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Neoplasia

Neoplasia. Cancer. Neoplasia A Disorder of Altered Cell Differentiation and Growth. Cancer. The second leading cause of death in the United States Estimated 1.45 million diagnosed 559,650 die each year Prostate is the most common cancer for men Breast is the most common cancer for women

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Neoplasia

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  1. Neoplasia Cancer

  2. Neoplasia A Disorder of Altered Cell Differentiation and Growth

  3. Cancer • The second leading cause of death in the United States • Estimated 1.45 million diagnosed • 559,650 die each year • Prostate is the most common cancer for men • Breast is the most common cancer for women • Excluding skin cancer • Lung cancer is the leading cause of death in both men and women

  4. Definitions • Benign – not capable of metastasizing and usually not capable of causing death • Malignant – capable of metastasizing and capable of causing death • Neoplasm – an uncontrolled growth of new cells, benign or malignant • Tumor – literally, a mass; however, in everyday language, a neoplasm • Cancer – any kind of malignant neoplasm • Carcinoma – a malignant neoplasm of epithelial cells • Sarcoma – a malignant neoplasm of mesenchymal cells

  5. Growth Layers

  6. More Definitions • -oma is used for benign tumors • There is a matching malignant variety for every benign variety • For example, adenoma – aden = gland and oma = swelling • A benign tumor of fibrous tissue is a fibroma

  7. Even More Definitions • Malignant tumors are named by adding carcinoma if the tumor is of epithelial origin • Breast duct epithelium, prostate epithelium, bronchial epithelium and so on • Sarcoma if the tumor is from mesenchymal tissue • Bone, cartilage, fat, muscle or fibrous tissue • Adenocarcinoma if the tumor is of glandular epithelial cells • Fibrosarcoma if the tumor

  8. Mutations • The root cause of all cancer is damaged (mutant) DNA • This causes the normal cycle of cellular reproduction to go awry

  9. Cell Cycle • Cell proliferation • Process of cell division • Inherent adaptive mechanism for replacing body cells • Sequence of events that occurs as a cell duplicates • Genetic information is also duplicated • Duplicated chromosomes are appropriately aligned for distribution between two genetically identical daughter cells • Process of specialization

  10. http://highered.mcgraw-hill.com/sites/9834092339/student_view0/chapter10/control_of_the_cell_cycle.htmlhttp://highered.mcgraw-hill.com/sites/9834092339/student_view0/chapter10/control_of_the_cell_cycle.html

  11. Interphase • G1 (gap 1) • From the end of the M phase until the beginning of DNA synthesis • Growth Phase • The cell determines its readiness to commit to DNA synthesis • S (DNA Synthesis) • DNA replication • G2 (gap 2) • DNA replication is assessed and errors are corrected • the gap between DNA synthesis and mitosis, the cell will continue to grow.

  12. Cell Cycle • M-Phase (Mitotic Phase) • The replicated chromosomes are separated and packaged into two new nuclei by mitosis • The cytoplasm is divided between the two daughter cells by cytokinesis • Prophase • Metaphase • Anaphase • Telophase

  13. http://highered.mcgraw-hill.com/sites/9834092339/student_view0/chapter10/stimulation_of_cell_replication.htmlhttp://highered.mcgraw-hill.com/sites/9834092339/student_view0/chapter10/stimulation_of_cell_replication.html

  14. Cyclins and CDK’s • Two key classes of regulatory proteins, Cyclinsand Cylin-Dependent Kinases (CDKs), determine a cell’s progress through the cell’s cycle

  15. Cell Cycle • Cyclins are proteins that control the entry and progression of cells through the cell cycle • Cyclins bind to cyclin-dependent kinases (CDK), which are enzymes that phosphorylate proteins • Cyclin-dependent kinase inhibitors-regulates cell cycle checkpoints to prevent DNA replication mistakes.

  16. Cyclins and CDK’s • Progression from one phase of the cell cycle to the next is controlled by the orderly activation of cyclin dependent kinases • Cyclin proteins bind to CDK’s to cause phosphorylation and activation

  17. http://highered.mcgraw-hill.com/sites/9834092339/student_view0/chapter10/how_tumor_suppressor_genes_block_cell_division.htmlhttp://highered.mcgraw-hill.com/sites/9834092339/student_view0/chapter10/how_tumor_suppressor_genes_block_cell_division.html

  18. Cell Growth Control Genes • All cells contain genes that function as “go” or “stop” switches (restrains cell growth) • The “go” genes are proto-oncogenes • Proto-oncogenes produce growth-promoting proteins that stimulate normal cell division • Oncogenes (cancer genes) come from mutations of proto-oncogenes • Their function is to stimulate uncontrolled cellular division

  19. Tumor Suppressor Genes • “stop” genes are the opposite of proto-oncogenes • Called Tumor suppressor genes • Produce proteins that inhibit cell division • Mutation of tumor suppressor genes leaves cell growth uninhibited

  20. http://highered.mcgraw-hill.com/sites/9834092339/student_view0/chapter9/cell_proliferation_signaling_pathway.htmlhttp://highered.mcgraw-hill.com/sites/9834092339/student_view0/chapter9/cell_proliferation_signaling_pathway.html

  21. Tumor Suppressor Genes • Retinoblastoma is a rare childhood cancer due to the inactivation of a specific tumor suppressor gene • Retinoblastoma (pRB) gene • Prevents cell division • Retinoblastoma tumor suppressor protein (pRB) • Phosphorylation of pRB causes progression of the cell into the S-phase • A point mutation renders the pRB pathway non-functional • Thought to occur in almost all human cancers

  22. Tumor Suppressor Genes • p53 gene • Found on the small arm of chromosome 17 • Its protein product is in virtually all normal tissues • Controls p53 protein levels • p53 proteins increase with damage to DNA • Initiates apoptosis of DNA-damaged cells

  23. p53 Gene • “Guardian of the genome” • Restricts uncontrolled cellular proliferation under circumstances in which cells with abnormal DNA might propagate • Deleted or mutated in 70% to 80% of cases of colorectal cancer, breast cancer, small cell carcinoma of the lung, hepatocellular carcinoma, astrocytoma and numerous other tumors

  24. Epigenetics • Involves changes of gene expression without a change in the DNA • “silence” genes such as tumor suppressor genes • Methylation of the promoter region • Prevents transcription to cause gene inactivity • Can be inherited

  25. Genetic and Molecular Basis of Cancer • Epigenetic factors • http://youtu.be/Xjq5eEslJhw • http://youtu.be/wFsxVkuChdU

  26. The Spread of Neoplasms • Direct invasion and extension • Seeding of cancer cells in body cavities • Metastases

  27. Premalignant States and Conditions • Neoplasms evolve over time from normal tissue • Dysplasia • A pre-malignant state of tissue that is atypical and clearly abnormal but not yet malignant • Dysplasia does NOT always progress to malignancy • Carcinoma in situ • Cancer that never metastasizes

  28. Invasion • Cancer is latin for crablike • Cancer grows by sending crablike projections into the surrounding tissues • Cancers secrete enzymes to break down proteins to increase invasion and penetration of surrounding tissues • Prevents sharp demarcation for surgical removal

  29. Seeding • A tumor erodes and shed cells into body cavities • Peritoneal, pleural, pericardial cavity and joint spaces • Floating in body space from one surface to another • These cancers grow in masses and secrete fluids • Ascites, pleural effusion

  30. Metastasis • The ability to skip from one place to another • Via lymphatics or the bloodstream • Breast via lymphatics to lymph nodes • Via blood to bone • Metastases may occur by seeding

  31. Metastasis

  32. Nourishment of Tumors • Angiogenesis • Neoplasms develop their own blood supply

  33. Liver Metastasis

  34. Human Papilloma Virus • Infection in the cervix • Causes dysplasia, carcinoma in situ and invasive carcinoma • Takes many years and repeated infections to produce dysplasia or malignancy

  35. Grading and Staging of Malignancies • Cancer Grading • Microscopic assessment of the degree of differentiation, atypia and other features of malignancy • Cancer Staging • Evaluation of behavior by assessing size of the primary tumor and its spread • Assessed by physical exam, history and pathologic and diagnostic imaging

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