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Understanding Cancer: The Battle Within Our Own Cells

Cancer represents a complex battle where our own cells turn against us, forming malignant tumors that invade normal tissues. By examining cancer's hallmarks—uncontrolled growth, evasion of cell death, and metastasis—we gain insight into its progression. This presentation explores how genetic mutations affect cell behavior and the therapeutic approaches taken, including surgery, radiation, and innovative targeted therapies. Understanding these mechanisms is crucial in the fight against cancer and its devastating impact on health and society.

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Understanding Cancer: The Battle Within Our Own Cells

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  1. Cancer: when our own cells become the enemy Erin Martinez, Ph.D. Trevecca University Physician Assistant Program September 30, 2013

  2. What is cancer? = a malignanttumor = cells that escape their normal surroundings, invading locally and travelling to distant locations = abnormal cell mass that develops when cells grow too much benign

  3. Moving from normal tissue to cancer Normal cells Benign tumor Basement membrane Blood vessel Malignant tumor = CANCER Bastid J, Ciancia C, Puisieux A, Ansieau S . Role of TWIST proteins in cancer progression. Atlas Genet CytogenetOncolHaematol. December 2009 .

  4. What does cancer look like? Breast cancer: normal to cancer Ductal carcinoma in situ DeNardo and CoussensBreast Cancer Research 2007 9:212

  5. What does cancer look like?Colon cancer: normal to cancer Cancer Normal Tumor Rose and Wu. The Internet Journal of Pathology. 12:1. 2011

  6. What does a cancer cell look like?The Hallmarks of Cancer CellHanahan and Weinberg, 2000.

  7. Hallmarks of Cancer: physiological changes 1 Keeping the foot on the gas of growth 3 2 Cells don’t die easily No brakes on growth! 6 5 Cells get more blood supply Cells escape and spread 4 Cells divide forever, and ever…

  8. Cell growth in cancer • Hallmarks 1 and 2: Keeping the foot on the gas of growth and no brakes on growth! • Progress though the cell cycle more quickly than a normal cell • Don’t follow normal rules for stopping the cell cycle (checkpoints) http://eishinoguchi.com/checkpoint.htm

  9. Cancer cells resist death • Hallmark 3: Cells don’t die easily • Things that can usually cause programmed cell death (apoptosis) • DNA and protein damage • lack of nutrition/oxygen • buildup of waste • lack of survival signals from other cells • death signals from other cells • Cancer cells ignore these and survive!

  10. Cancer cells are immortal • Hallmark 4: cells divide forever, and ever… • Normal cells stop growing or die when telomeres are gone • Cancer cells activate telomerase or do abnormal kinds of DNA recombination to survive! http://www.med.nyu.edu/skirball-lab/sfeirlab/Research.html

  11. Cancer cells induce angiogenesis • Hallmark 5: cells get more blood supply • Fast growing cells beginning to form a tumor need more nutrients and need to get rid of more waste than local blood vessels can provide • Promote formation of new blood vessels (angiogenesis) with signaling molecules (example: VEGF) http://www.cancer.gov/cancertopics/understandingcancer/angiogenesis/AllPages

  12. Cancer cells are on the move Prostate cancer metastasis imaged with PET • Hallmark 6: cells escape and spread • Normal cells die when they loose contact with surrounding cells or the basement membrane • Cancer cells gain ability to migrate locally and sometimes flow through bloodstream and grow in a distant site (metastasis) J Nucl Med February 2006 vol. 47 no. 2 287-297

  13. How do normal cells become cancerous? • Changes in gene expression and activity • most often caused by mutations • Mutations = changes in DNA that alter expression or activity of the gene • Two main types of genes with mutations in cancer: • Oncogene – genes that normally promote growth are mutated to be hyperactive • Tumor suppressor – genes that normally inhibit growth are mutated to be inactive • It takes several genetic alterations to cause cancer

  14. How do we fight cancer? • First surgery, then other therapies • Target fast-growing cells • - Radiation • - Chemotherapy Kill all fast-growing cells - bad side effects

  15. Other new cancer therapies Anti-angiogenesis therapy Avastin – anti-VEGF antibody for metastatic colorectal cancer, and advanced non-small cell lung cancer Targeted therapy to a oncogene in a tumor cell Gleevec - inhibitor of oncogene in chronic myelogenous leukemia Erbitux – inhibitor of oncogene in colorectal and head/neck cancer Herceptin - inhibitor of oncogene in breast cancer Activating immune system against cancer cells Provenge– activate man’s own immune cells against prostate cells

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