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Cancer A Disease Resulting from Uncontrolled Cell Growth Properties of Cancer Cells Due to lack of specialization, cancer cells have a different appearance than surrounding cells. Cancer cells have enlarged nuclei and may have extra chromosomes. They are genetically unstable and accumulate mutations. Normal cervical cells Precancerous cervical cells Cancerous cervical cells Non-cancerous cells form sheets. Properties of Cancer Cells Cancer cells grow into tumors, showing a lack of contact inhibition. Cancer cells do not respond to signals from Growth factors—stimulate or inhibit cell division Apoptosis factors—promote death of cells with damaged DNA Properties of Cancer Cells Cancer cells divide more frequently and for an unlimited number of times due to an abundance of telomerase, an enzyme that repairs the ends of chromosomes Cancer cells show metastasis, an invasion of other tissues Angiogenesis: cancerous tumors grow new blood vessels for delivery of nutrients and oxygen Cancer is the result of multiple mutations causing uncontrolled growth Angiogenesis: Formation of new blood vessels, allows tumor to grow to larger size Normal Cell Growth Involves the Cell Cycle with Mitosis G2 assembly of components for division S chromosomes replicate Mitosis P M A T Interphase includes G1 = growth phase 1 S = synthesis phase G2 = growth phase 2 cytokinesis G1 cytoplasm doubles Interphase Mitosis includes P = prophase M = metaphase A = anaphase T = telophase Chromosomes align individually at the cell equator so each daughter cell receives one copy of each chromosome Mitosis = Chromosomal Division Leading to Genetically Identical Nuclei Control of the Cell Cycle Mechanisms for controlling progress through the cell cycle Extracellular Signals Control the timing of cell division Transitions Orderly progression from one stage of cell cycle to another Depend on the production of proteins called cyclins Checkpoints Delay progression to next stage if cell must repair damage Control of the Cell Cycle Involves Activities at Transitions and Checkpoints Signals initiate self-destruction if DNA damage is severe Apoptosis Checkpoint G2M Checkpoint SG2 Transition G2M Transition P M G2 assembly of components for division S A T Mitosis cytokinesis G1 chromosomes replicate DNA Damage Checkpoint Spindle Assembly Checkpoint cytoplasm doubles G1S Transition G1S Checkpoint Cancer-Causing Mutations Occur in Two Types of Genes Proto-oncogene stimulates cell division mutation Oncogene overstimulates cell division Tumor Suppressor Gene inhibits cell division mutation Mutated Tumor Suppressor Gene cannot influence cell cycle Mutations That Cause Cancer Gene Type ProtoOncogene example Ras Tumor Suppressor Gene examples RB p53 Normal Function In Cancer In response to Oncogene extracellular or Promotes cell intracellular division in signals, promotes absence of cell division and signals prevents apoptosis Inhibits cell division and promotes apoptosis Active gene product no longer available to control cell division Mutation Type Dominant Recessive In cancer cells, the RAS gene product is locked into its GTP-binding shape and does not require a signal at the receptor in order to stimulate cell division Ras Proto-Oncogene In response to growth factor binding at receptor, the Ras gene product combines with GTP to promote cell division RB = product of Retinoblastoma gene, inhibits action of E2F until chemically modified due to buildup of CDK-cyclins (intracellular signals) In Normal Cells, the Rb Gene Product Controls the G1 S Transition E2F = transcription factor required to activate genes for DNA synthesis In people who are heterozygous for a mutation in the RB gene (Rb+Rb-), there is a tendency for the functional copy of the RB gene (Rb+) to mutate to Rb-. Retinal cancer develops because growth of tumor cells is no longer controlled at the the G1S transition. p53 = transcription factor that causes p21 to be produced In Normal Cells, the p53 Gene Product Acts at the G1 S Checkpoint Preventing Entry Into S Phase If DNA Is Damaged p21 inhibits intracellular signals that would activate E2F Cells with damaged DNA do not pass the G1S checkpoint In cancer cells the mutated p53 gene product no longer stimulates p21 production. Cells will pass the G1 S checkpoint even when chromosomal damage exists. In Normal Cells, the p53 Gene Product Stimulates Apoptosis If DNA Damage Cannot Be Repaired p53 gives an internal signal for apoptosis In cancer cells, a mutated p53 gene product no longer initiates self-destruction. Cells with damaged DNA can divide and more DNA damage can be accumulated. p53 is the most frequently mutated of all known cancer-causing genes, contributing to many types of cancer. Causes of Cancer • Heredity – tendency to develop cancer can be inherited due to mutations in tumor suppressors, such as BRCA1 and RB – Tendency to inherit thyroid cancer is linked to the RET proto-oncogene • Environmental Carcinogens – agents that contribute to cancer development, often by causing mutations Causes of Cancer • Environmental Carcinogens – Radiation • ultraviolet radiation in sunlight • nuclear radiation • radon gas – Organic chemicals found in • tobacco smoke • pollutants – Viruses • • • • hepatitis B and C viruses Epstein-Barr virus human papillomavirus HIV Cancer Prevention • Protective Behaviors – Avoid Carcinogens – Get regular screening tests – Get vaccinated • Dietary Habits – Avoid excess weight gain – Exercise regularly – Exclude foods that promote cancer– salt-cured or smoked foods, excess alcohol – Limit foods that are high in saturated fat – Include protective foods with fiber, vitamins A and C, and cruciferous vegetables Treatment of Cancer • Traditional Therapies – Surgery – Radiation – Chemotherapy • restore immune function with bone marrow transplants • Newer Therapies – Immunotherapy – p53 gene therapy • Genetically-engineered adenovirus that can infect and kill p53-deficient cancer cells – Antiangiogenic drugs to inhibit blood vessel formation – Targeted therapy acting on specific molecules • Herceptin blocks growth factor receptors on breast cancer cells • Gleevec inhibits the action of a faulty tyrosine kinase related to uncontrolled bone marrow cell reproduction in Chronic Myelogenous Leukemia
