Biochemistry of cancer

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Biochemistry of Cancer

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  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • NCI Web site: http://cancer.gov/cancertopics/understandingcancer
  • Biochemistry of cancer

    1. 1. Biochemistry of Cancer Ashok Katta
    2. 2. What Is Cancer?
    3. 3. Cancer • Cancer is uncontrolled growth and Cell proliferation results in a mass (tumor) that invades neighboring tissues and may metastasize to more distant sites. • Some cancers, however, such as blood cancers, do not form tumors. Cancer is one of the most common and severe problems of clinical medicine.
    4. 4. • Tumors can be of 2 major types: • Benign tumors are generally slow growing expansive masses often with a “Pushing margin” and enclosed within a fibrous capsule. Benign tumors are not cancer. • Malignant tumors are usually rapidly growing. • invading local tissue and spreading to distant sites. Malignant tumors are cancer.
    5. 5. Characteristics of cancer cells  Dedifferentiated;  Less adherent;  Loss of cell cycle control;  Tissue invasion and metastasis;  Evading apoptosis;  Insensitivity to antigrowth factor;  Increased mutation rate;  Induce local blood vessel formation (angiogenesis).
    6. 6. BIOCHEMICAL CHANGES IN CANCER CELLS AND NORMAL CELLS Loss of contact inhibition Growing cells forms multilayer Increased Synthesis of RNA & DNA Decreased catabolism of pyrimidine glycolysis leads to lactic acidosis Synthesis of fetal protein Increase in growth factor secretion Increase in oncogene expression Loss of tumor suppressor genes Contact inhibition Forms single layer Synthesis of RNA & DNA is normal. catabolism of pyrimidine also normal Mostly aerobic glycolysis Oncogene expression is rare Intermittent or co-ordinated growth factor secretion oncogene expression is absent Presence of tumor suppressor genes NORMAL CELLS Normal cell Few mitoses Frequent mitoses Nucleus Blood vessel Abnormal heterogeneous cells CANCER CELLS
    7. 7. Nomenclature of Cancer Lung Breast (women) Colon Bladder Prostate (men) Some common sarcomas: Fat Bone Muscle Lymphomas: Lymph nodes Leukemias: Bloodstream Some common carcinomas:
    8. 8. Naming Cancers Prefix Meaning adeno- gland chondro- cartilage erythro- red blood cell hemangio- blood vessels hepato- liver lipo- fat lympho- lymphocyte melano- pigment cell myelo- bone marrow myo- muscle osteo- bone Cancer Prefixes Point to Location
    9. 9. Naming Cancers Prefix Meaning adeno- gland chondro- cartilage erythro- red blood cell hemangio- blood vessels hepato- liver lipo- fat lympho- lymphocyte melano- pigment cell myelo- bone marrow myo- muscle osteo- bone Cancer Prefixes Point to Location
    10. 10. Loss of Normal Growth Control Cancer cell division Fourth or later mutation Third mutation Second mutation First mutation Uncontrolled growth Cell Suicide or Apoptosis Cell damage— no repair Normal cell division
    11. 11. Example of Normal Growth Cell migration Dermis Dividing cells in basal layer Dead cells shed from outer surface Epidermis
    12. 12. The Beginning of Cancerous Growth Underlying tissue
    13. 13. Tumors (Neoplasms) Underlying tissue
    14. 14. Invasion and Metastasis 3 Cancer cells reinvade and grow at new location 1 Cancer cells invade surrounding tissues and blood vessels 2 Cancer cells are transported by the circulatory system to distant sites
    15. 15. Malignant versus Benign Tumors Malignant (cancer) cells invade neighboring tissues, enter blood vessels, and metastasize to different sites Time Benign (not cancer) tumor cells grow only locally and cannot spread by invasion or metastasis
    16. 16. Why Cancer Is Potentially Dangerous Melanoma cells travel through bloodstream Melanoma (initial tumor) Brain Liver
    17. 17. What Causes Cancer? Some viruses or bacteria Heredity Diet Hormones RadiationSome chemicals
    18. 18. Etiology of Cancer •Genetic factors •hormonal •Racial & geographic factors •Environmental factors •Chemical factors •Age •Sex
    19. 19. Heredity Can Affect Many Types of Cancer Inherited Conditions That Increase Risk for Cancer
    20. 20. Mutagens / Carcinogens •Any substance which increase rate of mutation •All mutagens are carcinogens. •Examples are…… • Radiations like X-ray, UV-ray, gamma ray • Chemicals like benzopyrenes, Aflatoxins • Hormones like estrogen
    21. 21. Industrial Pollution Some of the chemical Carcinogens in the Workplace
    22. 22. Tobacco Use and Cancer Some Cancer-Causing Chemicals in Tobacco Smoke
    23. 23. Viruses and Cancer • Viruses promoting human cancer. These include both DNA viruses and retroviruses, type of RNA viruses. Tumor Viruses
    24. 24. DNA Tumor Viruses •Viruses can contribute to cancer by inserting their DNA into a chromosome in a host cell. •Insertion of the virus DNA directly into a proto-oncogene may mutate the gene into an oncogene, resulting in a tumor cell.
    25. 25. RNA Tumor Viruses • The ability of retroviruses to promote cancer is associated with the presence of oncogenes in these viruses. • An example of this is the normal cellular c-sis proto-oncogene, which makes a cell growth factor. The viral form of this gene is an oncogene called v-sis. Cells infected with the virus that has v-sis overproduce the growth factor, leading to high levels of cell growth and possible tumor cells.
    26. 26. Cancer Genes •Proto-oncogenes – normally promote normal cell growth; mutations convert them to oncogenes. •Tumor suppressor genes – normally restrain cell growth; loss of function results in unregulated growth. •Mutator or DNA repair genes – when faulty, result in an accumulated rate of mutations.
    27. 27. Proto-oncogenes • Proto-oncogenes are normal genes. • These code for proteins that help to regulate cell growth and differentiation. These are … Growth factor, Growth factor receptor, Transcription factors and Other proteins involved in proliferation of cell. • Mutation of Proto-oncogenes leads to abnormal production of these proteins that causes abnormal growth. • Excessive or inappropriate expression of these genes can also causes abnormal growth.
    28. 28. Tumor Suppressor genes Tumor Suppressor genes are normal genes. These genes switch off cell proliferation. These genes normally suppresses tumour formation. Mutation or deletion of these genes leads to the loss of their function result in malignant transformation. Example are…. Retinoblastoma gene (RB gene) P53 gene
    29. 29. Balance between factors stimulating and inhibiting cell growth Tumor suppressor inhibitors Proto- oncogenes stimulators Tumour suppressor Proto- oncogenes
    30. 30. Oncogenes Oncogenes or tumor genes are genes with potential properties for the induction of neoplastic transformation Oncogenes are genes able to produce cancer when overexpressed, amplified, or mutated. Most oncogenes are mutated forms of normal genes, called proto-oncogenes. Proto-oncogenes are activated to oncogenes by various mechanisms…. Point mutation, Promoter and enhancer insertion, Chromosomal translocation and Gene amplification.
    31. 31. Some oncogenes & their related cancer Oncogene Type of Cancer Gene modification Ab1 Chronic myeloid leukemia Translocation Myc Burkitt's lymphoma Small cell lung cancer Translocation Amplification L-myc Small cell lung cancer Amplification N-myc Neuroblastoma Amplification Ras Bladder cancer Mutation K-ras Colon cancer Mutation N-ras Acute myeloid leukemia Mutation
    32. 32. --- Physiological cell death --- Cell suicide --- Cell deletion --- Programmed cell death APOPTOSIS Cells are born, live for a given period of time and then die
    33. 33. WHERE can APOPTOSIS be ENCOUNTERED ? ... Growth of Embrio ... Tissue Homeostasis ... Immunology ... Chronic viral diseases ... Neurodegenerative diseases ... Reperfusion injury ... Insuline-dependent Diabetes ... Atheroschlerosis ... Miyokard Infarction ... AIDS ... Development and Treatment of Malignancies
    34. 34. GENERAL FEATURES OF APOPTOSIS • ... Occupation of death receptors • ... Dimerization of Bcl-2 family members • ... Release of cytochrome c • ... Activation of caspases • ... Activation of DNase 1) A number of activities take place
    35. 35. Cancer Detection and Diagnosis We will see in next class…

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