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Different types of cancer have different origins, mechanisms, rate of development, patterns and differ in their responses to treatment. Thus, accurate diagnoses and evaluation are important and critical at times. Classification includes identifying the origin tissue, extent of distribution, microscopic and immuno-histomical appearance and genetic changes.
Benign tumors are well differentiated and well organized stroma (the supportive tissue) of an epithelial organ, tumor, gonad (sex gland), etc., consisting of connective tissues and blood vessels. They do not spread, remain in their capsule and do not interrupt the tissue's structure. The suffix of “oma” is common for benign tumors. Malignant tumors have rapid growth rates and specific microscopic alterations such as loss of differentiation and abnormal tissue organization. A very distinctive mark of cancer is Anaplasia (loss of differentiation) and being Pleomorphic (of different size and shape). Often, the nuclei is dark and stained with mitotic cells.
The amount of stroma may be greater than usual, without a capsule, invading other cells and tissues. Invasion of blood vessels, lymphatic and surrounding structures is common. Metastasis is a malignant tumors’ ability to spread to other tissues, even far away. Cancerous cells invade other cells, tissues and systems in order to take over resources such as nutrients, blood supply, oxygen, and space.
As indicated, we distinct between different types of cancers; The suffix of “sarcoma” refers to cancers of connective tissue. Carcinomas are cancerous tumors originating from the epithelium, adenocarcinomas originate from a duct or gland, lymphomas are cancers of the lymphatic system, while leukemias are cancers of blood tissue. Some cancer names originate from historical reasons that do not follow this terminology; For example, Hodgkin Disease and Ewing Sarcoma.
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Genetic lesions accumulation is a significant process in the development of cancer. Early detection of genetic lesion accumulation can save lives if the cancer is violent. If they have not penetrated the basement membrane or invaded the surrounding stroma they are called Carcinoma in Situ (CIS; In situ means “on site”). Carcinoma in Situ have three possible reactions: 1) remain stable; 2) progress to become invasive/metastatic; 3) regress and disappear.
High grade Carcinoma in Situ are most likely to become invasive. Waiting to see if low-grade lesions develop to high-grade lesions is termed in medicine Watchful Waiting. Some medical professionals prefer to avoid watchful waiting and remove any Carcinoma in Situ in order to be on the safe side. As part of the process to better understand the exact treatment needed, we analyze the molecular and genetic attributes of the tissue. Cancer treatment, as are other disease treatments, are becoming more and more genetic mutation specific (see previous posts about genetic mutations). This is referred to as personalized medicine.
Tumor markers help in the prognosis process (which includes evaluation of future outcomes), and the treatment process. Biomarkers are very commonly found in blood tissue but also in other fluids such as spinal fluids and urine. The paraneoplastic syndrome occurs when a tumor marker has biological activity, causing clinical symptoms.Associating tumor markers with a disease is very helpful in the prognosis and treatment processes.
The biology of cancer cells:
Contact Inhibition is a phenomenon where the number of cells in a certain area of the body is too high, cells respond by decreased growth rate and do not present hypertrophy (increased mass) or hyperplasia (increased number of cells). Growth is the outcome of the combination of hypertrophy and hyperplasia. Cancerous cells lack contact inhibition and thus will continue to grow "crowding" spaces with more cancerous cells.
While normal cells must have a firm surface, cancerous cells do not, make them Anchorage Independent. A cell that lacks Contact Inhibition and are Anchorage Independent have two major advantages when it comes to their survival compared to regular cells. This combination always marks the beginning of something bad biologically. Any biological cell with these two biological advantages, is destined to overcome the other cells around it.
Cancerous cells become "immortal" by endlessly dividing, and regenerating themselves, to the point where cancerous cells may sometimes continue to grow even when transferred to other animals. There is no doubt as to the role that DNA has in the development of cancer, yet not all cancer types are inherited. Thus, some mutations are passed from generation to generation and some are acutely induced. Genetic changes may alter all levels and structures relevant to gene expression such as DNA, RNA, chromosomes, and histones.
Age is a leading factor increasing the chances of cancer development, meaning that the percentage of people with cancer in the older population is greater than in the younger population. It is believed that the combination of genetic mutation accumulation and decreased abilities to cope, defend, and repair the genetic mutations lead to increased chances of cancer in the advanced age and elderly.
Clonal expansion and clonal proliferation occur when the cancerous cells achieve an advantage over normal cells (as described before). Mutations that cause the progression of the cell to a cancerous state are called Driver Mutations, while other mutations that are present yet do not drive the progression, are called Passenger Mutations. Oncogenes are genes that increase proliferation and have become mutant; Before mutation accumulation they are defined as Proto-Oncogenes (i.e. precursor oncogenes). Tumor Suppressor Genes decrease proliferation, and are often called Anti-Oncogenes, since they cancel the effects of oncogenes.
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This is the second post in the mini series of posts dedicated to cancer. Stay tune, more post and empowering knowledge to come.
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