DIAGNOSA CANCER BY STAGING

In previous writings I wrote an article Diagnosis of Cancer by Detection of Cancer, now I'll write a continuation of the article. When a tumor is detected, the physician takes a biopsy by removing a sample of the tissue. The biopsy sample is inspected under a microscope to determine if the tumor is benign or malignant. Cancerous cells usually appear abnormal in shape and no longer orient themselves in orderly configurations. If the tumor is cancerous, the physician assigns it a stage, indicating how far cancer has spread. The stage is a key factor in determining both the cancer’s treatment and prognosis.

Oncologists, physicians who specialize in the diagnosis and treatment of cancer, use several different staging systems. In one system, tumors are grouped into four stages denoted by Roman numerals I through IV. Stage I cancers are small localized cancers that are usually curable. Stage II and III tumors are usually locally advanced and may or may not have invaded nearby lymph nodes, and stage IV tumors have usually metastasized—that is, spread to distant tissues in the body.

The most widely used staging system is the Tumor, Lymph Node, and Metastasis system, commonly abbreviated TNM. This system uses numbers between zero and three to assess the size of the tumor (T), the extent that it has spread to nearby lymph nodes (N), and the extent that it has spread throughout the body (M). A cancer’s stage depends on a combination of these numbers. For example, a T-1, N-0, and M-0 tumor is a stage 1 tumor. This tumor is 2 cm (1 in) or less (T-1) and has not spread to nearby lymph nodes (accounting for N-0) or metastasized (M-0). The five-year survival rate for a patient with this stage tumor is accordingly excellent. A T-3, N-1, and M-0 tumor is a stage 3 tumor.

This tumor is greater than 5 cm (2 in) and has spread to nearby lymph nodes, but there is no evidence that the cancer has spread to distant tissues. The five-year survival rate for a patient with this tumor is not as high as the T-1, N-0, M-0 patient. Stage 4 tumors are distinguished by an M-1 number. This means they have progressed to the point where metastasis is widespread, and the prognosis is usually quite poor.

DIAGNOSIS OF CANCER BY DETECTION OF CANCER

Diagnosis of cancer often begins when a person notices an unusual health symptom and consults a doctor. Early warning signs of cancer include changes in bowel or bladder habits, a sore that does not heal, unusual bleeding or discharge, thickening or a lump in the breast or any other part of the body, indigestion or difficulty swallowing, change in appearance of a wart or mole, or a nagging cough or hoarseness.

People with early warning signs should consult their family doctor, who will evaluate symptoms and may refer the patient to a physician who specializes in cancer. A physician will first take the patient’s medical history to learn about current symptoms, past history of disease, and family members diagnosed with cancer. The procedures used in a physical exam depend on the patient’s clinical symptoms and may include a digital rectal examination, in which the physician uses a gloved finger to gently check the smoothness of the rectal lining. The physician may perform a breast exam on female patients, in which the breasts are gently probed to feel for lumps or unusual masses.

During the examination the physician may use a thin, lighted tube called an endoscope to look for tumors in internal body cavities. The endoscopy procedure used depends on the organ or body cavity examined. In gastric endoscopy, the doctor feeds a specialized endoscope down the throat to examine the lining of the esophagus, stomach, and first part of the small intestine. Fiberoptic sigmoidoscopy, in which a flexible instrument is inserted into the lower intestinal tract through the anus, enables a physician to visually examine the interior of the colon and rectum. Colonoscopy uses a much longer flexible instrument to view the entire length of the large intestine.

A number of laboratory tests help narrow the possible diagnoses. In a Pap smear, cells are removed from the cervical epithelium with a small plastic brush. These cells are examined under a microscope for cell changes that are a sign that cancer may be developing as well as signs of malignancy. If a patient’s clinical signs suggest colorectal cancer, the doctor may search for blood in the stool using a fecal occult blood test. A small sample of the patient’s stool is smeared on a card coated with a chemical called guaiac, which reacts with blood. The card is analyzed in a laboratory for occult (hidden) blood. Certain blood tests determine if levels of red and white blood cells are low, a possible indication of leukemia. Others test for the presence of tumor markers, chemicals that are present in higher levels when certain cancers are present. For example, a prostate-specific antigen (PSA) test measures levels of prostate-specific antigen in the blood. Prostate cancer cells overproduce this protein, causing an elevation of PSA levels in blood.

Medical imaging techniques help doctors locate and evaluate a tumor. These include computed tomography (CT) and magnetic resonance imaging (MRI) scans. CT and MRI scans use computers to form a three-dimensional image of the tumor and surrounding tissues. X-ray images of the breast called mammograms help physicians detect and evaluate breast cancer. Ultrasound scanning bounces high-frequency sound waves off a tumor and surrounding tissue to create an image of the tumor. The multimodality display technique combines the images from several imaging tools into one picture, providing a final three-dimensional image with much greater detail. Computer-aided diagnosis uses complex computer programming technology called artificial intelligence to scan mammograms and X rays to help look for signs of cancer and offer an automated second opinion.

CAUSES OF CANCER

Cancer can develop in the human body, where this discussion has been detailed in previous posts. In this article will discuss about the things that cause cancer.

Scientists do not fully understand the causes of cancer, but studies show that some people are more likely to develop the disease than others. Scientists called epidemiologists study particular populations to identify why cancer rates vary. One method they use is to compare cancer patients with healthy people in terms of behavior such as diet, exercise, and smoking and traits such as gender, age, and race. Population studies provide useful information about risk factors that increase the likelihood of developing cancer.

1. Carcinogens

One of the greatest risk factors for cancer is prolonged or repeated exposure to carcinogens—chemical, biological, or physical agents that cause the cellular damage that leads to cancer. The details of how carcinogens cause cancer remain unclear. One theory is that exposure to carcinogens, when combined with the effects of aging, causes an increase in chemicals in the body called free radicals. An excessive number of free radicals causes damage by taking negatively charged particles called electrons from key cellular components of the body, such as DNA. This may make genes more vulnerable to the mutating effects of carcinogens.

2. Hereditary Factors

Evidence suggests that heredity plays a role in developing cancer. Some gene mutations associated with cancer are inherited. For example, inheriting mutated tumor suppressor genes BRCA1 or BRCA2 greatly increases a woman’s chances of developing breast cancer. About 50 to 60 percent of women with inherited BRCA1 or BRCA2 mutations will develop breast cancer by the age of 70. Inherited mutations in the genes MSH2, MLH1, PMS1, and PMS2, all of which repair DNA, are especially prevalent in a rare form of hereditary colon cancer.

Scientists suspect that many other hereditary factors contribute to cancer. In addition to inherited mutations, other genetic variations, particularly those influencing how the body responds to carcinogens, may create a greater susceptibility to cancer. The identities of the majority of these genetic variations are not yet known.

3. Steroid Hormones

Medical research suggests that cancers of the reproductive organs may be affected by naturally occurring steroid hormones produced by the endocrine system. These hormones stimulate reproductive organ cells to divide and grow. In women, relatively high or long exposure to the female sex hormone estrogen seems to increase the risk of breast and uterine cancers.

Thus, early age at first menstruation, late age at menopause, having a first child after age 30, and never having children, all of which affect the duration of estrogen exposure in the body, increase the risk for these cancers. Studies also indicate that hormone replacement therapy (HRT), in which women take estrogen to offset the unpleasant effects of menopause, increases the risk of breast cancer. Male sex hormones, particularly testosterone, appear to play a role in cancers of the male reproductive organs, but this role is not yet well understood.

4. Population Demographics

Population studies show that a person’s age, race, and gender affect the probability that he or she will develop cancer. Most cancers occur in adults middle-aged or older. The risk of cancer increases as individuals age because genetic mutations accumulate slowly over many years, and the older a person is, the more likely that he or she will have accumulated the collection of mutations necessary to turn an otherwise healthy cell into a cancerous cell.

More than three-fourths of all cancers in North America are diagnosed in people over age 55. Statistics show that men are more likely to develop cancer than women. In the United States, nearly half of all men will develop cancer at some point in their lifetimes, whereas slightly more than one-third of women will.

Stomach cancer is nearly twice as common in men as in women, as are certain types of kidney cancer. However, the reasons for the discrepancy between the sexes are unknown. Some cancers are more prevalent in particular races than others. In the United States, for example, bladder cancer is twice as common in white people as in black people. White women are slightly more likely to develop breast cancer than are black women, but black women are more likely to die of the disease.

Asian, Hispanic, and Native American women have the lowest breast cancer risk. On the whole, African Americans, especially men, are more likely to develop cancer—and more likely to die from it—than members of any other group in the United States. Reasons for the discrepancies between races are still not entirely clear, but many epidemiologists trace them to differences in diet and exercise, unequal access to medical care, and exposure to carcinogens.

HOW CAN CANCER DEVELOP IN OUR BODY: CELLS BREAK FREE AND SPREAD

More cancer, more cancer again, the reader may get bored with this article, but this information must I provide to be a lesson for us. Cancer can develop in the human body, therefore I think we need to know how the cancer can develop in the body. This article is a continuation of previous articles that discuss the same topic. Evading the many obstacles that guard against runaway cell division is still not enough for cancer to develop. A malfunctioning cell must also skirt a number of safety mechanisms designed to prevent cells from growing where they are not supposed to in the body.

Normal cells adhere to each other and to a fibrous meshwork called an extracellular matrix. This matrix exists throughout all tissues and provides the structural support on which cells grow and form organs and other complex tissues. While a normal cell will often die if it cannot adhere to an extracellular matrix, cancer cells survive without this matrix.

1. Tumor Forms

A tumor is a mass of cells not dependent upon an extracellular matrix. These cells can grow on top of each other, creating a mass of abnormal cells. Often a tumor develops its own network of tiny blood vessels to supply itself with nutrient-rich blood, a process called angiogenesis.

There are two general types of tumors. Benign tumors do not invade other tissues and are limited to one site, making surgical removal possible and the odds for a full recovery excellent. Some benign tumors are quite harmless and are not surgically removed unless they are unsightly or uncomfortable. For example, warts are benign tumors of the outer layer of the skin. Although they are usually not dangerous, warts may cause discomfort. Other benign tumors are thought to be precursors to cancerous, or malignant, tumors.

2. Tumors Spread

Tumors are malignant only if they can invade other parts of the body. Malignant tumors extend into neighboring tissue or travel to distant sites, forming secondary growths known as metastases. To metastasize, tumor cells break through a nearby blood vessel to enter the circulatory system or through a lymphatic vessel wall to enter the lymphatic system. Most metastases occur in organs that are the next site downstream in the circulatory system or the lymphatic system and contain a network of capillaries, or small blood vessels. For example, cancer of the large intestine often travels through the bloodstream to the liver, the organ immediately downstream from the intestines.
In the lymphatic system, tumor cells can spread to surrounding lymph nodes, or lymph glands. Normally, lymph nodes filter out and destroy infectious materials circulating in the lymphatic system.
The unique receptors on the surface of a cell may also play a role in where tumors metastasize. Specialized molecules on a cell’s surface identify where in the body the cell belongs. Similar cells adhere to one another when their surface receptors are compatible. Most often cells from different tissues and organs have incompatible surface receptors.

However, some tissue types share similar surface receptors, enabling cancerous cells to move between them and proliferate. Prostate cells and bone cells, for example, have similar surface receptors. This gives prostate cancer cells a natural affinity for bone tissue, where they can settle to form a new tumor.

Many cancers shed cells into the bloodstream early in their growth. Most of these cells die in the bloodstream, but some lodge against the surface of the blood vessel walls, eventually breaking through them and into adjacent tissue.

In some cases, these cells survive and grow into a tumor. Others may divide only a few times, forming a small nest of cells that remain dormant as a micrometastasis. They may remain dormant for many years, only to grow again for reasons not yet known.

HOW CAN CANCER DEVELOP IN OUR BODY: BODY SECURITY SYSTEM FAILED

Some time ago I wrote an article about how cancer develops?now I'll write a continuation of the article, how the cancer can develop in our body. While each human cell performs its own specialized function, it also exerts influence on the cells around it. Cells communicate with one another via receptors, protein molecules on the cell surface. A cell releases chemical messages, which fit into the surface receptors of cells nearby, much as a key fits into a lock. A cell may instruct other cells in its neighborhood to divide, for example, by releasing a growth-promoting signal, or growth factor.

The growth factor binds to receptors on adjacent cells, activating a message within each individual cell. This message travels to the nucleus, where a cell’s genes are located.

1. Proto-Oncogenes Become Oncogenes

When the growth factor message reaches the cell nucleus, it activates genes called proto-oncogenes. These genes produce proteins that stimulate the cell to divide. In cancerous cells, mutations in proto-oncogenes cause these genes to malfunction.

When a proto-oncogene mutates, it becomes an oncogene—a gene that instructs the cell to grow nd divide repeatedly without stimulation from neighboring cells. Some oncogenes overproduce growth factors, causing the cell to divide too often.

Other oncogenes stimulate the cell to reproduce even when no growth factor is present. Cancer researchers have identified about 100 different types of proto-oncogenes and their cancer-causing oncogene counterparts.

2. Tumor Suppressor Genes Stop Working

When runaway cell division occurs, it does not necessarily lead to cancer. Neighboring cells respond by excreting a growth inhibitor. This chemical binds to receptors in the malfunctioning cell, sending a signal to the nucleus that activates tumor suppressor genes. Tumor suppressor genes are like brakes for cell growth.

When activated, these genes halt the cell cycle, preventing further cell division. But if tumor suppressor genes malfunction due to mutations, the rapidly dividing cell ignores messages from its neighbors telling it to stop dividing. Malfunctioning tumor suppressor genes are not enough to cause cancer—the cell still must overcome a host of other safety mechanisms before it can cause truly significant damage.

3. Cell Cycle Clock Malfunctions

The cell nucleus contains a collection of interacting proteins that control cell division. Sometimes called the cell cycle clock, this group of proteins interprets incoming messages at several checkpoints in the cell division cycle.
At these checkpoints, the clock evaluates the health of the cell. If conditions are right, the clock activates certain proto-oncogenes, which produce proteins that trigger the cell to enter the next stage of the cell cycle. If conditions are not right, certain tumor suppressor genes produce proteins that prevent the cell from proceeding with cell division.