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General Pathology

Explore the basics of neoplasia and nonneoplastic growth disturbances, including molecular aspects, causes, and host-tumor interactions. Learn about DNA diseases, oncogenic viruses, and cell cycle regulators.

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General Pathology

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  1. General Pathology Basic Principles of Cellular and Organ Pathology Oncology - I Jaroslava Dušková Inst. Pathol. ,1st Med. Faculty, Charles Univ. Prague

  2. General Oncology - 1 • Disorders of the cell proliferation and growth (hypertrophy, hyperplasia, metaplasia) • Neoplasms – disorders of cell proliferation and differentiation • Molecular biology of neoplasia - oncogenesis • Host - neoplasm interactions

  3. Tumour swelling of any kind NEOPLASIA

  4. NEOPLASIA Def.: persistent abnormal relativelyautonomous proliferation of cells

  5. NEOPLASIA – history I. Ramayana – 2000 B.C. • therapy with knife • chemotherapy arsenical compounds

  6. NEOPLASIA – history II. Galen – AD 131–201 TUMOURS • according to nature pregnancy • exceeding nature inflammatory, reparative, callus • against nature true neoplasms

  7. Growth Disturbances & Their Relation to Neoplasms

  8. Nonneoplastic Growth Disturbances – I MALFORMATIONS • complete or partial lack of development(aplasia, hypoplasia) • asymmetry • oversize • hamartoma • choristoma • ectopic tissue - +

  9. Hamartia – Hamartoma Def.: A mass of disorganized tissue indigenous to the particular site.

  10. Choristia - Choristoma Def.: A mass of ectopic tissue (cells) with a limmited growth potency

  11. Nonneoplastic Growth Disturbances – II • repair • hypertrophy / atrophy - (incl.pseudohypertrophy) • hyperplasia • metaplasia • dysplasia • anaplasia – undifferentiation

  12. Nonneoplastic Growth Disturbances – II • repair • hypertrophy / atrophy - (incl.pseudohypertrophy) • hyperplasia • metaplasia • dysplasia • anaplasia – undifferentiation

  13. Nonneoplastic Growth Disturbances – II • repair • hypertrophy / atrophy • hyperplasia • metaplasia • dysplasia • anaplasia – undifferentiation

  14. Nonneoplastic Growth Disturbances – II • repair • hypertrophy / atrophy • hyperplasia • metaplasia • dysplasia • anaplasia – undifferentiation

  15. Nonneoplastic Growth Disturbances – II • repair • hypertrophy / atrophy • hyperplasia • metaplasia • dysplasia • anaplasia – undifferentiation

  16. Growth Disturbances to Neoplasms Relation • differential diagnosis pseudotumours • precursors precanceroses (preblastomatoses) • both 1. and 2.

  17. NEOPLASIA Def.: persistent abnormal relativelyautonomous proliferation of cells

  18. Neoplasia (Tumour) • DNA disease • Stepwise accumulation of genetic abnormalities • Escapeof immunological clearing systems

  19. External Irradiation chemical cancerogens oncogenic viruses Internal immunosupression (inborn, acquired) chronic irritation (inflammation) Neoplasia - causes

  20. DNA HPV SV 40 – polyoma Adenoviruses Herpesviruses Epstein– Barr Hepatitis B RNA Rous sarcoma Leukemia HIV Oncogenic Viruses

  21. Cell Cycle Regulators– control of cellular proliferation • polypeptide growth factors EGF, PDGF, FGF, TGFα,β (protooncogenes) • ligand receptor binding • activation via conformation alteration (kinase) • signal transduction – second messengers (tyrosine kinases) • activation of transcription factors • DNA synthesis initiation • cyclins and cyclin dependent kinases cdk • cdk associated inhibitors cki

  22. Polypeptide growth stimulators EGF, PDGF, TGF α(protooncogenes) cytokins IL-1, TNF angiogenesis Polypeptide growth inhibitors T(ransforming)GF β interferon α prostaglandin E-2 Cell Cycle Regulators – growth factors

  23. Cell Cycle Regulation Disorders– uncontroled cellular proliferation • polypeptide growth factors (e.g. EGF, PDGF, FGF,…) acting as oncogenes via overexpression • ligand receptor amplification • signal transducing proteins (e.g. ras oncoproteins) - activation othe mitogenic signaling pathway • nuclear DNA synthesis regulators (myc, jun, fos) • mitochondrial oncogenes (bcl-2) – prevention of apoptosis

  24. Molecular Biological and Morphological Tumour Progression Normal cell dysplasia adenoma infiltrating carcinoma Loss of growth control Loss of apoptosis control Loss of Senescence control genomic instability activation proteases Metastasising tumour cell Molecular biological Morphological Tumour Progression

  25. immune surveillance immune response spontaneous regression local preassure cachexia anaemia immunodepression products of neoplastic cells Host - Neoplasm Interactions

  26. NEOPLASIA – function NEOPLASTIC CELL PRODUCTS: • immunoglobulin • osteiod • keratin • mucus • melanin • hormones

  27. NEOPLASIA – function NEOPLASTIC CELL PRODUCTS: • immunoglobulin • osteiod • keratin • mucus • melanin • HORMONES

  28. ENDOCRINE NEOPLASIAHormone Production and Function • mayor may not be present • unregulated – may be excessive • benign tumours more likely to be active • size of tumour not related to the degree of function • metastases may cause hyperfunction

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