Lung Cancer - Causes

The main causes of lung cancer (and cancer in general) include carcinogens (such as those in tobacco smoke), ionizing radiation, and viral infection.This exposure causes cumulative changes to the DNA in the tissue lining the bronchi of the lungs (the bronchial epithelium).As more tissue becomes damaged, eventually a cancer develops

Smoking
Smoking, particularly of cigarettes, is by far the main contributor to lung cancer.
In the United States, smoking is estimated to account for 87% of lung cancer cases (90% in men and 85% in women). Among male smokers, the lifetime risk of developing lung cancer is 17.2%. Among female smokers, the risk is 11.6%. This risk is significantly lower in non-smokers: 1.3% in men and 1.4% in women. Cigarette smoke contains over 60 known carcinogens including radioisotopes from the radon decay sequence, nitrosamine, and benzopyrene. Additionally, nicotine appears to depress the immune response to malignant growths in exposed tissue. The length of time a person smokes as well as the amount smoked increases the person's chance of developing lung cancer. If a person stops smoking, this chance steadily decreases as damage to the lungs is repaired and contaminant particles are gradually removed. Across the developed world, almost 90% of lung cancer deaths are caused by smoking. In addition, there is evidence that lung cancer in never-smokers has a better prognosis than in smokers, and that patients who smoke at the time of diagnosis have shorter survival than those who have quit.

Passive smoking—the inhalation of smoke from another's smoking—is a cause of lung cancer in non-smokers. Studies from the U.S., Europe, the UK, and Australia have consistently shown a significant increase in relative risk among those exposed to passive smoke. Recent investigation of sidestream smoke suggests it is more dangerous than direct smoke inhalation.


Radon gas

Radon is a colorless and odorless gas generated by the breakdown of radioactive radium, which in turn is the decay product of uranium, found in the earth's crust. The radiation decay products ionize genetic material, causing mutations that sometimes turn cancerous. Radon exposure is the second major cause of lung cancer after smoking. Radon gas levels vary by locality and the composition of the underlying soil and rocks. For example, in areas such as Cornwall in the UK (which has granite as substrata), radon gas is a major problem, and buildings have to be force-ventilated with fans to lower radon gas concentrations. The United States Environmental Protection Agency (EPA) estimates that one in 15 homes in the U.S. has radon levels above the recommended guideline of 4 picocuries per liter (pCi/L) (148 Bq/m³). Iowa has the highest average radon concentration in the United States; studies performed there have demonstrated a 50% increased lung cancer risk with prolonged radon exposure above the EPA's action level of 4 pCi/L.


Asbestos
Asbestos can cause a variety of lung diseases, including lung cancer. There is a synergistic effect between tobacco smoking and asbestos in the formation of lung cancer.[10] In the UK, asbestos accounts for 2–3% of male lung cancer deaths. Asbestos can also cause cancer of the pleura, called mesothelioma (which is different from lung cancer).


Viruses
Viruses are known to cause lung cancer in animals and recent evidence suggests similar potential in humans. Implicated viruses include human papillomavirus, JC virus, simian virus 40 (SV40), BK virus and cytomegalovirus. These viruses may affect the cell cycle and inhibit apoptosis, allowing uncontrolled cell division.



Originally from Wikipedia.org

Lung Cancer - Epidemiology

Worldwide, lung cancer is the most common cancer in terms of both incidence and mortality with 1.35 million new cases per year and 1.18 million deaths, with the highest rates in Europe and North America. The population segment most likely to develop lung cancer is over-fifties who have a history of smoking. Lung cancer is the second most commonly occurring form of cancer in most western countries, and it is the leading cancer-related cause of death. Although the rate of men dying from lung cancer is declining in western countries, it is actually increasing for women due to the increased takeup of smoking by this group. Among lifetime non-smokers, men have higher age-standardized lung cancer death rates than women.

Not all cases of lung cancer are due to smoking, but the role of passive smoking is increasingly being recognized as a risk factor for lung cancer, leading to policy interventions to decrease undesired exposure of non-smokers to others' tobacco smoke. Emissions from automobiles, factories and power plants also pose potential risks.

Eastern Europe has the highest lung cancer mortality among men, while northern Europe and the U.S. have the highest mortality among women.Lung cancer incidence is currently less common in developing countries. With increased smoking in developing countries, the incidence is expected to increase in the next few years, notably in China[ and India.

Lung cancer incidence (by country) has an inverse correlation with sunlight and UVB exposure. One possible explanation is a preventative effect of vitamin D (which is produced in the skin on exposure to sunlight).


Originally from Wikipedia.org

10 method of release Pressure and Anxiety

Pressure and Anxiety not only causing Mental illness but also cancer. To release presure and anxiety, life will becaome better and live in happiness.

1. Tell about your pressure
Tell someone you would like to tell.
Remember that share the pressure, the pressure will reduce half. Share your hapiness, your happiness will double up.

2.Write out
when facing a problem, not to hide from the issue, write it down. This might help you to solve the problem, at least your pressure have been release out.

3. Exhaled pressure
Feeling heavy pressure, the most simple, rapid method is deep breathing, which is deeply absorbing anger, obturator two, three seconds, then slightly open mouth, exhaled slowly, so repeated several times, will resume normal blood circulation, heart rate slow down, and more natural feeling calm.

4. Sport
To find a quiet place outdoors, jogging or walking 20 to 30 minutes, the whole body muscle relaxant.

5.Punch pressure
if the pressure from the high authority and or powerful party, then you can find a sandbag or puppets, then punch it until you mind feel better.

6. Bath
Nice bubble bath can take away your pressure. Enjoy it and let the pressure claim dawn.

7. Sing
Let your voice bring the pressure out from your body. After sing, the pressure might be gone.

8. And some other methed like cheering, crying aloud might help you out from pressure as well. Just open your heart and find the way suitable for you.

Fnally, time keep running no matter what happen, either you choose to leave in pressure or live in happy. Open your mind and open your heart, tomorrow will always better.

Peritoneal Mesothelioma - History

There is a lot of depressing information on the internet about peritoneal mesothelioma and the survival associated with this cancer. Reading it you would think that no one has ever survived peritoneal mesothelioma beyond a year or so. This information is far from comprehensive. To help balance some of the negative information that is so prevalent on the Web, we present some case histories of long-term peritoneal mesothelioma survival as published in the peer reviewed medical literature.

9 Years +
In November 1979, a 73 year-old man had abdominal pain and distension and was found to have an abdominal mass. A laparotomy was performed that revealed peritoneal malignancy with ascites. A biopsy demonstrated that the tumor was malignant peritoneal mesothelioma. No special treatment was recommended other than draining of the ascites. In spite of the continuing ascites and the gradually-enlarging abdominal masses, the patient enjoys good health, and lives independently at home. How many more years (in excess of 9) this patient lived with peritoneal mesothelioma is not known.
See: Norman, P.E. and Whitaker, D., Nine-Year Survival in a Case of Untreated Peritoneal Mesothelioma, Med J Aust 1989; 150: 43-44.

15 Years +
A woman was diagnosed with peritoneal mesothelioma. She had surgery (“total excision”). Seven years later the peritoneal mesothelioma recurred and she had another surgery (“reexcision”). She remains well 15 years after the initial diagnosis. The patient did not receive chemotherapy.
See: Asensio, J.A., et al., Primary Malignant Peritoneal Mesothelioma: A Report of Seven Cases and a Review of the Literature, Arch Surg; Nov 1990, 125, 1477-1480.

17 + Years
In 1962, a 31 year-old woman had abdominal pain for several months and a mass was detected. She underwent exploratory laparotomy which found tumor nodules spread throughout her abdomen. The diagnosis of peritoneal mesothelioma was made. Complete surgical removal of the tumor was not possible. She was treated with radioactive phosphorus, radiation, and oral chemotherapy (cytoxan). She remained well for 17 years. In 1979 she had recurrent peritoneal mesothelioma. She was treated with cytoxan again and continued to live as of the writing of the published medical report.

5 step for famale to have beauty figure

Single muscle exercise is not the trend of the campaign, the world's top-class coach to mind are how to combine different types of movement to help practitioners achieve all-round balance and release tension.


1 A hands lateral lumbar action
Lateral lumbar hands: hands extended to the left, until the maximum, further downward rotation, stretching to the limit, to the right,then to the same limit, shrinkage abdomen to bring your top body up.
Imagine the entire fan-like movements such as open and close.


2 limit extension
No pause between every movement, the whole cycle of the same movements such as a clock. Each action should be extended to the limit as far as possible.


3 Strength up chest and shrinkage hip movements
Strength up chest and use your muscle to shrinkage hip. At the same time move your Cervical upward.Keep you hip shringkage and enforce upward by your leg muscle.
Beginner can use a paper as supporting by clamp it at your Knee & Thigh, this might help to maintain the shrinkage.



4.Abdomen Shrinkage
sharinkage abdomen and extend your hand to in front to form your body into a cave-like.Then lying down slowly, feeling his body like a slow rolling wheels.he mo Ensure that you must keep the action slow.




5 fantasy touch wall
Touch the wall: stretching arms (Imaging you are touch a walls in far distance), from the sacral Sacrococcygeal forward a little bit extended in an effort to pull back to a maximum point.
To the contrary, the strength, like a cat wings, and power from the lower abdomen, first mentioned at lower abdomen. A little bit up from the physical body. The whole process releases such as the bullwhip.

Lung Cancer - Signs and Symptoms

Symptoms that suggest lung cancer include:

  • Dyspnea (shortness of breath)
  • Hemoptysis (coughing up blood)
  • Chronic coughing or change in regular coughing pattern
  • Wheezing
  • Chest pain or pain in the abdomen
  • Cachexia (weight loss), fatigue and loss of appetite
  • Dysphonia (hoarse voice)
  • Clubbing of the fingernails (uncommon)
  • Dysphagia (difficulty swallowing).


If the cancer grows in the airway, it may obstruct airflow, causing breathing difficulties. This can lead to accumulation of secretions behind the blockage, predisposing the patient to pneumonia. Many lung cancers have a rich blood supply. The surface of the cancer may be fragile, leading to bleeding from the cancer into the airway. This blood may subsequently be coughed up.

Depending on the type of tumor, so-called paraneoplastic phenomena may initially attract attention to the disease. In lung cancer, these phenomena may include Lambert-Eaton myasthenic syndrome (muscle weakness due to auto-antibodies), hypercalcemia or syndrome of inappropriate antidiuretic hormone (SIADH). Tumors in the top (apex) of the lung, known as Pancoast tumors, may invade the local part of the sympathetic nervous system, leading to changed sweating patterns and eye muscle problems (a combination known as Horner's syndrome), as well as muscle weakness in the hands due to invasion of the brachial plexus.

Many of the symptoms of lung cancer (bone pain, fever, weight loss) are nonspecific; in the elderly, these may be attributed to comorbid illness. In many patients, the cancer has already spread beyond the original site by the time they have symptoms and seek medical attention. Common sites of metastasis include the bone, such as the spine (causing back pain and occasionally spinal cord compression), the liver and the brain. About 10% of people with lung cancer do not have symptoms at diagnosis; these cancers are incidentally found on routine chest x-rays.



Originally from Wikipedia.org

Lung Cancer - Classification

The vast majority of lung cancers are carcinomas—malignancies that arise from epithelial cells. There are two main types of lung carcinoma, categorized by the size and appearance of the malignant cells seen by a histopathologist under a microscope: non-small cell (80.4%) and small-cell (16.8%) lung carcinoma.This classification, based on histological criteria, has important implications for clinical management and prognosis of the disease


Non-small cell lung carcinoma (NSCLC)
The non-small cell lung carcinomas are grouped together because their prognosis and management are similar. There are three main sub-types: squamous cell lung carcinoma, adenocarcinoma and large cell lung carcinoma.
Accounting for 31.1% of lung cancers, squamous cell lung carcinoma usually starts near a central bronchus. Cavitation and necrosis within the center of the cancer is a common finding. Well-differentiated squamous cell lung cancers often grow more slowly than other cancer types.
Adenocarcinoma accounts for 29.4% of lung cancers. It usually originates in peripheral lung tissue. Most cases of adenocarcinoma are associated with smoking. However, among people who have never smoked ("never-smokers"), adenocarcinoma is the most common form of lung cancer. A subtype of adenocarcinoma, the bronchioloalveolar carcinoma, is more common in female never-smokers, and may have different responses to treatment.
Accounting for 10.7% of lung cancers, large cell lung carcinoma is a fast-growing form that develops near the surface of the lung. It is often poorly differentiated and tends to metastasize early.


Small cell lung carcinoma (SCLC)
Small cell lung carcinoma (microscopic view of a core needle biopsy)
Small cell lung carcinoma (SCLC, also called "oat cell carcinoma") is less common.
It tends to arise in the larger airways (primary and secondary bronchi) and grows rapidly, becoming quite large.] The "oat" cell contains dense neurosecretory granules (vesicles containing neuroendocrine hormones) which give this an endocrine/paraneoplastic syndrome association. While initially more sensitive to chemotherapy, it ultimately carries a worse prognosis and is often metastatic at presentation. Small cell lung cancers are divided into Limited stage and Extensive stage disease. This type of lung cancer is strongly associated with smoking.


Metastatic cancers
The lung is a common place for metastasis from tumors in other parts of the body. These cancers are identified by the site of origin, thus a breast cancer metastasis to the lung is still known as breast cancer. They often have a characteristic round appearance on chest x-ray. Primary lung cancers themselves most commonly metastasize to the adrenal glands, liver, brain, and bone.

Staging
Lung cancer staging is an assessment of the degree of spread of the cancer from its original source. It is an important factor affecting the prognosis and potential treatment of lung cancer. Non-small cell lung carcinoma is staged from IA ("one A", best prognosis) to IV ("four", worst prognosis). Small cell lung carcinoma is classified as limited stage if it is confined to one half of the chest and within the scope of a single radiotherapy field.
Otherwise it is extensive stage.



Origenally Form :Wikipedia.org

Sport Vs Fat Burning

Sport is the most healthy way to keep your body fit. To lose 1 kg of fat , need to consume 7,700 calories. Let's see the sport listed and how good the effectiveness of remove the fat.

Swimming:
Consumption of calories every half hour 175 cards. It is a coordinating body movements sport and good for the empowerment of cardiorespiratory function, exercise flexibility and strength.
Besides, It is also beneficial to the patient back to health, after the restoration of women's reproductive fitness, and the elder people.

Athletics:
Every half hour calorie consumption is 450 cards.
It can be trained human body.

Basketball:
Consumption of calories every half hour 250 card.
It can increase flexibility and strengthen cardiorespiratory function.


Cycling:
Consumption of calories every half hour 330 cards.
Good for heart and lungs, and stregthen the legs.


Horse Riding:
Consumption of calories every half hour 175 cards.
Train your leg muscle and your mind.

Water Skiing:
Consumption of calories every half hour 240 cards.
Good for whole body, limbs, muscle and the body balancing between the training role.

Golf:
Consumption of calories every half hour 125 cards.
It results from the exercise of the need to travel long distances and hitting action. If so as to maintain a beautiful lines is extremely advantageous.

Jogging:
Consumption of calories every half hour 300 cards.
Benefit cardiopulmonary and blood circulation. Run the longer distance, the greater the consumption of calories.

Walking:
Consumption of calories every half hour 75 cards.
On the enhancement of cardiopulmonary function useful, it can improve blood circulation, joint activities and contribute to weight loss.

Roller-blading:
Consumption of calories every half hour 175 cards.
Body can be enhanced flexibility and strength of the partial muscle.

Rope Skipping:
Consumption of calories every half hour 400 cards.
This is a fitness campaign to improve people's posture. People over the age of 35 can not do too much rope skipping.

Squash:
Consumption of calories every half hour 300 cards.
Better flexibility for leg, weight loss, increased speed capability. However, people with poor heart and lung function, it is not appropriate in this campaign.

Tennis:
Consumption of calories every half hour 220 cards.
This is a fierce campaign, it can exercise cardiopulmonary function, exercise flexibility.

Table Tennis:
Consumption of calories every half hour 180 cards.
Is a systemic campaign to benefit heart, can be the focus of training and coordination of movement.

Volleyball:
Consumption of calories every half hour 175 cards.
Main increased flexibility, jumping ability and physical strength, cardiovascular benefit.

Sport Vs Fat burning (Table)

Below is the table of Sport Vs Fat burning. Athletics and Rope Skipping providing a better result compare with others according to the table.



Consumption of calories mean more fat are getting burned. Even the higher consumption provide a better fat burning. However, we need to consider whether the sport is suit for ourself. More related information can look for title " Sport Vs Fat Burning"

Lung Cancer - Prognosis

Prognostic factors in non- small-cell lung cancer include presence or absence of pulmonary symptoms, tumor size, cell type (histology), degree of spread (stage) and metastases to multiple lymph nodes, and vascular invasion. For patients with inoperable disease, prognosis is adversely affected by poor performance status and weight loss of more than 10%. Prognostic factors in small-cell lung cancer include performance status, gender, stage of disease, and involvement of the central nervous system or liver at the time of diagnosis.

For non-small cell lung carcinoma, prognosis is generally poor. Following complete surgical resection of stage IA disease, five-year survival is 67%. With stage IB disease, five-year survival is 57%. The 5-year survival rate of patients with stage IV NSCLC is about 1%.

For small cell lung carcinoma, prognosis is also generally poor. The overall five-year survival for patients with SCLC is about 5%. Patients with extensive-stage SCLC have an average five-year survival rate of less than 1%. The median survival time for limited-stage disease is 20 months, with a five-year survival rate of 20%.

According to data provided by the National Cancer Institute, the median age of incidence of lung cancer is 70 years, and the median age of death by lung cancer 71 years.

Lung Cancer - Signs & Symtoms

The early symptoms of lung cancer

Ten following symptoms we should be on high alert:

  1. Body such as breasts, abdomen or neck of the growing mass;
  2. A non-physical injury caused by ulcers, especially perishable Fuyu, such as skin, buccal mucosa, and tongue ulcer, etc.;
  3. Heizhi suddenly increased, hair loss or rupture hemorrhage;
  4. Plugging long nose, nasal bleeding, unilateral headache with or diplopia;
  5. Persistent dry cough and bloody sputum or persistent hoarseness;
  6. Increasing the swallowing will not ring true or nausea after eating at the sternum bulging, burning sensation;
  7. Stool habits change, alternating constipation and diarrhea or recurrent hematochezia;
  8. Unexplained indigestion or long-term sexual anorexia, emaciated;
  9. A painless hematuria;
  10. Middle-aged and older women in irregular vaginal bleeding or Leucorrhea increasing.

Above normal in one or more of the performance should be cause for concern, to hospital checks to clear reasons. However, it must be pointed out that more than a certain kind of performance may be related to the early symptoms similar to the tumor, but not all people with these symptoms tumor disease, and many more other diseases can also cause the various manifestations of the above.

How early detection of cancer?

Early detection of cancer related to the first, is timely to conduct self-examination, as many tumor growth in the surface, it can be self-censorship. Found that certain internal growth in the tumor, as growth in certain special location, can cause certain symptoms, such as the 10 symptoms of certain performance, early detection of these self-abnormal feeling, and promptly requested the doctors for a medical examination, there will be a clear diagnosis . The older people, the nearest regular inspection, and we can rule out the cancer and early detection.

Health Care - Diet Therapy

Eggs slimming food therapy - 1 week 26 eggs, total two weeks need 52 eggs, 10 kg weight loss two weeks.

Denmark National Hospital make this recipe as an obese patients by prescription, unlike the general method of dieting. Take the eggs slimming food therapy, in the two weeks after that the Organization of the chemical will change, the organization refused to excess nutrients, reduce appetite and thus difficult to body fat, but with the starch diet food to avoid.

Take the eggs slimming food therapy, prescription should be included in the finished food, if for some reason, weight reduction process was interrupted when, it must be re-started from scratch.



Monday
Breakfast
Boiled egg three, a grapefruit, an Andean soil, coffee.
Lunch
Boiled egg three, tomatoes, coffee.
Dinner
Boiled egg three, cucumber, carrots, celery made vinegar stains vegetable salad vegetables.



Tuesday
Breakfast
Boiled Eggs three, grapefruit, coffee.
Lunch
Boiled Eggs three, Grapefruit, an Andean soil, coffee.
Dinner
Steak, tomatoes, celery, vegetables, vinegar stains vegetables, coffee.


Wednesday
Breakfast
Boiled egg one grapefruit, coffee.
Lunch
Vegetable salad, grapefruit, an Andean soil, coffee.
Dinner
Boiled Egg two, mutton, celery, tomatoes, vinegar stains vegetables, coffee.


Thursday
Breakfast
Boile Egg one grapefruit, coffee.
Lunch
Vegetable salad, grapefruit, an Andean soil, coffee.
Dinner
Boiled egg three, cheese, spinach, coffee.


Friday
Breakfast
Boiled egg one grapefruit, an Andean soil, coffee.
Lunch
Boiled egg three, spinach, a Slovak soil, coffee.
Dinner
Fish, vegetable salad, two Andean soil, coffee.


Saturday
Breakfast
Boiled egg 2, Grapefruit, an Andean soil, coffee.
Lunch
Fruit salad (do not use apples, bananas, canned fruit).
Dinner
Steak, celery, tomatoes, vinegar stains vegetables, coffee.


Sunday
Breakfast
Boiled Egg one grapefruit, coffee.
Lunch
Cold roast chicken, tomatoes, grapefruit, coffee. D
inner
Vegetable salad, grilled chicken, tomatoes, boiled cabbage, celery, grapefruit, coffee.



Notes:
Do not apply Salad oil to make the salad.
No sugar or milk in Coffee
Grilled meat only , can not use any oil.
Fish to eat can be sashimi, steam or grill.
Salt to use as less as possible.
The weight of a chicken in the leg, Mutton is the weight of 135 grams. Beef about 50-200 grams.
Must be boiled eggs.


Anyway, the best way to keep fit is Exercises and take a balance food.

Lung Cancer - History

Lung cancer was extremely rare before the advent of cigarette smoking. Lung cancer was first recognized as a distinct disease in 1761. Different aspects of lung cancer were described further in 1810.[109] Malignant lung tumors made up only 1% of all cancers seen at autopsy in 1878, but had risen to 10–15% by the early 1900s. Case reports in the medical literature numbered only 374 worldwide in 1912. A review of autopsies showed that the incidence of lung cancer had increased from 0.3% in 1852 to 5.66% in 1952. In Germany, in 1929 physician Fritz Lickint recognized the link between smoking and lung cancer. This led to an aggressive anti-smoking campaign. The British Doctors Study, published in the 1950s, was the first solid epidemiological evidence of the link between lung cancer and smoking. As a result, in 1964 the Surgeon General of the United States recommended that smokers should stop smoking.

The connection with radon gas was first recognized among miners in the Ore Mountains near Schneeberg, Saxony. Silver has been mined there since 1470. However these mines are rich in uranium, with accompanying radium and radon gas. Miners developed a disproportionate amount of lung disease, eventually recognized as lung cancer in the 1870s. An estimated 75% of former miners died from lung cancer. Despite this discovery, mining continued into the 1950s due to the USSR's demand for uranium.


Treatment
The first successful pneumonectomy for lung cancer was carried out in 1933. Initially, pneumonectomy was the surgical treatment of choice.[118] However with improvements in cancer staging and surgical techniques, lobectomy with lymph node dissection has now become the treatment of choice.

Palliative radiotherapy has been used since the 1940s. Radical radiotherapy, initially used in the 1950s, was an attempt to use larger radiation doses in patients with relatively early stage lung cancer, but who were otherwise unfit for surgery. In 1997, continuous hyperfractionated accelerated radiotherapy (CHART) was seen as an improvement over conventional radical radiotherapy.[

With small cell lung carcinoma, initial attempts in the 1960s at surgical resection and radical radiotherapy were unsuccessful. In the 1970s, successful chemotherapy regimens were developed.



Originally from Wikipedia.org

Lung Cancer - Introduction

Lung cancer is a disease of uncontrolled cell growth in tissues of the lung. This growth may lead to metastasis, invasion of adjacent tissue and infiltration beyond the lungs. The vast majority of primary lung cancers are carcinomas of the lung, derived from epithelial cells. Lung cancer, the most common cause of cancer-related death in men and the second most common in women, is responsible for 1.3 million deaths worldwide annually. The most common symptoms are shortness of breath, coughing (including coughing up blood), and weight loss.


The main types of lung cancer are small cell lung carcinoma and non-small cell lung carcinoma. This distinction is important because the treatment varies; non-small cell lung carcinoma (NSCLC) is sometimes treated with surgery, while small cell lung carcinoma (SCLC) usually responds better to chemotherapy and radiation. The most common cause of lung cancer is long term exposure to tobacco smoke. The occurrence of lung cancer in non-smokers, who account for fewer than 10% of cases, appears to be due to a combination of genetic factors, radon gas, asbestos, and air pollution, including second-hand smoke.


Lung cancer may be seen on chest x-ray and computed tomography (CT scan). The diagnosis is confirmed with a biopsy. This is usually performed via bronchoscope or CT-guided biopsy. Treatment and prognosis depend upon the histological type of cancer, the stage (degree of spread), and the patient's performance status. Possible treatments include surgery, chemotherapy, and radiotherapy. With treatment, the five-year survival rate is 14%.


Origenally Form :Wikipedia.org

Cancer - Preventive

Cancer prevention is defined as active measures to decrease the incidence of cancer. This can be accomplished by avoiding carcinogens or altering their metabolism, pursuing a lifestyle or diet that modifies cancer-causing factors and/or medical intervention (chemoprevention, treatment of pre-malignant lesions). The epidemiological concept of "prevention" is usually defined as either primary prevention, for people who have not been diagnosed with a particular disease, or secondary prevention, aimed at reducing recurrence or complications of a previously diagnosed illness.


Observational epidemiological studies that show associations between risk factors and specific cancers mostly serve to generate hypotheses about potential interventions that could reduce cancer incidence or morbidity. Randomized controlled trials then test whether hypotheses generated by epidemiological trials and laboratory research actually result in reduced cancer incidence and mortality. In many cases, findings from observational epidemiological studies are not confirmed by randomized controlled trials.


About a third of the twelve most common cancers worldwide are due to nine potentially modifiable risk factors. Men with cancer are twice as likely as women to have a modifiable risk factor for their disease. The nine risk factors are tobacco smoking, excessive alcohol use, diet low in fruit and vegetables, limited physical exercise, human papillomavirus infection (unsafe sex), urban air pollution, domestic use of solid fuels, and contaminated injections (hepatitis B and C).




Modifiable ("lifestyle") risk factors

Examples of modifiable cancer risk factors include alcohol consumption (associated with increased risk of oral, esophageal, breast, and other cancers), smoking (although 20% of women with lung cancer have never smoked, versus 10% of men), physical inactivity (associated with increased risk of colon, breast, and possibly other cancers), and being overweight (associated with colon, breast, endometrial, and possibly other cancers). Based on epidemiologic evidence, it is now thought that avoiding excessive alcohol consumption may contribute to reductions in risk of certain cancers; however, compared with tobacco exposure, the magnitude of effect is modest or small and the strength of evidence is often weaker. Other lifestyle and environmental factors known to affect cancer risk (either beneficially or detrimentally) include certain sexually transmitted diseases, the use of exogenous hormones, exposure to ionizing radiation and ultraviolet radiation, and certain occupational and chemical exposures.


Every year, at least 200,000 people die worldwide from cancer related to their workplace. Millions of workers run the risk of developing cancers such as lung cancer and mesothelioma from inhaling asbestos fibers and tobacco smoke, or leukemia from exposure to benzene at their workplaces. Currently, most cancer deaths caused by occupational risk factors occur in the developed world. It is estimated that approximately 20,000 cancer deaths and 40,000 new cases of cancer each year in the U.S. are attributable to occupation.


See alcohol and cancer for more on that topic.




Diet
Main article: Diet and cancer
The consensus on diet and cancer is that obesity increases the risk of developing cancer. Particular dietary practices often explain differences in cancer incidence in different countries (e.g. gastric cancer is more common in Japan, while colon cancer is more common in the United States). Studies have shown that immigrants develop the risk of their new country, often within one generation, suggesting a substantial link between diet and cancer. Whether reducing obesity in a population also reduces cancer incidence is unknown.


Despite frequent reports of particular substances (including foods) having a beneficial or detrimental effect on cancer risk, few of these have an established link to cancer. These reports are often based on studies in cultured cell media or animals. Public health recommendations cannot be made on the basis of these studies until they have been validated in an observational (or occasionally a prospective interventional) trial in humans.


Proposed dietary interventions for primary cancer risk reduction generally gain support from epidemiological association studies. Examples of such studies include reports that reduced meat consumption is associated with decreased risk of colon cancer, and reports that consumption of coffee is associated with a reduced risk of liver cancer. Studies have linked consumption of grilled meat to an increased risk of stomach cancer, colon cancer, breast cancer, and pancreatic cancer, a phenomenon which could be due to the presence of carcinogens such as benzopyrene in foods cooked at high temperatures.


A 2005 secondary prevention study showed that consumption of a plant-based diet and lifestyle changes resulted in a reduction in cancer markers in a group of men with prostate cancer who were using no conventional treatments at the time. These results were amplified by a 2006 study in which over 2,400 women were studied, half randomly assigned to a normal diet, the other half assigned to a diet containing less than 20% calories from fat. The women on the low fat diet were found to have a markedly lower risk of breast cancer recurrence, in the interim report of December, 2006.


Recent studies have also demonstrated potential links between some forms of cancer and high consumption of refined sugars and other simple carbohydrates. Although the degree of correlation and the degree of causality is still debated, some organizations have in fact begun to recommend reducing intake of refined sugars and starches as part of their cancer prevention regemins.




Vitamins
There is a concept that cancer can be prevented through vitamin supplementation stems from early observations correlating human disease with vitamin deficiency, such as pernicious anemia with vitamin B12 deficiency, and scurvy with Vitamin C deficiency. This has largely not been proven to be the case with cancer, and vitamin supplementation is largely not proving effective in preventing cancer. The cancer-fighting components of food are also proving to be more numerous and varied than previously understood, so patients are increasingly being advised to consume fresh, unprocessed fruits and vegetables for maximal health benefits.


The Canadian Cancer Society has advised Canadians that the intake of vitamin D has shown a reduction of cancers by close to 60%, and at least one study has shown a specific benefit for this vitamin in preventing colon cancer.


Vitamin D and its protective effect against cancer has been contrasted with the risk of malignancy from sun exposure. Since exposure to the sun enhances natural human production of vitamin D, some cancer researchers have argued that the potential deleterious malignant effects of sun exposure are far outweighed by the cancer-preventing effects of extra vitamin D synthesis in sun-exposed skin. In 2002, Dr. William B. Grant claimed that 23,800 premature cancer deaths occur in the US annually due to insufficient UVB exposure (apparently via vitamin D deficiency). This is higher than 8,800 deaths occurred from melanoma or squamous cell carcinoma, so the overall effect of sun exposure might be beneficial. Another research group estimates that 50,000–63,000 individuals in the United States and 19,000 - 25,000 in the UK die prematurely from cancer annually due to insufficient vitamin D.


The case of beta-carotene provides an example of the importance of randomized clinical trials. Epidemiologists studying both diet and serum levels observed that high levels of beta-carotene, a precursor to vitamin A, were associated with a protective effect, reducing the risk of cancer. This effect was particularly strong in lung cancer. This hypothesis led to a series of large randomized clinical trials conducted in both Finland and the United States (CARET study) during the 1980s and 1990s. This study provided about 80,000 smokers or former smokers with daily supplements of beta-carotene or placebos. Contrary to expectation, these tests found no benefit of beta-carotene supplementation in reducing lung cancer incidence and mortality. In fact, the risk of lung cancer was slightly, but not significantly, increased by beta-carotene, leading to an early termination of the study.


Results reported in the Journal of the American Medical Association (JAMA) in 2007 indicate that folic acid supplementation is not effective in preventing colon cancer, and folate consumers may be more likely to form colon polyps.




Chemoprevention
The concept that medications could be used to prevent cancer is an attractive one, and many high-quality clinical trials support the use of such chemoprevention in defined circumstances.
Daily use of tamoxifen, a selective estrogen receptor modulator (SERM), typically for 5 years, has been demonstrated to reduce the risk of developing breast cancer in high-risk women by about 50%. A recent study reported that the selective estrogen receptor modulator raloxifene has similar benefits to tamoxifen in preventing breast cancer in high-risk women, with a more favorable side effect profile.


Raloxifene is a SERM like tamoxifen; it has been shown (in the STAR trial) to reduce the risk of breast cancer in high-risk women equally as well as tamoxifen. In this trial, which studied almost 20,000 women, raloxifene had fewer side effects than tamoxifen, though it did permit more DCIS to form.
Finasteride, a 5-alpha-reductase inhibitor, has been shown to lower the risk of prostate cancer, though it seems to mostly prevent low-grade tumors. The effect of COX-2 inhibitors such as rofecoxib and celecoxib upon the risk of colon polyps have been studied in familial adenomatous polyposis patients and in the general population. In both groups, there were significant reductions in colon polyp incidence, but this came at the price of increased cardiovascular toxicity.




Genetic testing
Genetic testing for high-risk individuals is already available for certain cancer-related genetic mutations. Carriers of genetic mutations that increase risk for cancer incidence can undergo enhanced surveillance, chemoprevention, or risk-reducing surgery. Early identification of inherited genetic risk for cancer, along with cancer-preventing interventions such as surgery or enhanced surveillance, can be lifesaving for high-risk individuals.



Vaccination
Considerable research effort is now devoted to the development of vaccines to prevent infection by oncogenic infectious agents, as well as to mount an immune response against cancer-specific epitopes) and to potential venues for gene therapy for individuals with genetic mutations or polymorphisms that put them at high risk of cancer.

As reported above, a preventive human papillomavirus vaccine exists that targets certain sexually transmitted strains of human papillomavirus that are associated with the development of cervical cancer and genital warts. The only two HPV vaccines on the market as of October 2007 are Gardasil and Cervarix.


Screening
Cancer screening is an attempt to detect unsuspected cancers in an asymptomatic population. Screening tests suitable for large numbers of healthy people must be relatively affordable, safe, noninvasive procedures with acceptably low rates of false positive results. If signs of cancer are detected, more definitive and invasive follow up tests are performed to confirm the diagnosis.
Screening for cancer can lead to earlier diagnosis in specific cases. Early diagnosis may lead to extended life, but may also falsely prolong the lead time to death through lead time bias or length time bias.

A number of different screening tests have been developed for different malignancies. Breast cancer screening can be done by breast self-examination, though this approach was discredited by a 2005 study in over 300,000 Chinese women. Screening for breast cancer with mammograms has been shown to reduce the average stage of diagnosis of breast cancer in a population. Stage of diagnosis in a country has been shown to decrease within ten years of introduction of mammographic screening programs. Colorectal cancer can be detected through fecal occult blood testing and colonoscopy, which reduces both colon cancer incidence and mortality, presumably through the detection and removal of pre-malignant polyps. Similarly, cervical cytology testing (using the Pap smear) leads to the identification and excision of precancerous lesions. Over time, such testing has been followed by a dramatic reduction of cervical cancer incidence and mortality. Testicular self-examination is recommended for men beginning at the age of 15 years to detect testicular cancer. Prostate cancer can be screened using a digital rectal exam along with prostate specific antigen (PSA) blood testing, though some authorities (such as the US Preventive Services Task Force) recommend against routinely screening all men.

Screening for cancer is controversial in cases when it is not yet known if the test actually saves lives. The controversy arises when it is not clear if the benefits of screening outweigh the risks of follow-up diagnostic tests and cancer treatments. For example: when screening for prostate cancer, the PSA test may detect small cancers that would never become life threatening, but once detected will lead to treatment. This situation, called overdiagnosis, puts men at risk for complications from unnecessary treatment such as surgery or radiation. Follow up procedures used to diagnose prostate cancer (prostate biopsy) may cause side effects, including bleeding and infection. Prostate cancer treatment may cause incontinence (inability to control urine flow) and erectile dysfunction (erections inadequate for intercourse). Similarly, for breast cancer, there have recently been criticisms that breast screening programs in some countries cause more problems than they solve. This is because screening of women in the general population will result in a large number of women with false positive results which require extensive follow-up investigations to exclude cancer, leading to having a high number-to-treat (or number-to-screen) to prevent or catch a single case of breast cancer early.

Cervical cancer screening via the Pap smear has the best cost-benefit profile of all the forms of cancer screening from a public health perspective as, being largely caused by a virus, it has clear risk factors (sexual contact), and the natural progression of cervical cancer is that it normally spreads slowly over a number of years therefore giving more time for the screening program to catch it early. Moreover, the test itself is easy to perform and relatively cheap.

For these reasons, it is important that the benefits and risks of diagnostic procedures and treatment be taken into account when considering whether to undertake cancer screening.
Use of medical imaging to search for cancer in people without clear symptoms is similarly marred with problems. There is a significant risk of detection of what has been recently called an incidentaloma - a benign lesion that may be interpreted as a malignancy and be subjected to potentially dangerous investigations. Recent studies of CT scan-based screening for lung cancer in smokers have had equivocal results, and systematic screening is not recommended as of July 2007. Randomized clinical trials of plain-film chest X-rays to screen for lung cancer in smokers have shown no benefit for this approach.

Canine cancer detection has shown promise, but is still in the early stages of research.



Originally from Wikipedia.org

Cancer - Pathophysiology


Cancers are caused by a series of mutations. Each mutation alters the behavior of the cell somewhat.

Cancer is fundamentally a disease of regulation of tissue growth. In order for a normal cell to transform into a cancer cell, genes which regulate cell growth and differentiation must be altered. Genetic changes can occur at many levels, from gain or loss of entire chromosomes to a mutation affecting a single DNA nucleotide. There are two broad categories of genes which are affected by these changes. Oncogenes may be normal genes which are expressed at inappropriately high levels, or altered genes which have novel properties. In either case, expression of these genes promotes the malignant phenotype of cancer cells. Tumor suppressor genes are genes which inhibit cell division, survival, or other properties of cancer cells. Tumor suppressor genes are often disabled by cancer-promoting genetic changes. Typically, changes in many genes are required to transform a normal cell into a cancer cell.


There is a diverse classification scheme for the various genomic changes which may contribute to the generation of cancer cells. Most of these changes are mutations, or changes in the nucleotide sequence of genomic DNA. Aneuploidy, the presence of an abnormal number of chromosomes, is one genomic change which is not a mutation, and may involve either gain or loss of one or more chromosomes through errors in mitosis.


Large-scale mutations involve the deletion or gain of a portion of a chromosome. Genomic amplification occurs when a cell gains many copies (often 20 or more) of a small chromosomal locus, usually containing one or more oncogenes and adjacent genetic material. Translocation occurs when two separate chromosomal regions become abnormally fused, often at a characteristic location. A well-known example of this is the Philadelphia chromosome, or translocation of chromosomes 9 and 22, which occurs in chronic myelogenous leukemia, and results in production of the BCR-abl fusion protein, an oncogenic tyrosine kinase.


Small-scale mutations include point mutations, deletions, and insertions, which may occur in the promoter of a gene and affect its expression, or may occur in the gene's coding sequence and alter the function or stability of its protein product. Disruption of a single gene may also result from integration of genomic material from a DNA virus or retrovirus, and such an event may also result in the expression of viral oncogenes in the affected cell and its descendants.






Epigenetics
Epigenetics is the study of the regulation of gene expression through chemical, non-mutational changes in DNA structure. The theory of epigenetics in cancer pathogenesis is that non-mutational changes to DNA can lead to alterations in gene expression. Normally, oncogenes are silent, for example, because of DNA methylation. Loss of that methylation can induce the aberrant expression of oncogenes, leading to cancer pathogenesis. Known mechanisms of epigenetic change include DNA methylation, and methylation or acetylation of histone proteins bound to chromosomal DNA at specific locations. Classes of medications, known as HDAC inhibitors and DNA methyltransferase inhibitors, can re-regulate the epigenetic signaling in the cancer cell.




Oncogenes
Oncogenes promote cell growth through a variety of ways. Many can produce hormones, a "chemical messenger" between cells which encourage mitosis, the effect of which depends on the signal transduction of the receiving tissue or cells. In other words, when a hormone receptor on a recipient cell is stimulated, the signal is conducted from the surface of the cell to the cell nucleus to effect some change in gene transcription regulation at the nuclear level. Some oncogenes are part of the signal transduction system itself, or the signal receptors in cells and tissues themselves, thus controlling the sensitivity to such hormones. Oncogenes often produce mitogens, or are involved in transcription of DNA in protein synthesis, which creates the proteins and enzymes responsible for producing the products and biochemicals cells use and interact with.


Mutations in proto-oncogenes, which are the normally quiescent counterparts of oncogenes, can modify their expression and function, increasing the amount or activity of the product protein. When this happens, the proto-oncogenes become oncogenes, and this transition upsets the normal balance of cell cycle regulation in the cell, making uncontrolled growth possible. The chance of cancer cannot be reduced by removing proto-oncogenes from the genome, even if this were possible, as they are critical for growth, repair and homeostasis of the organism. It is only when they become mutated that the signals for growth become excessive.


One of the first oncogenes to be defined in cancer research is the ras oncogene. Mutations in the Ras family of proto-oncogenes (comprising H-Ras, N-Ras and K-Ras) are very common, being found in 20% to 30% of all human tumours. Ras was originally identified in the Harvey sarcoma virus genome, and researchers were surprised that not only was this gene present in the human genome but that, when ligated to a stimulating control element, could induce cancers in cell line cultures.





Tumor suppressor genes
Tumor suppressor genes code for anti-proliferation signals and proteins that suppress mitosis and cell growth. Generally, tumor suppressors are transcription factors that are activated by cellular stress or DNA damage. Often DNA damage will cause the presence of free-floating genetic material as well as other signs, and will trigger enzymes and pathways which lead to the activation of tumor suppressor genes. The functions of such genes is to arrest the progression of the cell cycle in order to carry out DNA repair, preventing mutations from being passed on to daughter cells. The p53 protein, one of the most important studied tumor suppressor genes, is a transcription factor activated by many cellular stressors including hypoxia and ultraviolet radiation damage.


Despite nearly half of all cancers possibly involving alterations in p53, its tumor suppressor function is poorly understood. p53 clearly has two functions: one a nuclear role as a transcription factor, and the other a cytoplasmic role in regulating the cell cycle, cell division, and apoptosis.
The Warburg hypothesis is the preferential use of glycolysis for energy to sustain cancer growth. p53 has been shown to regulate the shift from the respiratory to the glycolytic pathway.
However, a mutation can damage the tumor suppressor gene itself, or the signal pathway which activates it, "switching it off". The invariable consequence of this is that DNA repair is hindered or inhibited: DNA damage accumulates without repair, inevitably leading to cancer.


Mutations of tumor suppressor genes that occur in germline cells are passed along to offspring, and increase the likelihood for cancer diagnoses in subsequent generations. Members of these families have increased incidence and decreased latency of multiple tumors. The tumor types are typical for each type of tumor suppressor gene mutation, with some mutations causing particular cancers, and other mutations causing others. The mode of inheritance of mutant tumor suppressors is that an affected member inherits a defective copy from one parent, and a normal copy from the other. For instance, individuals who inherit one mutant p53 allele (and are therefore heterozygous for mutated p53) can develop melanomas and pancreatic cancer, known as Li-Fraumeni syndrome. Other inherited tumor suppressor gene syndromes include Rb mutations, linked to retinoblastoma, and APC gene mutations, linked to adenopolyposis colon cancer. Adenopolyposis colon cancer is associated with thousands of polyps in colon while young, leading to colon cancer at a relatively early age. Finally, inherited mutations in BRCA1 and BRCA2 lead to early onset of breast cancer.


Development of cancer was proposed in 1971 to depend on at least two mutational events. In what became known as the Knudson two-hit hypothesis, an inherited, germ-line mutation in a tumor suppressor gene would only cause cancer if another mutation event occurred later in the organism's life, inactivating the other allele of that tumor suppressor gene.


Usually, oncogenes are dominant, as they contain gain-of-function mutations, while mutated tumor suppressors are recessive, as they contain loss-of-function mutations. Each cell has two copies of the same gene, one from each parent, and under most cases gain of function mutations in just one copy of a particular proto-oncogene is enough to make that gene a true oncogene. On the other hand, loss of function mutations need to happen in both copies of a tumor suppressor gene to render that gene completely non-functional. However, cases exist in which one mutated copy of a tumor suppressor gene can render the other, wild-type copy non-functional. This phenomenon is called the dominant negative effect and is observed in many p53 mutations.


Knudson’s two hit model has recently been challenged by several investigators. Inactivation of one allele of some tumor suppressor genes is sufficient to cause tumors. This phenomenon is called haploinsufficiency and has been demonstrated by a number of experimental approaches. Tumors caused by haploinsufficiency usually have a later age of onset when compared with those by a two hit process.




Cancer cell biology

Tissue can be organized in a continuous spectrum from normal to cancer.


Often, the multiple genetic changes which result in cancer may take many years to accumulate. During this time, the biological behavior of the pre-malignant cells slowly change from the properties of normal cells to cancer-like properties. Pre-malignant tissue can have a distinctive appearance under the microscope. Among the distinguishing traits are an increased number of dividing cells, variation in nuclear size and shape, variation in cell size and shape, loss of specialized cell features, and loss of normal tissue organization. Dysplasia is an abnormal type of excessive cell proliferation characterized by loss of normal tissue arrangement and cell structure in pre-malignant cells. These early neoplastic changes must be distinguished from hyperplasia, a reversible increase in cell division caused by an external stimulus, such as a hormonal imbalance or chronic irritation.


The most severe cases of dysplasia are referred to as "carcinoma in situ." In Latin, the term "in situ" means "in place", so carcinoma in situ refers to an uncontrolled growth of cells that remains in the original location and has not shown invasion into other tissues. Nevertheless, carcinoma in situ may develop into an invasive malignancy and is usually removed surgically, if possible.



Clonal evolution
The process of malignancy can be explained from an evolutionary perspective. Millions of years of biological evolution insure that the cellular metabolic changes that enable cancer to grow occur only very rarely. Most changes in cellular metabolism that allow cells to grow in a disorderly fashion lead to cell death. Cancer cells undergo a process analogous to natural selection, in that the few cells with new genetic changes that enhance their survival continue to multiply, and soon come to dominate the growing tumor, as cells with less favorable genetic change are outcompeted. This process is called clonal evolution. Tumors often continue to evolve in response to chemotherapy treatments, and on occasion aberrant cells may acquire resistance to particular anti-cancer pharmaceuticals.



Biological properties of cancer cells
In a 2000 article by Hanahan and Weinberg, the biological properties of malignant tumor cells were summarized as follows:


  • Acquisition of self-sufficiency in growth signals, leading to unchecked growth.

  • Loss of sensitivity to anti-growth signals, also leading to unchecked growth.

  • Loss of capacity for apoptosis, in order to allow growth despite genetic errors and external anti-growth signals.

  • Loss of capacity for senescence, leading to limitless replicative potential (immortality)
    Acquisition of sustained angiogenesis, allowing the tumor to grow beyond the limitations of passive nutrient diffusion.

  • Acquisition of ability to invade neighbouring tissues, the defining property of invasive carcinoma.

  • Acquisition of ability to build metastases at distant sites, the classical property of malignant tumors (carcinomas or others).

The completion of these multiple steps would be a very rare event without :



  • Loss of capacity to repair genetic errors, leading to an increased mutation rate (genomic instability), thus accelerating all the other changes.

  • These biological changes are classical in carcinomas; other malignant tumor may not need all to achieve them all. For example, tissue invasion and displacement to distant sites are normal properties of leukocytes; these steps are not needed in the development of Leukemia. The different steps do not necessarily represent individual mutations. For example, inactivation of a single gene, coding for the P53 protein, will cause genomic instability, evasion of apoptosis and increased angiogenesis.







Originally from Wikipedia.org

Peritoneal Mesothelioma - Introduction

Peritoneal mesothelioma in the primary peritoneal mesothelial organizations and epithelial tumors, clinical rarely see.

Disease Arguments can be divided into adenomatous mesothelioma,cystic mesothelioma and peritoneal malignant mesothelioma(PMM).

The first two are benign. Cystic mesothelioma was particularly prevalent in women,
Cause unknown, occurred in the surrounding pelvic or attachments, a single or multiple cystic masses; patients often palpable abdominal mass and attendance. PMM about vicious Mesothelioma of 30%; in its close relationship with exposure to asbestos, about 5% of the patients have a history of exposure ; asbestos fibers after oral intake through Translocation to the wall and peritoneal disease. Exposure to asbestos from confirmed, the disease incubation period could be as long as 25 to 40 years. But from 1951 to 1993 domestic 20 reported 161 cases of the literature only one case of PMM a history of exposure to asbestos. In the absence of a history of exposure to asbestos in the crowd, the incidence rate of about 1 / 1 million years, Infection may be related to certain genetic factors. Reported one case of international, PMM patients more than 40 years ago dioxide contacts glial
Thorium (Thorotrast) .

PMM often occur in men over 40 years of age. Dirty floor or layer can be permanently and peritoneal tumor can be a direct violation of abdominal, pelvic Organ, 50% to 70% of the patients with lymph node and (or) blood distant metastasis such as liver, kidney, adrenal gland, lung, bone and lymph nodes, etc..

Clinical manifestations of this disease Lack of specificity, have abdominal pain, constipation, abdominal distension, weight loss and other intestinal obstruction performance. Physical or ascites can be found, such as abdominal mass. Ascites To exudate, some bloody. The disease often misdiagnosed as tuberculosis peritonitis and recurrent spontaneous bacterial peritonitis, mesenteric inflammation or peritoneal carcinomatosis Etc..

Ascites hyaluronic acid increased significantly,> 0.8 g / L found only PMM. Ascites exfoliated cells also check some value, but the result often difficult Judgement. -125 Serum carbohydrate antigen (CA125) increased help diagnose this disease .

B-ultrasound and CT performance varied, the typical irregular, peritoneal Thickening and omental adhesion was popular among hungry students, mesenteric a tissue sample; CT can also display enhanced Peripancreatic large mass, or intraperitoneal substantive diffuse large Mass, and bowel and mesenteric violations or peritoneal nodules, or a cystic mass, multi-with varying degrees of ascites .

Guided by ultrasound or CT wear Thorn biopsy a certain value. PMM diagnostic laparoscopy is a simple and effective method microscope peritoneum, omentum diffuse plaques and nodules, Open biopsy and pathological examination. We sent one case of 83-year-old male patient with laparoscopy, peritoneal biopsy report mesothelial cell hyperplasia, After immunohistochemical tests confirmed the PMM. Butchart, and so will be divided into four PMM: Phase I, confined to the peritoneal tumor; Ⅱ stage, tumor invasion Intra-abdominal lymph nodes; Ⅲ, tumor metastasis to the lymph nodes outside the abdominal cavity; Ⅳ period, blood distant metastasis. The above categories will help choose the method of treatment.


PMM has no effective standard treatment. Poor prognosis, the survival period after diagnosis in a median survival of more than two years of less than 20%. Main
Dioxin or died of intestinal obstruction of the death of little distant metastasis and tumor.

Cancer - Causes

Main article: Carcinogenesis
Cancer is a diverse class of diseases which differ widely in their causes and biology. The common thread in all known cancers is the acquisition of abnormalities in the genetic material of the cancer cell and its progeny. Research into the pathogenesis of cancer can be divided into three broad areas of focus. The first area of research focuses on the agents and events which cause or facilitate genetic changes in cells destined to become cancer. Second, it is important to uncover the precise nature of the genetic damage, and the genes which are affected by it. The third focus is on the consequences of those genetic changes on the biology of the cell, both in generating the defining properties of a cancer cell, and in facilitating additional genetic events, leading to further progression of the cancer.


Chemical carcinogens

Cancer pathogenesis is traceable back to DNA mutations that impact cell growth and metastasis. Substances that cause DNA mutations are known as mutagens, and mutagens that cause cancers are known as carcinogens. Particular substances have been linked to specific types of cancer. Tobacco smoking is associated with lung cancer and bladder cancer. Prolonged exposure to asbestos fibers is associated with mesothelioma.

Many mutagens are also carcinogens, but some carcinogens are not mutagens. Alcohol is an example of a chemical carcinogen that is not a mutagen. Such chemicals are thought to promote cancers through their stimulating effect on the rate of cell mitosis. Faster rates of mitosis leaves less time for repair enzymes to repair damaged DNA during DN replication, increasing the likelihood of a genetic mistake. A mistake made during mitosis can lead to the daughter cells receiving the wrong number of chromosomes (see aneuploidy ).

Decades of research have demonstrated the strong association between tobacco use and cancers of many sites, making it perhaps the most important human carcinogen. Hundreds of epidemiological studies have confirmed this association. Further support comes from the fact that lung cancer death rates in the United States have mirrored smoking patterns, with increases in smoking followed by dramatic increases in lung cancer death rates and, more recently, decreases in smoking followed by decreases in lung cancer death rates in men.


Ionizing radiation
Sources of ionizing radiation, such as radon gas, can cause cancer. Prolonged exposure to ultraviolet radiation from the sun can lead to melanoma and other skin malignancies.


Infectious diseases
Furthermore, many cancers originate from a viral infection; this is especially true in animals such as birds, but also in humans, as viruses are responsible for 15% of human cancers worldwide. The main viruses associated with human cancers are human papillomavirus, hepatitis B and hepatitis C virus, Epstein-Barr virus, and human T-lymphotropic virus. Experimental and epidemiological data imply a causative role for viruses and they appear to be the second most important risk factor for cancer development in humans, exceeded only by tobacco usage. The mode of virally-induced tumors can be divided into two, acutely-transforming or slowly-transforming. In acutely transforming viruses, the viral particles carry a gene that encodes for an overactive oncogene called viral-oncogene (v-onc), and the infected cell is transformed as soon as v-onc is expressed. In contrast, in slowly-transforming viruses, the virus genome is inserted, especially as viral genome insertion is an obligatory part of retroviruses, near a proto-oncogene in the host genome. The viral promoter or other transcription regulation elements in turn cause overexpression of that proto-oncogene, which in turn induces uncontrolled cellular proliferation. Because viral genome insertion is not specific to proto-oncogenes and the chance of insertion near that proto-oncogene is low, slowly-transforming viruses have very long tumor latency compared to acutely-transforming viruses, which already carry the viral oncogene.

Hepatitis viruses, including hepatitis B and hepatitis C, can induce a chronic viral infection that leads to liver cancer in 0.47% of hepatitis B patients per year (especially in Asia, less so in North America), and in 1.4% of hepatitis C carriers per year. Liver cirrhosis, whether from chronic viral hepatitis infection or alcoholism, is associated with the development of liver cancer, and the combination of cirrhosis and viral hepatitis presents the highest risk of liver cancer development. Worldwide, liver cancer is one of the most common, and most deadly, cancers due to a huge burden of viral hepatitis transmission and disease.

Advances in cancer research have made a vaccine designed to prevent cancer available. In 2006, the US FDA approved a human papilloma virus vaccine, called Gardasil. The vaccine protects against four HPV types, which together cause 70% of cervical cancers and 90% of genital warts. In March 2007, the US CDC Advisory Committee on Immunization Practices (ACIP) officially recommended that females aged 11-12 receive the vaccine, and indicated that females as young as age 9 and as old as age 26 are also candidates for immunization.

In addition to viruses, researchers have noted a connection between bacteria and certain cancers. The most prominent example is the link between chronic infection of the wall of the stomach with Helicobacter pylori and gastric cancer.


Hormonal imbalances
Some hormones can act in a similar manner to non-mutagenic carcinogens in that they may stimulate excessive cell growth. A well-established example is the role of hyperestrogenic states in promoting endometrial cancer.


Immune system dysfunction
HIV is associated with a number of malignancies, including Kaposi's sarcoma, non-Hodgkin's lymphoma, and HPV-associated malignancies such as anal cancer and cervical cancer. AIDS-defining illnesses have long included these diagnoses. The increased incidence of malignancies in HIV patients points to the breakdown of immune surveillance as a possible etiology of cancer. Certain other immune deficiency states (e.g. common variable immunodeficiency and IgA deficiency) are also associated with increased risk of malignancy.


Heredity

Most forms of cancer are "sporadic", and have no basis in heredity. There are, however, a number of recognised syndromes of cancer with a hereditary component, often a defective tumor suppressor allele. Famous examples are:

  • certain inherited mutations in the genes BRCA1 and BRCA2 are associated with an elevated risk of breast cancer and ovarian cancer
  • tumors of various endocrine organs in multiple endocrine neoplasia (MEN types 1, 2a, 2b)
  • Li-Fraumeni syndrome (various tumors such as osteosarcoma, breast cancer, sof tissue sarcoma, brain tumors) due to mutations of p53
  • Turcot syndrome (brain tumors and colonic polyposis)
  • Familial adenomatous polyposis an inherited mutation of the APC gene that leads to early onset of colon carcinoma.
  • Hereditary nonpolyposis colorectal cancer (HNPCC, also known as Lynch syndrome) can include familial cases of colon cancer, uterine cancer, gastric cancer, and ovarian cancer, without a preponderance of colon polyps.
  • Retinoblastoma, when occurring in young children, is due to a hereditary mutation in the retinoblastoma gene.
  • Down syndrome patients, who have an extra chromosome 21, are known to develop malignancies such as leukemia and testicular cancer, though the reasons for this difference are not well understood.

Other causes
A few types of cancer in non-humans have been found to be caused by the tumor cells themselves. This phenomenon is seen in Sticker's sarcoma, also known as canine transmissible venereal tumor. The closest known analogue to this in humans is individuals who have developed cancer from tumors hiding inside organ transplants.

Originally from Wikipedia.org

Cancer - Prognosis

Cancer has a reputation for being a deadly disease. While this certainly applies to certain particular types, the truths behind the historical connotations of cancer are increasingly being overturned by advances in medical care. Some types of cancer have a prognosis that is substantially better than nonmalignant diseases such as heart failure and stroke.

Progressive and disseminated malignant disease has a substantial impact on a cancer patient's quality of life, and many cancer treatments (such as chemotherapy) may have severe side-effects. In the advanced stages of cancer, many patients need extensive care, affecting family members and friends. Palliative care solutions may include permanent or "respite" hospice nursing.

Cancer patients, for the first time in the history of oncology, are visibly returning to the athletic arena and workplace. Patients are living longer with either quiescent persistent disease or even complete, durable remissions. The stories of Lance Armstrong, who won the Tour de France after treatment for metastatic testicular cancer, or Tony Snow, who was working as the White House Press Secretary as of June, 2007 despite relapsed colon cancer, continue to be an inspiration to cancer patients everywhere.


Emotional impact
Many local organizations offer a variety of practical and support services to people with cancer. Support can take the form of support groups, counseling, advice, financial assistance, transportation to and from treatment, films or information about cancer. Neighborhood organizations, local health care providers, or area hospitals may have resources or services available.
Counseling can provide emotional support to cancer patients and help them better understand their illness. Different types of counseling include individual, group, family, peer counseling, bereavement, patient-to-patient, and sexuality.
Many governmental and charitable organizations have been established to help patients cope with cancer. These organizations often are involved in cancer prevention, cancer treatment, and cancer research.


Originally from Wikipedia.org

Health Care - Cancer Preventive

Theoritically, everyone is likely to be suffering from cancer, but medical confirm any of the following people suffering from cancer more likely, early prevention.

First, the hot tea Changhe

Regular drinking high temperature (above 70 degrees Celsius) water tea is not only easy to burn the esophagus, chronic ulcers, and the tannin in tea can be deposited on the injury site, stimulate epithelial cells of the esophagus injuries, chronic ulcers caused prolonged Fuyu, lead to cancer.

Second, often stay up late

Night cell division is the most productive period, if enough sleep at night, lower the body's immunity, the cells mutate to not be timely clearance, which may lead to cancer.

And stay up late, often smoking for the refreshing drink coffee, but also to more easily enter the human carcinogens.

Third, hold urine

Urine contains one or more of the carcinogenic substances, it can stimulate the bladder epithelial carcinogenesis. In the feces of the more harmful, such as hydrogen sulfide, skatole, cholesterol and sub-acid metabolites, such as carcinogens, if often stimulate the intestinal mucosa, will lead to cancer.

4, allergies physique

Have a history of allergic women suffering from breast cancer is higher than normal risk of 30 percent of men are suffering from allergies risk of prostate cancer is 40 percent higher than normal.

5, low serum cholesterol

Experts believe that the low serum cholesterol, the higher the incidence of colon cancer. Serum cholesterol below 110 mg / dl people, the risk of colon cancer than the normal high of more than three times.

6, migraine eat meat

Experts found that day to pigs, cattle, sheep, etc. Churu-eating people, with the proportion of colorectal cancer than those eating several small amount of the monthly Roushizhe high 2.5 times the risk of developing pancreatic cancer also of the Carnivore increase.

7, the children of cancer patients

Medicine confirmed that the incidence of human cancer and genetic factors have great relations. The descendants of cancer patients significantly the risk of cancer than the general population.

8, one of the spouses cancer

Data show that both the husband and wife have cancer or phenomenon, a growing trend known as "husband and wife cancer." Experts believe that the same root cause of their poor lifestyle.

9, hypertension

Hypertension Although not directly cause cancer, but the occurrence of the two diseases share a common mechanism. Obesity, alcohol, smoking, too much salt can make blood pressure rise, etc., can induce cancer.

10, a lack of vitamin

Experts believe that in the protection of the people less vulnerable to vitamin cancer violations. Vitamin A, the lack of β-carotene, the risk of lung cancer increased three times a lack of vitamin C, suffering from esophageal cancer, the risk of gastric cancer were increased by 2 times and 3.5 times less than in the vitamin E group, lip cancer, Oral cancer, skin cancer, cervical cancer, gastric cancer, colorectal cancer, lung cancer incidence rates have increased.

Cancer - Treatment

Cancer can be treated by surgery, chemotherapy, radiation therapy, immunotherapy, monoclonal antibody therapy or other methods. The choice of therapy depends upon the location and grade of the tumor and the stage of the disease, as well as the general state of the patient (performance status). A number of experimental cancer treatments are also under development.

Complete removal of the cancer without damage to the rest of the body is the goal of treatment. Sometimes this can be accomplished by surgery, but the propensity of cancers to invade adjacent tissue or to spread to distant sites by microscopic metastasis often limits its effectiveness. The effectiveness of chemotherapy is often limited by toxicity to other tissues in the body. Radiation can also cause damage to normal tissue.

Because "cancer" refers to a class of diseases, it is unlikely that there will ever be a single "cure for cancer" any more than there will be a single treatment for all infectious diseases.



Surgery
In theory, non-hematological cancers can be cured if entirely removed by surgery, but this is not always possible. When the cancer has metastasized to other sites in the body prior to surgery, complete surgical excision is usually impossible. In the Halstedian model of cancer progression, tumors grow locally, then spread to the lymph nodes, then to the rest of the body. This has given rise to the popularity of local-only treatments such as surgery for small cancers. Even small localized tumors are increasingly recognized as possessing metastatic potential.

Examples of surgical procedures for cancer include mastectomy for breast cancer and prostatectomy for prostate cancer. The goal of the surgery can be either the removal of only the tumor, or the entire organ. A single cancer cell is invisible to the naked eye but can regrow into a new tumor, a process called recurrence. For this reason, the pathologist will examine the surgical specimen to determine if a margin of healthy tissue is present, thus decreasing the chance that microscopic cancer cells are left in the patient.

In addition to removal of the primary tumor, surgery is often necessary for staging, e.g. determining the extent of the disease and whether it has metastasized to regional lymp nodes. Staging is a major determinant of prognosis and of the need for adjuvant therapy.

Occasionally, surgery is necessary to control symptoms, such as spinal cord compression or bowel obstruction. This is referred to as palliative treatment.


Radiation therapy
Main article: Radiation therapy

Radiation therapy (also called radiotherapy, X-ray therapy, or irradiation) is the use of ionizing radiation to kill cancer cells and shrink tumors. Radiation therapy can be administered externally via external beam radiotherapy (EBRT) or internally via brachytherapy. The effects of radiation therapy are localised and confined to the region being treated. Radiation therapy injures or destroys cells in the area being treated (the "target tissue") by damaging their genetic material, making it impossible for these cells to continue to grow and divide. Although radiation damages both cancer cells and normal cells, most normal cells can recover from the effects of radiation and function properly. The goal of radiation therapy is to damage as many cancer cells as possible, while limiting harm to nearby healthy tissue. Hence, it is given in many fractions, allowing healthy tissue to recover between fractions.

Radiation therapy may be used to treat almost every type of solid tumor, including cancers of the brain, breast, cervix, larynx, lung, pancreas, prostate, skin, stomach, uterus, or soft tissue sarcomas. Radiation is also used to treat leukemia and lymphoma. Radiation dose to each site depends on a number of factors, including the radiosensitivity of each cancer type and whether there are tissues and organs nearby that may be damaged by radiation. Thus, as with every form of treatment, radiation therapy is not without its side effects.


Chemotherapy
Main article: Chemotherapy

Chemotherapy is the treatment of cancer with drugs ("anticancer drugs") that can destroy cancer cells. In current usage, the term "chemotherapy" usually refers to cytotoxic drugs which affect rapidly dividing cells in general, in contrast with targeted therapy (see below).

Chemotherapy drugs interfere with cell division in various possible ways, e.g. with the duplication of DNA or the separation of newly formed chromosomes. Most forms of chemotherapy target all rapidly dividing cells and are not specific for cancer cells, although some degree of specificity may come from the inability of many cancer cells to repair DNA damage, while normal cells generally can. Hence, chemotherapy has the potential to harm healthy tissue, especially those tissues that have a high replacement rate (e.g. intestinal lining). These cells usually repair themselves after chemotherapy.

Because some drugs work better together than alone, two or more drugs are often given at the same time. This is called "combination chemotherapy"; most chemotherapy regimens are given in a combination.

The treatment of some leukaemias and lymphomas requires the use of high-dose chemotherapy, and total body irradiation (TBI). This treatment ablates the bone marrow, and hence the body's ability to recover and repopulate the blood. For this reason, bone marrow, or peripheral blood stem cell harvesting is carried out before the ablative part of the therapy, to enable "rescue" after the treatment has been given. This is known as autologous stem cell transplantation. Alternatively, hematopoietic stem cells may be transplanted from a matched unrelated donor (MUD).


Targeted therapies
Main article: Targeted therapy

Targeted therapy, which first became available in the late 1990s, has had a significant impact in the treatment of some types of cancer, and is currently a very active research area. This constitutes the use of agents specific for the deregulated proteins of cancer cells. Small molecule targeted therapy drugs are generally inhibitors of enzymatic domains on mutated, overexpressed, or otherwise critical proteins within the cancer cell. Prominent examples are the tyrosine kinase inhibitors imatinib and gefitinib.

Monoclonal antibody therapy is another strategy in which the therapeutic agent is an antibody which specifically binds to a protein on the surface of the cancer cells. Examples include the anti-HER2/neu antibody trastuzumab (Herceptin) used in breast cancer, and the anti-CD20 antibody rituximab, used in a variety of B-cell malignancies.

Targeted therapy can also involve small peptides as "homing devices" which can bind to cell surface receptors or affected extracellular matrix surrounding the tumor. Radionuclides which are attached to this peptides (e.g. RGDs) eventually kill the cancer cell if the nuclide decays in the vicinity of the cell. Especially oligo- or multimers of these binding motifs are of great interest, since this can lead to enhanced tumor specificity and avidity.

Photodynamic therapy (PDT) is a ternary treatment for cancer involving a photosensitizer, tissue oxygen, and light (often using lasers). PDT can be used as treatment for basal cel carcinoma (BCC) or lung cancer; PDT can also be useful in removing traces of malignant tissue after surgical removal of large tumors.


Immunotherapy
Main article: Cancer immunotherapy

Cancer immunotherapy refers to a diverse set of therapeutic strategies designed to induce the patient's own immune system to fight the tumor. Contemporary methods for generating an immune response against tumours include intravesical BCG immunotherapy for superficial bladder cancer, and use of interferons and other cytokines to induce an immune response in renal cell carcinoma and melanoma patients. Vaccines to generate specific immune responses are the subject of intensive research for a number of tumours, notably malignant melanoma and renal cell carcinoma. Sipuleucel-T is a vaccine-like strategy in late clinical trials for prostate cancer in which dendritic cells from the patient are loaded with prostatic acid phosphatase peptides to induce a specific immune response against prostate-derived cells.

Allogeneic hematopoietic stem cell transplantation ("bone marrow transplantation" from a genetically non-identical donor) can be considered a form of immunotherapy, since the donor's immune cells will often attack the tumor in a phenomenon known as graft-versus-tumor effect. For this reason, allogeneic HSCT leads to a higher cure rate than autologous transplantation for several cancer types, although the side effects are also more severe.


Hormonal therapy
Main article: Hormonal therapy (oncology)

The growth of some cancers can be inhibited by providing or blocking certain hormones. Common examples of hormone-sensitive tumors include certain types of breast and prostate cancers. Removing or blocking estrogen or testosterone is often an important additional treatment. In certain cancers, administration of hormone agonists, such as progestogens may be therapeutically beneficial.


Angiogenesis inhibitor
Main article: Angiogenesis inhibitor

Angiogenesis inhibitors prevent the extensive growth of blood vessels (angiogenesis) that tumors require to survive. Some, such as bevacizumab, have been approved and are in clinical use. One of the main problems with anti-angiogenesis drugs is that many factors stimulate blood vessel growth, in normal cells and cancer. Anti-angiogenesis drugs only target one factor, so the other factors continue to stimulate blood vessel growth. Other problems include route of administration, maintenance of stability and activity and targeting at the tumor vasculature.



Symptom control
Although the control of the symptoms of cancer is not typically thought of as a treatment directed at the cancer, it is an important determinant of the quality of life of cancer patients, and plays an important role in the decision whether the patient is able to undergo other treatments. Although doctors generally have the therapeutic skills to reduce pain, nausea, vomiting, diarrhea, hemorrhage and other common problems in cancer patients, the multidisciplinary specialty of palliative care has arisen specifically in response to the symptom control needs of this group of patients.

Pain medication, such as morphine and oxycodone, and antiemetics, drugs to suppress nausea and vomiting, are very commonly used in patients with cancer-related symptoms. Improved antiemetics such as ondansetron and analogues, as well as aprepitant have made aggressive treatments much more feasible in cancer patients.

Chronic pain due to cancer is almost always associated with continuing tissue damage due to the disease process or the treatment (i.e. surgery, radiation, chemotherapy). Although there is always a role for environmental factors and affective disturbances in the genesis of pain behaviors, these are not usually the predominant etiologic factors in patients with cancer pain. Furthermore, many patients with severe pain associated with cancer are nearing the end of their lives and palliative therapies are required. Issues such as social stigma of using opioids, work and functional status, and health care consumption are not likely to be important in the overall case management. Hence, the typical strategy for cancer pain management is to get the patient as comfortable as possible using opioids and other medications, surgery, and physical measures. Doctors have been reluctant to prescribe narcotics for pain in terminal cancer patients, for fear of contributing to addiction or suppressing respiratory function. The palliative care movement, a more recent offshoot of the hospice movement, has engendered more widespread support for preemptive pain treatment for cancer patients.

Fatigue is a very common problem for cancer patients, and has only recently become important enough for oncologists to suggest treatment, even though it plays a significant role in many patients' quality of life.



Complementary and alternative
Complementary and alternative medicine (CAM) treatments are the diverse group of medical and health care systems, practices, and products that are not part of conventional medicine. Oncology, the study of human cancer, has a long history of incorporating unconventional or botanical treatments into mainstream cancer therapy. Some examples of this phenomenon include the chemotherapy agent paclitaxel, which is derived from the bark of the Pacific Yew tree, and ATRA, all-trans retinoic acid, a derivative of Vitamin A that induces cures in an aggressive leukemia known as acute promyelocytic leukemia. Many "complementary" and "alternative" medicines for cancer have not been studied using the scientific method, such as in well-designed clinical trials, or they have only been studied in preclinical (animal or in-vitro) laboratory studies. Many times, "complementary" and "alternative" medicines are supported by marketing materials and testimonials from users of the substances. Frequently, when these treatments are subjected to rigorous scientific testing, they are found not to work. A recent example was reported at the 2007 annual meeting of the American Society of Clinical Oncology: a Phase III clinical trial comparing shark cartilage extract to placebo in non-small cell lung cancer demonstrated no benefit of the shark cartilage extract, AE-491.

"Complementary medicine" refers to methods and substances used along with conventional medicine, while "alternative medicine" refers to compounds used instead of conventional medicine. A study of CAM use in patients with cancer in the July 2000 issue of the Journal of Clinical Oncology found that 69% of 453 cancer patients had used at least one CAM therapy as part of their cancer treatment.

Some complementary measures include botanical medicine, such as an NIH trial currently underway testing mistletoe extract combined with chemotherapy for the treatment of solid tumors; acupuncture for managing chemotherapy-associated nausea and vomiting and in controlling pain associated with surgery; and psychological approaches such as "imaging" or meditation to aid in pain relief or improve mood.
A wide range of alternative treatments have been offered for cancer over the last century. The appeal of alternative cures arises from the daunting risks, costs, or potential side effects of many conventional treatments, or in the limited prospect for cure. Some people resort to these so-called "alternative" forms of treatment in desperation or as a last resort. However, no alternative therapies have been shown in any scientific study to effectively treat cancer. Some express the view that the promotion and sale of certain alternative modalities known to be ineffective constitute quackery.


Treatment trials
Clinical trials, also called research studies, test new treatments in people with cancer. The goal of this research is to find better ways to treat cancer and help cancer patients. Clinical trials test many types of treatment such as new drugs, new approaches to surgery or radiation therapy, new combinations of treatments, or new methods such as gen therapy.

A clinical trial is one of the final stages of a long and careful cancer research process. The search for new treatments begins in the laboratory, where scientists first develop and test new ideas. If an approach seems promising, the next step may be testing a treatment in animals to see how it affects cancer in a living being and whether it has harmful effects. Of course, treatments that work well in the lab or in animals do not always work well in people. Studies are done with cancer patients to find out whether promising treatments are safe and effective.

Patients who take part may be helped personally by the treatment(s) they receive. They get up-to-date care from cancer experts, and they receive either a new treatment being tested or the best available standard treatment for their cancer. Of course, there is no guarantee that a new treatment being tested or a standard treatment will produce good results. New treatments also may have unknown risks, but if a new treatment proves effective or more effective than standard treatment, study patients who receive it may be among the first to benefit.


Originally from Wikipedia.org