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Principles of Cancer

Learn about the basics of cancer, including its classification, cell cycle, characteristics, and clinical features. Gain knowledge on the rate of growth, cancer phenotype, stem cells, and microscopic patterns. Written by Ms. Santoshi Naik, Assistant Professor at Yenepoya Pharmacy College and Research Centre.

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Principles of Cancer

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  1. PRINCIPLES OF CANCER By: Ms. Santoshi Naik Assistant Professor Yenepoya Pharmacy College and Research Centre

  2. Introduction • Neoplasia means ‘newgrowth’ • New growth produced is Neoplasm or tumour • Howeverall ‘new growths’ are not neoplasms as it also exist in the processes of embryogenesis, regeneration and repair, hyperplasia. • The proliferation and maturation of cells in normal adults is controlled as a result of which some cells proliferate throughout life (labile cells), some have limited proliferation (stable cells), while others do not replicate (permanent cells). • On the other hand, neoplastic cells lose control and regulation of replication and form an abnormal mass of tissue.

  3. Tumour is defined as ‘a mass of tissue formed as a result of abnormal, excessive, uncoordinated, autonomous and purposeless proliferation of cells even after cessation of stimulus for growth which caused it’. • Thebranch of science dealing with the study of neoplasms ortumours is called oncology (oncos=tumour, logos=study).

  4. Differences between normal and cancercell

  5. CLASSIFICATION OF TUMOURS

  6. CLASSIFICATION OF TUMOURS • BENIGN TUMOURS • Slow-growing • Localised • No harm to host. • Suffix ‘-oma’is added to denote benign tumours. • MALIGNANT TUMOURS • Proliferate rapidly • spread throughout the body • May cause death of the host. • Malignant tumours of epithelial origin are called carcinomas. • Malignant mesenchymal tumours are named sarcomas.

  7. Classification of tumours

  8. CELL CYCLE

  9. Phases of cell cycle • G1 phase- DNA synthesis • S phase – DNA replication • G2 phase – short gap phase in which correctness of DNA synthesised is assessed. • M phase – mitosis phase to form two daughter cells. It includes Prophase, Metaphase, Anaphase and Telophase. • G0 phase – Resting phase

  10. CHARACTERISTICS OF TUMOURS

  11. Majority of neoplasms can be categorized clinically and morphological into benign and malignant on the basis of certain characteristics listedbelow: • Rate ofgrowth • Cancer phenotype and stemcells • Clinical and grossfeatures • Microscopicfeatures • Local invasion (directspread) • Metastasis (distantspread)

  12. Rate of growth • Thetumourcellproliferatemorerapidlythanthenormalcells. • The tumour enlarge rate dependsupon • Rateofcellproduction,growthfractionandrateofcellloss: • Doubling time (mitotic rate) oftumour cells • Numberofcellsremaininginpreoperativepool(growthfraction) • Rateoflossoftumourcellsbycellshedding

  13. Degree ofdifferentiation • Well differentiated cancer cells look like normal cells and grow & spread slowly than poorly differentiated cancer cells. • Rate of growth of malignant tumour is directly proportionate to the degree ofdifferentiation. • Some tumours after a period of slow grow show spurt in growth, whereas some tumours may cease to grow. • Rarely, a malignant tumour may disappear spontaneously from the primarysite,duetogoodhostimmuneattack , to reappear as secondary tumour.

  14. 2. Cancer phenotype and stemcells • Cancercells • disobey the growth control – proliferaterapidly • escape from death signals –immortality • imbalance between cell proliferation and cell death – excessivegrowth • lose differentiation properties – little or nofunction • are genetically unstable – newermutations • overrun their neighboring tissue – invadelocally • have the ability to travel from the site of origin to other part ofbody – • distantmetastasis • Cancer stem cells/ tumour-initiating cells have the properties of self-renewal, asymmetric replication and transdifferentiation (i.e.plasticity).

  15. 3. Clinical and grossfeatures • Clinical features: • Benign tumour are generally slow growing and depending upon location remains asymptomatic (subcutaneous lipoma) or may cause serious symptoms (meningioma in the nervous system). • Malignant tumor grow rapidly, invade locally into deeper tissue and spread to distant sites (metastasis) & produce systemic features such as weight loss, anorexia and anaemia.

  16. b) Gross features • Benign tumours - are generally spherical or ovoid in shape. They are encapsulated or well-circumscribed, freely movable, more often firm and uniform. • Malignant tumours- are usually irregular in shape, poorly-circumscribed and extend into the adjacent tissues. Sarcomas have fish flesh like consistency while carcinomas are firm.

  17. 4. Microscopicfeatures • Microscopicpattern • Tumours cells may be arranged in variety of patterns. • The epithelial tumours generally consist of acini, sheets, columns or cords of epithelial tumour cells that may be arranged in solid or papillary pattern.

  18. The mesenchymal tumours have mesenchymal tumour cells arranged as interlacing bundles or whorls, lying separated from each other.

  19. b) Cytomorphologyof neoplasticcells • Differentiation is defined as the extent of morphological and functional resemblance of tumour cells to corresponding normal cells.

  20. Anaplasia is lack of differentiation and is a characteristic feature of most malignant tumours. • Poorly differentiated malignant tumours have high degree of anaplasia.

  21. Basal polarity - the nuclei of epithelial cells are oriented along the basement membrane which is termed as basal polarity. Pleomorphism- means variation in size and shape of the tumour cells. N/C ratio – Nucleocytoplasmic ratio (size of nucleus to cytoplasm). Anisonucleosis- means variation in size and shape of nucleus. Hyperchromatism – increased nuclearchromatin of malignant cell resulting in dark-staining nuclei. Aneuploidy – is the presence of abnormal number of chromosomes ie. Other than 46 chromosomes.

  22. c) Tumour Angiogenesis and Stroma • Tumor angiogenesis – is the formation of new blood vessels from the pre-existing one to provide nourishment to growing tumour cell. • Tumour stroma: • When collagenous tissue in stroma is scanty- tumour is soft and fleshy (ie. In sarcomas). • When collagenous tissue in stroma is excessive- tumour is hard and gritty (i.e in carcinoma).

  23. d) Inflammatory reaction • In some instances inflammatory reaction may be present in and around the tumours which may be acute or chronic. • Cause - cell-mediated immunologic response by the host in an attempt to destroy the tumour. • In some instances such reaction may reduce the prognosis.

  24. 5. Local invasion (directspread) • Benign: expand and push aside without invading, infiltrating ormetastasising the surrounding tissue. • Malignant: expand, invasion, infiltration and destruction of the surroundingtissue.

  25. 6. Metastasis (distantspread) • Metastasis(meta= transformation, stasis= residence):is defined as spreadof tumour byinvasion in such a way that secondary tumours are formed at the site of lodgement. • Benign tumours – don’t metastasise • Malignant tumours - metastasise

  26. Routes of Metastasis

  27. Lymphatic spread • In general, carcinomas metastasise by lymphatic route while sarcomas favour haematogenous route • Mechansim: • Lymphatic permeation- The cancer cells permeate through the walls of the lymphatic vessels. • Lymphatic emboli- The malignant cells may detach to form tumour emboli so as to be carried along the lymph to the next draining lymph node.

  28. 2) Haematogenous spread • Blood-borne metastasis is the common route for sarcomas but certain carcinomas may also metastasise by this mode • Systemic veins drain blood into vena cava from limbs, head, neck and pelvis. Therefore, cancers of these sites more often metastasise to the lungs. • Portal veins drain blood from the bowel, spleen and pancreas into the liver. Thus, tumours of these organs frequently have secondaries in the liver.

  29. Arterial spread of tumours is less likely because they are thick-walled and contain elastic tissue which is resistant to invasion.

  30. c) Spread along body cavities and natural passages • Transcoelomicspread. Certain cancers invade through the coelomic cavity (body cavities). • Example: • a) Carcinoma of the stomach seeding to both ovaries • B) Carcinoma of the bronchus and breast seeding to the pleura and pericardium.

  31. ii. Spread along epithelium-lined surfaces • It is unusual for a malignant tumour to spread along the epithelium-lined surfaces because intact epithelium and mucus coat are quite resistant to penetration by tumour cells. • In some instances it may spread. • Example: • Bronchus to alveoli • Fallopian tube to ovary

  32. iii. Spread via cerebrospinal fluid • Malignant tumour of the meninges may spread by release of tumour fragments and tumour cells into the CSF and produce metastasis at other sites in the CNS. • iv. Implantation • Rarely, a tumour may spread by implantation by surgeon’s scalpel, needles, sutures, or may be implanted by direct contact such as transfer of cancer of the lower lip to the apposing upper lip.

  33. Difference between benign and malignant tumour

  34. Difference between benign and malignant tumour

  35. BENIGN TUMOUR MALIGNANT TUMOUR

  36. Mechanism & Biology of Invasion & Metastasis

  37. Aggressive clonal proliferation and angiogenesis The first step in the spread of cancer cells is the development of rapidly proliferating clone of cancer cells and angiogenesis (formation of new blood vessels). 2. Tumour cell loosening Normal cells remain attached to each other due to presence of cell adhesion molecules (CAMs) i.e. E(epithelial)-cadherin. In cancer cells, there is either loss or inactivation of E cadherin and also other CAMs which results in loosening of cancer cells.

  38. 3. Tumour cell-ECM interaction Loosened cancer cells are now attach to ECM proteins, mainly laminin and fibronectin. There is also loss of integrins, the transmembrane receptors, further favouring invasion. 4. Degradation of ECM Tumour cells overexpress proteases and matrix-degrading enzymes, metalloproteinases (collagenases and gelatinase).

  39. 5. Entry of tumour cells into lumen The tumour cells after degrading the basement membrane are ready to migrate into lumen of capillaries or venules. 6. Thrombus formation The tumour cells protruding in the lumen of the capillary are now covered with constituents of the circulating blood and form the thrombus. Thrombus provides nourishment to the tumour cells and also protects them from the immune attack by the circulating host cells.

  40. 7. Extravasation of tumour cells Tumour cells in the circulation (capillaries, venules, lymphatics) will move out into surrounding tissues. 8. Survival and growth of metastatic deposit The extravasatedmalignant cells on lodgement in the right environment grow further under the influence of growth factors produced by host tissues & tumour cells.

  41. Tumoursgrading

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