What causes cancer?
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What causes cancer?

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This article discusses the causes of cancer and outlines the current issues that limit standard approaches to treating cancer.

This article discusses the causes of cancer and outlines the current issues that limit standard approaches to treating cancer.

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What causes cancer? What causes cancer? Document Transcript

  • What Causes Cancer?Most, if not all cancers are caused and perpetuated by a small population of tumor-initiating cellsthat exhibit numerous stem cell-like properties. Adult stem cells (SC) are involved in theregeneration and maintenance of our body tissues and account for one out of every 6 millioncells. Each tissue has a unique population of specific SCs located in regions known as niches. Inthe SC niche, the SCs exist in a unique dormant state known as quiescence, and remain in thisstate until they are given the cues to be activated.Activated stem cells go through two stages of development referred to as proliferation anddifferentiation. During proliferation, biochemical cues cause the cells to reproduce, resulting inan expanded population of similar cells. Differentiation puts a stop to proliferation with specificbiochemical cues that cause the proliferating cells to differentiate into a specific type of cell.Once a stem cell has differentiated, it has a finite life span and is limited in how many times itcan reproduce. The number of times a differentiated cell can reproduce is referred to as itsHayflick number.Cancer results when a stem cell is stuck in proliferation, and is therefore not given the cues todifferentiate. This situation results in a continually expanding population of undifferentiated cellsthat can not only exist anywhere in the body (metastasis), but also have unlimited life spans (noHayflick number).The biochemical cues for proliferation and differentiation are based on genes specific to eachtissue type. In general, genes that initiate proliferation are called oncogenes while genes thatinitiate differentiation are called tumor suppressors. Cancer, therefore, could be seen as an over-activation of oncogenes accompanied by the inhibition of tumor suppressors. It is the ratio ofoncogenes to tumor suppressors that determines the aggressiveness of the cancer.Another key piece in the growth of cancers is a process called angiogenesis. Angiogenesis is thephysiological process that tumors use in order to recruit new blood vessels in order to sustaintheir continual growth. They do this by over-expressing genes that initiate and direct the growthof new, leaky blood vessels from existing ones. Both angiogenesis and the spontaneousformation of new blood vessels (vasculogenesis) are initiated by unique combinations of genes.Standard chemotherapeutic agents inhibit rapidly dividing cells during treatment, but do notaffect dormant cancer initiating SCs. An example of this is shown in a side affect of treatment.During chemotherapy, patients lose their hair (rapidly dividing cells), but their hair typicallygrows back soon after treatment. This is due to the dormant SCs located in the hair shaft, whichwere not affected by the chemotherapy. It is this presence of dormant cancer initiating SCscombined with the occurrence of angiogenesis in-between treatment regimes that leads to diseaserecurrence.The following link allows you to access the genes involved with various types of cancers.http://www.genome.jp/kegg/Alex Rolland is a cancer researcher, educator, and CEO of Cancer treatment Options andManagement (www.CTOAM.com). CTOAM is a personalized cancer research company thatspecializes in using the most current peer reviewed scientific research on cancer diagnostics,treatments, nutraceuticals, and clinical trials to educate patients on the treatments and diets thatprovide the best statistical chances for success.