What are Cancer Cell?
Carcinomas are cells that grow and divide uncontrollably, forming malignant tumors and invading nearby parts of the body. Carcinomas can also spread to other organs through the blood and lymph systems. This process is referred to as metastasis. Normal cells grow and divide to form new cells as the body needs them. However, in carcinomas this orderly process goes wrong. The genetic alterations in carcinomas give them the properties of uncontrolled growth, avoidance of programmed cell death or cell senescence, ability to evade the immune system, and ability to induce formation of new blood vessels. The uncontrolled growth of these defective carcinomas leads to the formation of malignant tumors that grow locally and spread to other parts of the body.
How Cancer Cell Form?
Cancer Cell typically begins when defects accumulate in the DNA of cells that trigger erratic cell division and prevent normal cell death. As cells divide, these genetic defects are duplicated and passed along to new cells. Cancer is a result of multiple mutations, with many mutations often needed before a cell turns cancerous. Environmental exposures, lifestyle factors, inheritable genes, and random DNA copying mistakes all play a role in determining one’s cancer risk by increasing the chances of DNA mutations occurring over a lifetime. Some of the main causes for genomic instability and mutations that can trigger cancer include tobacco smoke, various cancers causing viruses, certain chemicals, ionizing radiation, obesity, and certain inherited syndromes.
The Hallmarks of Carcinomas
In 2000, scientists Douglas Hanahan and Robert Weinberg proposed six hallmarks of cancer as the common biological capabilities acquired during the development of all types of human tumors. These hallmarks include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Later in 2011, they added two more emerging hallmarks, which include reprogramming of energy metabolism and evading immune destruction. Carcinomas must develop all of these hallmark capabilities to become malignant and metastatic. The acquisition of these hallmarks results from genetic and epigenetic alterations that ultimately corrupt normal cell physiology.
Evading Immune Destruction
One of the emerging hallmarks of carcinomas that allow them to thrive is the ability to evade destruction by the immune system. Normally, when aberrant or stressed cells arise, the immune system is able to identify and eliminate them before they become tumorigenic. However, carcinomas use several mechanisms to avoid recognition and destruction by the immune system. Some of the common mechanisms used by carcinomas include downregulating molecules that are recognized by immune cells, secretion of suppressive cytokines in the tumor microenvironment that creates local immune suppression, recruitment of immunosuppressive cells like regulatory T cells in the tumor vicinity, and expression of checkpoint molecules like PD-L1 that inhibit T cell function. Ongoing research aims to understand these immune evasion mechanisms by carcinomas to devise better immunotherapies against cancer.
The Role of Metabolism in Cancer
Another capability that carcinomas develop to thrive is reprogramming of their metabolism. In the 1920s, biologist Otto Warburg observed that carcinomas predominantly produce energy by a high rate of glycolysis followed by lactic acid fermentation even in the presence of sufficient oxygen. This phenomenon is known as the Warburg effect and it allows carcinomas to produce energy and macromolecules rapidly to meet the high demands of unchecked growth and division. Some of the key metabolic adaptations in carcinomas include increased glucose uptake and glycolysis, increased uptake of glutamine that fuels the tricarboxylic acid cycle, enhanced fatty acid synthesis to generate membrane phospholipids, adaptation of oxidative stress response, and reliance on alternative nutrient sources like lactate in nutrient-deprived tumor microenvironments. Novel cancer drugs now target various key enzymes and pathways in the altered metabolism of carcinomas.
Hijacking of Angiogenesis Process
To fuel their uncontrolled growth, carcinomas hijack the normal angiogenesis process by secreting various pro-angiogenic factors. Angiogenesis is the process by which new blood vessels are formed. It plays an important role in reproduction, embryonic development and wound healing. But in cancer, tumor cells co-opt this normally beneficial process to promote the growth of blood vessels that supply nutrients and oxygen and remove waste products. Some of the key pro-angiogenic factors secreted by carcinomas include vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and platelet-derived growth factor (PDGF). These factors activate quiescent endothelial cells, stimulating them to proliferate and migrate into the tumor, remodelling the extracellular matrix and generating neovasculature required to support the rapidly growing tumor. Angiogenesis inhibitors are now widely used as anticancer drugs that target this hallmark capability of carcinomas.
Evasion of Programmed Cell Death
Another strategy used by carcinomas to proliferate indefinitely is evading programmed cell death or apoptosis. This capacity prevents the elimination of cells with DNA damage or other defects. Normal cells activate an intrinsic suicide program called apoptosis to eliminate themselves when they become damaged or unstable. But carcinomas acquire genetic changes that disable apoptotic pathways allowing them to circumvent this natural tumor suppression mechanism. Some common evasion strategies include downregulating pro-apoptotic factors like p53, upregulating anti-apoptotic factors like Bcl-2, or activating growth-promoting signaling pathways like PI3K/Akt that antagonize apoptosis. Compounds that reactivate apoptosis or inhibit anti-apoptotic factors are under development as novel targeted therapies against cancers with defects in cell death pathways. In understanding the complex biology of carcinomas that allow them to evolve these hallmark capabilities provides opportunities to identify new therapeutic strategies. Targeted drugs interfering with carcinoma metabolism, angiogenesis and immune evasion are improving treatment outcomes. With ongoing research elucidating additional hallmarks and vulnerabilities, more personalized and effective anticancer therapies can be developed. This improved understanding of carcinoma dynamics guides precision oncology approaches tailored for individual patients.
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