Cancer Flash Cards.

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What is cancer?	A group of diseases resulting in the spreading of mutated cells throughout the body characterised by unregulated cell growth and invasion and spread of cells from the site of origin to other sites in the body. (> 200 different types causing different symptoms)
Name the five characteristics of cancer cells.	Evasion of Apoptosis (Bcl-2 anti-apoptotic protein). Growth signal autonomy (growth factor signal independence). Evasion of Growth inhibitory signals. Unlimited replicative potential, Angiogenesis, Invasion, metastasis.
Metastasis.	* Formation of discontinuous tumour. Implants at a distance from main tumour mass. Loss of cell cohesion- travels in blood of lymph nodes. Tumour will spread and duplicate in new environment. Nearly all malignant tumours can metastasize and form angiogenesis.
Survival and statistics.	4/10 will develop cancer at some stage. 5 year survival rate varies from 95% (testes) to 2% pancreas. In UK 331,487 people were diagnosed with cancer in 2011. doubling to 4 million over the next 20 years
Which demographic does cancer hit most frequently?	Old people, 64% of cases are =/> 65 years. Less than 1% occurs in children. Accumulation of genetic damage, life expectancy is increasing. Women in 30-50's at higher risk of cancer than men.
What are tumours (Neoplasms)?	Accumulation of multiple genetic alterations and epigenetic changes in cells, these changes = abnormal cell growth forming mass barrier cells. Malignant tumours develop in 25% of individuals, the incidence increases with age. Structure comprises neoplastic cells and connective tissue stroma of which the vascular supply is essential for growth
Sarcoma	Malignant connective tissue tumour.
Teratoma	Tumour arising from embryonic/ germ cells, and composed of endoderm, ectoderm and misoderm.
Leukaemia	Lymphoma bone marrow tissue.
Behaviour of Benign neoplasms.	Often encapsulated. Well differentiated. * Low mitotic/ growth rate. * Non-invasive. * Non metastasizing
Benign Neoplasms characteristics.	local growth, no infiltration or destruction of tissues. Close histological resembelance to parent tissue.
Behaviour of Malignant tumours.	* Non encapsulated. * Poorly differentiated. * High mitotic rate. * Invasive. * Metastisizing.
Malignant neoplasm characteristics.	Infiltration, destruction, dissemination. Variable histological resembelance to parent tissue.
Histogenic classification.	A degree of histological resemblance to parent tissue allows tumours to be graded, which correlates (grading) with clinical behaviour.
Grading	Dependant on resembalance to native cells. Grade 1- Well differentiated. *Grade 2- Moderately. Grade 3- Poorly. Grade 4- Undifferentiated. (Cell has loss of features.)
Grading in depth.	A well-differentiated neoplasm is composed of cells that closely resemble the cell of origin. A higher grade is a lower degree of differentiation. A higher grade is a worsening of biological behaviour. Poorly differentiated cells are difficult to assign to the cell of origin.
Causes of cancer	smoking, chemicals, radiation, infection, viruses, alcohol etc, anything that affects DNA. Cancer is considered a genetic disease at the cellular level. Major factor different in each target tissue e.g. UV radiation -> skin.
Genetic and Epigenetic factors of cancer.	Hereditary predispositions e.g. lung cancer mortality is four times higher in non-smoking relatives of lung cancer patients. Epigenetic- UV radiation, occupational agents.
Major Viral Cancers	* Viral cancers are involved in 10-15% of human cancers: Cervical Cancer. Liver Cancer. *Some Leukaemias and Lymphomas.
Hepatitis B Virus.	Small RNA replicates in the liver cells. Prevalent in many areas esp. Africa and S.E. Asia. Chronic HBV carriers are 20-100 fold higher risk of cancer. Tumours arise after 30 years of chronic infection. * Precise causative mechanism possibly inflammatory.
Causes of Cancer (infections)	*Will induce tumour formation by genetic amplification, inflammation cell cycle deregulation and immunosuppression.
Genes stimulated during cancer caused by infection.	Multiple mutations (6-10), accumulated in a slow progression to malignancy. * Growth providing and inhibitory genes. * DNA repair genes. Genes regulating blood supply and cell adherence. Mutation of protoncogens and tumour suppression.
Genetic changes in cancer.	Alterations. Point mutations-Protein changes. deletions- Protein changes. Amplification- over-expression of genes. Multiple copies- gene and chromosomal duplication. *Chromosomal translocations.
Diagnosis of cancer.	Biopsy. Endoscopy. Bone marrow aspiration. Genetic analysis. *Imaging techniques e.g. mammograms etc.
Staging.	Describes how far cancer has progressed. T (tumour),;primary site, size and depth. Tis-T4 N (node); involvemnet of lymph nodes. N0-N3 M (metastasis); distantce of metastaseses *M0-M1
What are primitive cells, and what is dedifferentiation associated with?	Primmative cells are very immature cells. Dedifferentiation is associated with aggressive behaviour.
HPV (Human Papilloma Virus).	Infects cervical epithelium. Inhibits P53 (Tumour suppressor gene). * Increases risk of cervical cancer.
DNA repair genes and cancer.	Many cells lack proper DNA repair. You can inherit a mutation of DNA repair gene e.g. BRCA-1. *Genes regulating DNA repair are mutated making them more likely to lead to mutation of other genes.
Principles of Cancer treatment.	* Cytotoxic- Kills cells Cytostatic- Prevents cells from multiplying (doesn't kill). Combination therapy reduces side affects and resistance.
Principles of Cancer therapy.	Requires death of all cancer cells. Balances between toxic effect on healthy and cancerous cells. *Aims to allow more rapid recovery of normal cells.
Chemotherapy: Tumour antibiotics and Mitotic disrupters.	Alkalising agents & Platinum-based drugs. both work in similar modes of action. Alkalising agents- Alter the configuration of double helix/ prevents DNA strand separation and interferes with DNA replication. *Platinum-based drugs: Results in DNA damage of cancer cells which triggers apoptosis.
Chemotherapy: Antimetabolites	Structurally similar to nitrogenous bases of DNA and can mimic their role and inhibit nucleic acid synthesis. Some drugs interfere with enzymes involved in DNA synthesis. *Organic drugs interrupt the mitotic spindle and primarily are used to treat solid tumours (e.g. in the breast.)
Radiotherapy.	Lethal dose of ionising radiation to tumour tissue. Causes DNA strand Cell death and breakage at mitosis. *Damage can occur to normal cells however they tend to recover faster than tumorous cells.
Nomenclature of tumours.	* All have the suffix -OMA Papilloma's/ Adenomas: Benign epithelial tumours. Carcinoma's: Malignant epithelial tumours. *Adenocarcinoma's: glandular epithelial tumours.
Classification of Tumours.	Anatomy: Organ of origin. Histogenesis: Cell type and origin. Histology: degree of cell maturity/differentiation. Anaplastic cells have complete loss of identity. Biological behaviour: Malignant/benign.
Oncogenes.	A proto-oncogene: A normal gene which, when altered by mutation, becomes an oncogene that can contribute to cancer. A proto-oncogene get stuck in the on position- produce growth promoting signals (e.g. RAS proteins).
Tumour suppressor genes.	Normally inhibit cell growth   Do not permit cell replication unless everything is “in  order” * Examples: p53  ,retinoblastoma gene ,adenomatous polyposis coli (APC) , breast cancer 1 and 2 (BRCA-1, BRCA-2)
Inactivation of P53- its role in pre cancer cells.	*The inactivation of p53 is a crucial step in allowing many pre-cancer cells to survive and mutate further.
Retinoblastoma (RB) Protein	Maintenance of ordered cell cycle progression and proliferation.   Regulator of the critical G1 to S-phase transition in the cell cycle.   * Functionally inactivated in over 60% of all human tumours.
Blood Vessel Genes	neovascularisation: formation of new blood vessels, similar to Angiogenesis. p53 releases thrombospondin-1, which inhibits angiogenesis, but if it is mutated thrombospondin-1 levels fall, and angiogenesis is promoted. *Stopping this is one possibility for treatment, as angiogenesis does not normally occur in many tissues.

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