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Cancer Notes

Medicine Notes > Physiology Notes

This is an extract of our Cancer document, which we sell as part of our Physiology Notes collection written by the top tier of Bristol University students.

The following is a more accessble plain text extract of the PDF sample above, taken from our Physiology Notes. Due to the challenges of extracting text from PDFs, it will have odd formatting:

Cancer Risk increase with; age >55, diet, exposure to risk factors [tobacco, radiation, carcinogens] & hereditary Tissue homeostasis ? cell birth = cell death

Neoplasia A growth disorder characterised by genetic alterations that lead to a loss of the normal control mechanisms that regulate cell growth and differentiation Apoptosis is dysregulated Loss of normal constraints on cell proliferation Differentiation program distorted Labile cells - cells continuously in cell cycle bone marrow, skin, GIT highly susceptible to cancer Stable cells - cells in reversible G0 hepatocytes and renal cells less susceptible Permanent cells - cells in irreversible G0 cardiac muscle fibres and neurons cancer is rare Stem cell ? transit-amplifying cell ? terminally differentiated cell ? cell death

Anaplasia Lack of differentiation, which is a hallmark of cancer Cancer evades apoptosis signals and so inducing apoptosis is the main aim of chemotherapy and radiotherapy

Cell cycle machinery Restriction point Mitogenic stimulation only in the first 2/3 of G1 At the end of G1 it is the restriction point where the cell may either: Commit to the cell cycle Enter G0 Commit to post-mitotic differentiated state HYPERTROPHY HYPERPLASIA HYPOPLASIA APLASIA ATROPHY DEGENERATION METAPLASIA DYSPLASIA CANCER CARCINOMA CARCINOMA-IN-SITU SARCOMA

Increase in the size of tissue due to an increase in size Increase in the size of tissue due to an increase in cell number Partial failure to develop Complete failure to develop Regression after full development Wasting away with decay Replacement of one cell type with another Abnormal proliferation - not cancer A malignant neoplasm Malignant epithelial tumour Malignant tumour, not invaded BM Malignant connective tissue tumour

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POLYP HARMATOMA

An abnormal growth of tissue projecting from a mucus membrane Mass of disorganised but mature specialised cells

Difference between Benign & Malignant Neoplasms SIZE BORDERS DIFFERENTIATION/ANAPLASIA

BENIGN Generally smaller Circumscribed border, often encapsulated Usually closely resemble their parent tissue

MITOTIC ACTIVITY

Slow growth Intact basement membrane

INVASION

METASTASIS/SPREAD

Do not invade lymphatics Do not show perineural invasion Do not metastasise

MALIGNANT Generally larger Invasive growth Los resemblance to normal tissues Rapid growth and have more mitotic figures Invade through basement membrane Invades lymphatics and spreads Invade perineurally Process of spread from site of origin. Haematogenous, lymphatic, transcoelomic or direct

All tumours have the suffix -oma Benign epithelial tumours - papillomas or adenomas Malignant epithelial tumours - carcinomas Benign connective tissue tumours - have a prefix fibroma Malignant connective tissue tumours - sarcomas

GRADING OF TUMOURS Grade 1 - well differentiated Grade 2 - moderately differentiated Grade 3 - poorly differentiated Anaplastic or undifferentiated

STAGING OF TUMOURS Extent of disease spread T Tumour N Lymph Node M Metastasis Or

Stage I to IV

Adenoma-carcinoma sequence and CRC Cancer DevelopmentTumour Suppressor Gene = brake pedal Oncogene = accelerator

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