Lung Cancer Awareness - Know How This Could Help You ?

Lung Cancer Awareness - Know How This Could Help You

Only about 10% of all patients cured at the end considering that the majority of the tumor was diagnosed at stage relatively late. There's a chance 50% death in less than one year, if the person with lung cancer can't be cured with surgery when cancer was found.

Who's at risk?

There are several a risk factor that can make it more likely to develop cancer in the lungs. Some kind of cancer has a risk factor different. Although there are several causes, the researchers found that most of them are associated with smoking.

A risk factor for lung cancer cells are small, including smoking. This is the most famous because of lung cancer. This includes smoking cigarettes, cigars or pipes in the past; Exposure cigarette smoke; Exposure asbestos or radon.

Up to 90% of patients or smokers. A lot of left wing 10% were exposed to second hand cigarette smoke. karsinogen in tobacco is the substance dangerous damaged cells in the lungs. Cells are damaged, then it could be cancer. broken cells in the tissue lung gradually returns to normal when someone stops smoking before the cancer began to develop.

Probability got cancer smokers is difficult to predict, but in general the extent of the cancer depends on: age started smoking; How long they have been smoking; How many cigarettes they smoke per day.

Cigar and pipe

Some factors must also be considered as cigar and pipe smokers have a risk higher have cancer in the lungs compared to non-smokers: the number of years someone smokes; the Number of pipes or cigars are smoked per day; How in their secretary of defense. Even the smoking of cigars and pipes that don't breathe are at increased risk for lung, mouth, and kind of-kind of keganasan, as well as the risk of developing lung cancer.

Kind of

A gene called GRPR causes the growth of cells that are not used in people exposed to cigarette smoke. The gene is more active in women than in men. This may explain why women are more vulnerable to cancer in the lungs compared to men.

Diet

Some evidence shows fruit and vegetables can protect against lung cancer. Research has shown a diet low in fruit and vegetables can increase the odds of got cancer if exposed to smoke tobacco.

Disease

Lung disease-lung specific, like tuberkulosis (TB) can increase the odds of someone exposed to lung cancer. Lungs marked with TB seems to develop adenokarsinoma lung cancer.

Some facts more about lung cancer: lung Cancer kills more people than another form of cancer. Only 10% of all patients healed in the end because most of the cancer in the lungs was diagnosed at stage relatively late. Eight of ten tumor in the lungs caused smoke tobacco. The American Cancer Society estimates 164.000 case of a new cancer is diagnosed every year in the U.S. and around 157.000 people died because of this disease every year. This is a good reason to compete with the awareness of cancer.

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The Lung Cancer Epidemic

The Lung Cancer Epidemic

Lung cancer is the leading cause of death due to cancer in the population of the U.S. and the Western world. Lung cancer became the leading cause of death due to cancer in the united States, but since 1988, women have caught up with men and then lung cancer is the leading cause of death due to cancer in women too. More than 170.000 cases of lung cancer diagnosed in the United States every year. Very lucky few recover from a terrible disease this is. Approximately 157.000 people died as a direct result of lung cancer.

Death is associated with lung cancer beyond the level of combined death of (breast cancer) second, third (cancer of his prostate) and fourth (cancer colon) leading cause of death cancer. How will we react if it crashes every day a Boing 747 and all the passengers die? That's what happens with lung cancer. About 430 people die every day because of lung cancer.

Despite the high mortality rate due to cancer, lung cancer received a lot of attention less than any other kind of cancer, especially breast cancer. Research about lung cancer receives far less funding, and the general public to take interest far lower on lung cancer. Although lung cancer is the leading cause of death due to cancer among men and women, in the field of lung cancer going on very little research and scientific advance.

An estimated $ 1.723 death due to cancer is spent on research about lung cancer where as the number that is appropriate for breast cancer ($ 13.953), cancer of his prostate ($ 10,318) and cancer kolorektal (4618) much higher. It should be noted that the Department of Defense breast cancer, cancer of the ovarium and cancer his prostate but no lung cancer.

Part of the problem associated with the funding of research for lung cancer is the fact that, there are not many survivors of lung cancer to lobbied the cause of lung cancer. mortality rate high associated with lung cancer leaves very few survivors to fight for their goals, and even those who survived was lucky not to be in health which is very good, because most of the victim this is the patient who has to undergo reseksi vast lungs .

There is also the stigma associated with lung cancer. Not like any other kind of risk cancer lung cancer linked closely with smoking. Many who deal with patients lung cancer and patients think that disease is a direct result of behavior. It filled the guilt of a patient with lung cancer tend to blame themselves. It also acts against any program fundraiser devoted to lung cancer, where people unconsciously feel that lung cancer is a disease that these patients brought on themselves.

More funding and research is needed for lung cancer. We all should join our hands to fight the enemy this sad of the human species.

Lung Cancer Causes - Pathogenesis

Lung Cancer Causes - Pathogenesis

Patogenesis lung cancer like cancer of the other, starting early diinduksi agent events of a long period promotion and progress in the process of multi steps. Smoking is started and promote karsinogenesis. The initiation done soon to change the same genetic between smokers and ex-event (z 3P removal of mutated p53), as proven. The smoke thus causing the "effect field" epitel lungs, populations of large cells starting distribution and the increase in the probability transformation. Keep exposure smoke tobacco has been allowed to accumulate mutations extra because of irritating the chronics and promoters in cigarette smoke (amount of nicotine's formalin for example., Is phenol) promotion because. The time delay between smoking and cancer, the early beginning is usually long and requires 20-25 years to the development of cancer. Reduce the risk of cancer after quitting smoking, but cells getting there can flourish. If karsinogen else continue with process.

SCLC and NSCLC were treated different, because it (i) comes from the cells are different, (ii) undergo the process of patogenesis different and (iii) to accumulate genetic mutations are different. SCLC carries frequent mutations in c-KIT, p53 and R.B., while often NSCLC, MYC, Bcl2, mutations EGFR, KRAS, CD44 and p16. This is all well onkogen or gen supresor tumor. See genetics and biology chapter cancer cancer for an explanation of how a mutation like this can cause cancer.

Similar to a lot of cancer other lung cancer begins with the activation onkogen or inaktivasi gen supresor tumor. Karsinogen causing mutation on the gene this causes the development of cancer. Mutation in K-ras proto-onkogen responsible for 10-30% of adenokarsinoma the lungs. About 4% of cancer cell lung non-small involving gene fusion EML4-ALK tyrosine kinase. Change epigenetik - like changes metilasi DNA, modification of histon tails or rules microRNA - it can cause inaktivasi gen supresor tumor. Reseptor to reseptor factor the growth of epidermal (EGFR) regulates proliferation of cells, apoptosis, angiogenesis and invasion of tumor. Mutation and amplifikasi EGFR are common in cell karsinoma lung non-small, and give the basis for treatment with inhibitor EGFR. HER2 / neu is influenced more rare. genes other that is often mutated or amplified are c-MET, NKX2-1, LKB1, PIK3CA, and BRAF. Line cells is not fully understood origin. The mechanism might include activation abnormal stem cells. In stem cells the drains breath proksimal express keratin 5 are more likely to be affected, usually causing karsinoma sel skuamosa the lungs. In the air central, the stem cells involved the club cells and the cells neuroepithelial who expressed protein cell sekretori club. Karsinoma sel small lungs that can be derived from the line cell or cell neuroendokrin and can express CD44. Metastasis of lung cancer requires transition from epitel to cell types mesenchymal. This problem can happen with the path signal activated Akt / GSK3Beta, MEK-ERK, Fas and Par6.

Smoking Lung Cancer

Smoking Lung Cancer

Smoking is a major risk factor and is the main cause of lung cancer. Chemicals in tobacco smoke are carcinogens. These are substances which can damage cells and lead to cancer developing. About 9 in 10 cases of lung cancer are caused by smoking.

Everyone knows smoking can cause lung cancer. But it also causes a whole array of other varieties of the disease, from pancreatic cancer to leukemia. Now, new research sheds light on just how deadly tobacco can be when smokers get cancer.

Compared with non-smokers, those who smoke between 1-14 cigarettes a day have eight times the risk of dying from lung cancer. Those who smoke 25 or more cigarettes a day have 25 times the risk. However, the risk of lung cancer depends more on the length of time a person has smoked. So, smoking one pack of cigarettes a day for 40 years is more hazardous than smoking two packs a day for 20 years.

Smoking causes more than 48% of deaths from the 12 types of cancer sometimes caused by smoking, according to new research in JAMA Internal Medicine. Smoking caused more than 80% of lungcancer deaths as well as 77% of larynx cancer deaths. Other top cancers caused by smoking include esophagus, kidney and liver cancer.

After about fifteen years from stopping smoking, that person's risk of developing lung cancer is similar to that of a non-smoker.

Researchers analyzed 2011 data from interviews conducted by the Centers for Disease Control and Prevention for the study. Overall, approximately 168,000 people are estimated to die of cancer due to smoking in the United States each year.

Most statistics look at the overall risk of lung cancer, combining both people who smoke and those who have never smoked. Based on United States statistics, the lifetime risk that a man will develop lung cancer is 7.62 percent, or 1 in 13 people.

The study’s researchers note that the prevalence of smoking has been on the decline in recent decades but argue that more needs to be done.

For women, lifetime risk is 6.61 percent or 1 in 15.  The lifetime risk of a man dying from lung cancer is 6.26 percent or 1 in 16, and 4.99 percent or 1 in 20 women will die from the disease.  Clearly these numbers would be higher for people who smoke and much lower for people who have never smoked.

Continued progress in reducing cancer mortality, as well as deaths from many other serious diseases, will require more comprehensive tobacco control, including targeted cessation support,” they conclude.

Studies in other countries have broken down the risk further to differentiate between never smokers, former smokers, and current smokers.

Small Cell Lung Cancer

 Small Cell Lung Cancer

Chemotherapy and Radiation Therapy

 For people with small cell lung cancer, regardless of stage, chemotherapy is an essential part of treatment. Radiation treatment may be used as well depending on the stage of cancer.

In the earliest stages of non-small cell lung cancer, chemotherapy is sometimes given before surgery to reduce tumor size and eliminate early spreading. Doctors call this approach neoadjuvant chemotherapy. For patients with limited lymph node involvement, chemotherapy can also be given post-surgery to kill any remaining cancer cells. This is known as adjuvant chemotherapy and helps prevent the chance of cancer recurrence.

For people with limited-stage small cell lung cancer, combination chemotherapy plus radiation therapy given at the same time is the recommended treatment. The most commonly used initial chemotherapy regimen is etoposide (Toposar or Vepesid) plus cisplatin (Platinol), known as EP.

For later stage cancers when surgery is no longer an option, chemotherapy is often administered with simultaneous radiation therapy. Known as combined chemoradiation therapy, this option often boasts survival rates higher than either treatment given alone or one after the other. This treatment is common if the cancer has spread to the mediastinal lymph nodes, which are located outside of the lung near the trachea and esophagus.

For people with extensive-stage small cell lung cancer, chemotherapy alone using the EP regimen is the standard treatment. However, another regimen that may be used is carboplatin (Paraplatin) plus irinotecan (Camptosar)

Radiation therapy of the brain may be used before or after chemotherapy for some people whose cancer has spread to the brain.

Preventive Radiation Therapy to the Brain

In more than half of the people with small cell lung cancer, the cancer also spreads to the brain. For people whose lung cancer has responded to chemotherapy, doctors may prescribe radiation therapy to the brain to help prevent the cancerfrom spreading to the brain. This procedure is known as prophylactic cranial irradiation (PCI). This can benefit patient with both limited-stage and extensive-stage small cell lung cancers.

Three-dimensional conformal radiation therapy delivers radiation beams tailored to the size, shape, and location of the cancer. Using a linear accelerator, the oncologist aims radiation beams at the cancer from different directions. Treatment is typically done twice a day, five days a week, over the course of three weeks. Breaking the total dose of radiation into smaller doses, called fractions, provides enough therapy to manage the tumor, while reducing the risk of side effects.

NYU Langone physicians use several different approaches for external beam radiation therapy, which is delivered using a machine called a linear accelerator. This machine can be moved around you during treatment sessions, helping oncologists to target the entire tumor. These approaches have different degrees of targeting, and our doctors can talk to you about the best treatment option for you.

Lung Cancer Staging

TX Primary tumor cannot be assessed, or tumor proven by the presence of malignant cells in sputum or bronchial washings but not visualized by imaging or bronchoscopy

T0 No evidence of primary tumor

Tis Carcinoma in situ

T1 Tumor 3 cm or less in greatest dimension, surrounded by lung or visceral pleura, without bronchoscopic evidence of invasion more proximal than the lobar bronchus (for example, not in the main bronchus)1

T1a Tumor 2 cm or less in greatest dimension

T1b Tumor more than 2 cm but 3 cm or less in greatest dimension

T2 Tumor more than 3 cm but 7 cm or less or tumor with any of the following features (T2 tumors with these features are classified T2a if 5 cm or less): involves main bronchus, 2 cm or more distal to the carina; invades visceral pleura (PL1 or PL2); associated with atelectasis or obstructive pneumonitis that extends to the hilar region but does not involve the entire lung

T2a Tumor more than 3 cm but 5 cm or less in greatest dimension

T2b Tumor more than 5 cm but 7 cm or less in greatest dimension

T3 Tumor more than 7 cm or one that directly invades any of the following: parietal pleural (PL3), chest wall (including superior sulcus tumors), diaphragm, phrenic nerve, mediastinal pleura, parietal pericardium; or tumor in the main bronchus less than 2 cm distal to the carina1 but without involvement of the carina; or associated atelectasis or obstructive pneumonitis of the entire lung or separate tumor nodule(s) in the same lobe

T4 Tumor of any size that invades any of the following: mediastinum, heart, great vessels, trachea, recurrent laryngeal nerve, esophagus, vertebral body, carina, separate tumor nodule(s) in a different ipsilateral lobe

Distant Metastasis (M)

M0 No distant metastasis

M1 Distant metastasis

M1a Separate tumor nodule(s) in a contralateral lobe, tumor with pleural nodules or

malignant pleural (or pericardial) effusion2

M1b Distant metastasis (in extrathoracic organs)

Regional Lymph Nodes (N)

NX Regional lymph nodes cannot be assessed

N0 No regional lymph node metastases

N1 Metastasis in ipsilateral peribronchial and/or ipsilateral hilar lymph nodes and intrapulmonary nodes, including involvement by direct extension

N2 Metastasis in ipsilateral mediastinal and/or subcarinal lymph node(s)

N3 Metastasis in contralateral mediastinal, contralateral hilar, ipsilateral or contralateral scalene, or supraclavicular lymph node(s)

 

			N0	N1	N2	N3
			No regional lymph node metastasis	Metastasis in ipsilateral pulmonary or hilar lymph nodes	Metastasis in ipsilateral mediastinal/subcarinal lymph nodes	Metastasis in contralateral mediastinal/hilar or lymph supraclavicular nodes
T1	Tumor < 3 cma
	T1a	Tumor ≤ 2 cma	IA-T1aN0	IIA-T1aN1	IIIA-T1aN2	IIIB-T1aN3
	T1b	Tumor > 2 cm but ≤ 3 cma	IA-T1bN0	IIA-T1bN1	IIIA-T1bN2	IIIB-T1bN3
T2	Tumor > 3 cm but ≤ 7 cma or tumor with#. Invading visceral pleura, bronchus ≥ 2 cm from carina, atelectasis extending to hilum, but not involving the entire lung
	T2a	Tumor > 3 cm but ≤ 5 cma	IB-T2aN0	IIA-T2aN1	IIIA-T2aN2	IIIB-T2aN3
	T2b	Tumor > 5 cm but ≤ 7 cma	IIA-T2bN0	IIB-T2bN1	IIIA-T2bN2	IIIB-T2bN3
T3	Tumor > 7 cma; OR invading chest wall diaphragm, phrenic nerve, mediastinal pleura, pericardium; OR tumor < 2 cm distal to the carina, OR atelectasis of entire lung; OR separate tumor nodule(s) in same lobe
	T3>7	Tumor > 7 cma	IIB-T3>7N0	IIIA-T3>7N1	IIIA-T3>7N2	IIIB-T3>7N3
	T3Inv	Invading chest wall diaphragm, phrenic nerve, mediastinal pleura, pericardium	IIB-T3InvN0	IIIA-T3InvN1	IIIA-T3InvN2	IIIB-T3InvN3
	T3Centr	Tumor < 2 cm distal to the carina	IIB-T3CentrN0	IIIA-T3CentrN1	IIIA-T3CentrN2	IIIB-T3CentrN3
	T3Satell	Separate tumor nodule(s) in same lobe	IIB-T3SatellN0	IIIA-T3SatellN1	IIIA-T3SatellN2	IIIB-T3SatellN3
T4	Tumor invading heart, great vessels, trachea, recurrent laryngeal nerve, esophagus, spine; OR tumor nodules(s) in a different ipsilateral lobe
	T4Inv	Tumor invading heart, great vessels, trachea, recurrent laryngeal nerve, esophagus, spine	IIIA-T4InvN0	IIIA-T4InvN1	IIIB-T4InvN2	IIIB-T4InvN3
	T4Ipsi Nod	Tumor nodules(s) in a different ipsilateral lobe	IIIA-T4Ipsi NodN0	IIIA-T4Ipsi NodN1	IIIB-T4Ipsi NodN2	IIIB-T4Ipsi NodN3