|
Publish in the Journal of carcinogenesis |
Despite the advances in the treatment of cancer and the increasing knowledge of the processes responsible for the disease, there is a gap in the understanding of molecular events leading to cancer and the mechanisms of action by anticancer agents
The field of carcinogenesis is far from being completely explored. Many novel ideas and concepts still need to be introduced into the field, and the results of several provocative experiments are yet to be disseminated and shared. There is a need for multidisciplinary research in the field and a forum for accelerated publication of results.
|
|
Read More |
|
|
|
|
|
|
|
CARCINOGENESIS
|
Carcinogenesis is a process through which normal cells are transformed into cancer cells. Cell division is a normal biological process, which happens in almost every tissue. Every day, in human body several cells die and new cells are born. But, there is a balance between cell growth and controlled cell death, known as apoptosis. Mutations (changes in genes) in genes which play vital roles in cell division, apoptosis and DNA repair cause a cell to lose control of its growth leading the way for cancer. Uncontrolled growth of cells leads to tumors. This is a generally accepted and simplified higher level model of carcinogenesis.
|
| |
 |
 |
All tumors are not harmful. Benign tumors do not migrate to other parts of the body or invade other tissues. They are rarely a threat to life unless they compress vital structures or are physiologically active. Malignant tumors can invade other organs and spread to distant locations (metastasis) and become life-threatening.
|
|
 |
|
Carcinogenesis is a multi-step genetic process. The three main steps are initiation, promotion and progression. A host of mutations in genes bring about these steps. Two distinct classes of genes, proto-oncogenes and tumor-suppressor genes are involved in the cancer process. Mutations in proto-oncogenes which promote cell growth turn the proto-oncogenes into oncogenes (cancer genes) driving cells to grow uncontrollably. When oncogenes go into overdrive, tumor suppressor genes are inactivated. Tumor suppressor genes code for proteins that put brakes on the growth of cells and protect cells� DNA against damage. There are various sources of carcinogenesis � chemical, familial, physical, viral, bacterial, occupational, and environmental. Chemical carcinogenesis is caused by carcinogens (chemicals) rich in electrons that bind to DNA causing mutations. In 1915, for the first time carcinogenesis was identified in laboratory by applying coal tar to rabbit skin. A year before this, Theodor Boveri propounded somatic mutation theory of carcinogenesis in his book ZurFrage der Entstehung Maligner Tumoren (On the Problem of the Origin of Malignant Tumors).
Familial carcinogenesis runs in family. Of all the tumors, 15 per cent have hereditary component. Among the cancers, breast cancer and colorectal cancer have a family component. In physical carcinogenesis, ionizing radiation, ultraviolet rays and asbestos inhalation can cause malignant tumors.
Many cancers originate from a viral infection. Viruses cause 15 per cent of human cancers. First viral cancer gene was detected in chicken in 1911. Of all the viruses, human papillomaviruses cause cervical and other genital cancers and hepatitis B viruses cause liver cancer. One good example of bacterial carcinogenesis is gastric cancer which is induced by Helicobacter pylori.
Research has shown that typical sporadic (not familial) colorectal cancers on average contain at least 11,000 genomic alterations per cell. According to the research, such genomic instability begins very early in cancer process and can be found in adenomatous polyps, which are known to be the precursors of cancer in the colon and rectum. In any tumor, multiple oncogenes may be activated or multiple tumor-suppressor genes may be inactivated. Identification of the genes involved in carcinogenesis and elucidation of the mechanisms of their activation or inactivation allows a better understanding of how chemical carcinogens influence the process of cancer evolution.
|
|
|
|
|
|
|
 |
|
 |
|
|
|
|
|
|
 |
| WHO Recommendations for Cancer Prevention |
 |
|
|
| Lifestyle and Cancer incidence (Source: National Cancer Institute, USA) |
 |
|
|
|
 |
|
|