What is cancer?
In simple terms, cancer is a group of more than 100 diseases that develop across time and involve the uncontrolled division of the body’s cells. Cancers arise when critical genes are mutated, causing unregulated proliferation of cells. These rapidly dividing cells pile up on top of each other to forming a lesion or a lump in some part of the body. This mass of abnormal cells is tumour. When it grows in confined area we call is a benign tumour and when it develops capability of invading surrounding tissues it becomes a malignant tumour. Cellular condition where tumour cells invade neighboring tissues and spread via body fluids to other parts of the body is called cancer.
How normal cells become cancerous and how malignant cells spread to other parts of the body?
A tumour develops as a result of mutations (damage to DNA), and the number of mutations involved in different types of tumours can vary. We do not know the exact number of mutations required for a normal cell to become a fully malignant cell. The tumour begins to develop when a cell experiences a mutation that makes the cell more likely to divide than it normally would. The altered cell and its descendants grow and divide too often, a condition called hyperplasia. At some point, one of these cells experiences another mutation that further increases its tendency to divide. This cell’s descendants divide excessively and look abnormal, a condition called dysplasia. As time passes, one of the cells experiences yet another mutation. This cell and its descendants are very abnormal in both growth and appearance. If the tumuor that has formed from these cells is still contained within its tissue of origin, it is called in situ cancer. In situ cancer may remain contained indefinitely. If some cells experience additional mutations that allow the tumour to invade neighboring tissues and shed cells into the blood or lymph, the tumour is said to be malignant. The escaped cells may establish new tumors (metastases) at other locations in the body.
How cancers grow?
Cancer develops and progresses through avoiding apoptosis (programmed cell death), which is a naturally-occurring method by which the body rids itself of damaged or unwanted cells and maintains healthy tissue function. Normal cells generally trigger apoptosis in response to a variety of factors: cell stress, DNA damage, developmental cues and other signals initiated in the body. Cancer cells, however, are able to avoid apoptosis, thereby allowing them to survive, develop and spread.
How cancer cells are different from normal cells?
Cancer cells are different to normal cells in several ways. They don’t die and unlike normal cells, cancer cells do not stop reproducing after they have doubled 50 or 60 times.
Further, cancer cells override the normal signaling system. This may be because the genes that tell the cell to reproduce keep on and on sending signals. Or because the genes that normally tell the cell to stop reproducing have been damaged or lost. So the cancer cell keeps on doubling, regardless of the damage the extra cells cause to the part of the body where the cancer is growing. Cancer cells can lose the molecules on their surface that keep normal cells in the right place. So they can become detached from their neighbors.
What are the treatment options available for cancer treatment?
The most common types of cancer treatment include surgery, chemotherapy, radiation therapy, immunotherapy and stem cell transplant.
How cancer fights back or become resistant to chemotherapy?
Typically, a first course of chemotherapy may prove highly beneficial, nearly annihilating a tumour. But a few resistant cancer cells often survive and proliferate. Too often, despite more aggressive second and third courses of chemotherapy, the remaining drug-defiant cells thrive, displaying increasing resistance to drug therapy and eventually displaying virtual invulnerability to chemotherapy.
Why cancer cells are so difficult to kill?
There could be several reasons why cancer cells refuse to die. First, a group of proteins known as drug metabolizing enzymes are responsible for metabolizing a vast array of xenobiotics, including drugs, as well as endogenous compounds. In normal cells, the levels of these enzymes are maintained at a low level. However, in cancer cells the levels of these enzymes are elevated and thus these cells become capable of effectively metabolizing anticancer drugs. Some tumors have the ability to constantly change. For example, in case of nutrient starvation they change their biology to be able to grown in low oxygen, low pH and low nutrient environment. Cancer cells also enhance the expression of those genes which play important roles in survival, proliferation, division and differentiation. Moreover, it is very difficult to
Is there hope for cancer patients in future?
The recent finding has undoubtedly advanced our understanding of cancer and patient survival has significantly increased in the past decade. In the next decade, our research focus should be to identify targets that are essential for the survival of cancer cells and develop targeted cancer therapies (drugs that interfere with specific molecules involved in cancer cell growth and survival).
Associate Professor & HOD
Department of Biotechnology
School of Engineering and Technology
1. Drug metabolism and anti-cancer drug resistance.
2. Modulation of MAP Kinase signaling and Apoptosis by anti-cancer drugs.
3. Protein phosphorylation by PKCs and EGFR.
4. Cancer stem cell culture and resistance to therapy.