In his riveting book One Renegade Cell, leading scientist and cell-biology expert Robert Weinberg reveals the internal ‘thrust-and-parry’ that goes on between a cancerous cell and the immune system, with stunning precision and clarity.
Is Cancer Inevitable?
Weinberg proposes that the extraordinary complexity of the human body dictates the inevitability of cancer. He sees cancer as a disease of damaged genes and shows conclusively that the appearance of a tumour requires many successive genetic mutations.
These clever mutations must bypass the complex proteins that determine how a cell behaves and override the cell-cycle clock which governs decisions on when a cell grows, differentiates or dies.
He reveals 5 key natural ‘barriers’ that the malignant cell must overcome, for the body to develop cancer.
Barrier no. 1 – Body’s first line of defence
A dormant (proto) onco-gene needs to be bio-chemically transformed into an active onco-gene, by a mutagen (genetic or environmental carcinogen).
Simultaneously, the body’s first line of defence – a corresponding tumour-suppressor gene – needs to be deactivated. Both these destabilizing processes are resisted by the in-built circuit-breakers of the cell. .
Barrier no. 2 : Growth factors produced by the body that neutralise cancer cells
To bypass this internal set of controls, the cell releases ‘growth-factors’ into its immediate surroundings, flooding it with unrelenting growth-stimulating signals.
To neutralise these, the body also produces growth-inhibiting h2 factors, which some tumour cells manage to escape.
Barrier no. 3 : Natural death cycle of each cell
A normal cell is endowed with a limited number of ‘doublings’, which naturally caps uncontrolled growth. Every cell contains a ‘generational clock’ i.e. a counting device which registers and records each time the cell passes through growth and division.
When the cell reaches its pre-determined limit of allotted doublings, the clock sounds a ‘telomerase alarm’ which tells the cell to stop growing, turn senescent and ultimately die.
Tumour cells not only learn to ignore this telomerase alarm, they actually resurrect telomerase, by accessing hidden information in their DNA and using it to make telomerase. Now they are able to regenerate indefinitely and bypass the generational clock.
Barrier no. 4 : Self-destruct program of every cell
The more drastic way is to induce a damaged cell to commit suicide. Apoptosis (a Greek word that describes a tree shedding its leaves) is a self-destruct program wired into every human cell.
When the cell senses serious DNA damage to itself, its p-53 protein acts as an emergency brake and activates its repair mechanism. However, should the DNA damage be massive, the p-53 protein will also activate the apoptosis program and instead of attempting repair, the cell will kill itself.
Tumour cells avoid or subvert apoptosis by undergoing a second mutation which somehow inactivates the p-53 protein. With its damage-response mechanism crippled, the cell can race ahead and replicate its damaged DNA, passing it on to descendent cells.
The absence of p-53 can amplify and enhance the rate of replication almost a thousand-fold. Worse still, if p-53 is knocked out by the mutation, such cells can survive for extended periods without oxygen or nutrients.
Barrier no. 5 : Immune system’s additional defence
The immune system erects various additional lines of defence, including for example, natural killer (NK) cells and many others.
The book beautifully outlines how the errant cell successfully counters these 5 barriers … and how modern scientists are tantalisingly close to finding a lasting cure to the disease!
If all these hurdles are overcome, yet other difficulties loom.
How The Primary Tumour Grows
Once the clump of cells reaches the one millimeter size, the normal process of diffusion no longer provides adequate nutrition or waste removal. Soon the cells starve (anoxis) and begin to choke on their own wastes. Once again, apoptosis can kick in and the cells may die.
Tumour cells respond by inventing a better way to access nutrients and remove wastes: they develop their own blood circulation system. By aping the surrounding normal cells, they secrete (angiogenic) growth factors and induce capillaries to grow into the clump of cancer cells. Finally, the tumour cells have direct access to oxygen-rich and nutrient-rich blood and their numbers begin to increase explosively.
How Metastasis Takes Place
- The process of metastasis is also very complex, with the odds stacked against its success.
- To begin with, cells in the primary tumour must breach surrounding physical barriers. They release enzymes (called proteases) which break and dissolve the membrane-like meshwork of proteins.
- Protease enzymes are used by normal cells during the formation and repair of normal tissue. As they enter other types of tissue, the tumour cells learn how to subvert, exploit and misuse normal protease enzymes; rather than releasing them selectively and in small doses, they flood their surroundings with them.
- As the tumour grows (a 1-cm tumour can contain a billion cells), individual or small clumps of cells may break off from the primary mass. Using the blood vessels or the lymphatic system, they can end up in distant locations. The journey is fraught with risk.
- They must survive the swim through the circulation system, to which they are not adapted. They must reattach and cling to the wall of the blood or lymph vessel using ‘anchoring receptors’. They must push aside endothelial cells and burrow through the sheathing around the vessel into the adjacent or underlying tissue.
- Each new site is a foreign environment that represents a major challenge to the tumour cells; they must confront physical structures and growth factors to which they are unaccustomed.
- By this time, the tumour cells themselves have become unstable. In continuously adapting their own genes to such different demands and environments, very few actually survive and a great many simply die.
- However, what keeps the process going is simple arithmetic. The primary tumour may have grown quite large and can dispatch a large, continuous stream of cells to the distant sites. At any given time, more tumour cells are being produced compared to those dying.
How Death Occurs
Sooner or later, these distant colonies of tumour cells begin to compromise the functioning of the host tissues and organs. Only then does the overall system begin to break down and the patient placed at death’s door. It is truly a ‘fight-to-the-finish’.
‘One Renegade Cell‘ By Robert Weinberg
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