MCBoM- Tumours Flashcards
Malignant, bone
Osteosarcoma
Benign, cartilage
Chondroma
Malignant, cartilage
Chondrosarcoma
Benign, fat
Lipoma
Malignant, fat
Liposarcoma
Benign, smooth muscle
Leiomyoma
Malignant, smooth muscle
Leiomyosarcoma
Benign, skeletal muscle
Rhabdomyoma
Malignant, skeletal muscle
Rhabdomyosarcoma
Benign, blood vessels
Hemangioma
Malignant, blood vessels
Angiosarcoma
Benign, melanocytic (skin pigment)
Naevus
Malignant, melanocytic
Melanoma
Benign, meningeal
Meningeioma
Benign, nerve sheath
Neurofibroma
Malignant, nerve sheath
Malignant peripheral nerve sheath tumour
Benign, mixed structures
Mature teratoma
Malignant, mixed structures
Immature teratoma
Benign, bone
Osteoma
Hamartoma
Developmental malformation, mass of disorganised but mature specialised tissue indigenous to site, eg birthmark
Dysplasia
Disordered growth Variable cell shape and size Deeply stained nuclei Increased number of cell divisions High nuclear:cytoplasm ratio
Grading
Degree of differentiation
1-3-anaplastix
Staging
Extent of disease spread
TNM or I - IV
Apoptosis mechanism
Mitochondria release cytochrome c to cytoplasm
Binds to APAF 1 (apoptosis protease factor) to form wheel of death
Activates to form apoptosome
Proto oncogenes examples
C ras, c myc, N myc, EGF
Promote proliferation
Tumour suppressor genes examples
Rb, p53, APC (adenomatous polyposis coli), TGF beta
Arrest growth at G1/S checkpoint
Primary abnormalities
Gatekeepers
Genes whose mutation or altered expression relieves normal controls and promotes outgrowth of cancer cells
Secondary abnormalities
Caretakers
Genes whose disruption caused genome instability, increasing the frequency of alteration in gatekeeper genes
Gain of function mutation
Dominant effect, one defective allele needed
Proto oncogene to oncogene
Loss of function mutation
Both alleles need to be inactivated to give phenotypic change
Tumour suppressor gene to non functioning
Growth factors
Epidermal and platelet derived GFs-> stimulates growth and leads to cascade for cyclin D and proliferation
Transforming growth factor beta-> inhibitory, switches on CDK inhibitor protein so stops proliferation
Colorectal tumour initiation
Mutation stops destruction complex from forming, so beta catenin is deregulated
Beta catenin can then switch on genes that drive cell survival and proliferation
E-cadherin
Cell surface transmembrane proteins expressed by cells
Mediates cell-cell adhesion
Acts as receptor and ligand, bind to each other and to catenins in cell which are bound to cytoskeleton
Ca dependent
Tumour suppressor, down regulated in tumour invasion
Integrins
Cell surface transmembrane proteins
Alpha and beta units
Mediate cell-ECM adhesion
Provides polarity for survival and migration
Lymphatic spread
Mainly carcinomas (epithelial)
Haematogenous spread
Mainly sarcomas (mesenchymal) through blood vessels
Transcoelomic spread
Through body cavities
Mainly carcinoma
HPV
DNA oncogenic virus
Viral DNA integrated to host genome
Clonal integration, same site on same chromosome
Leads to overexpression of E6 and E7 proteins, prevents inhibition of CDK4 and facilitates degradation of p53 gene product
Epstein-barr
DNA oncogenic virus
BURKITTS LYMPHOMA
B cell neoplasm
Should be controlled by immune system, but in Africa chronic malaria favours spread, endemic
Overexpression of c-myc oncogene
B CELL LYMPHOMA
In immunosuppressed individuals
Tumours in lymphoid tissue or CNS
HODGKINS DISEASE
Distinctive neoplastic giant cells
Express LMP1 which has transforming activity
NASOPHARYNGEAL CARCINOMA
Affects epithelial cells of oropharynx and B lymphocytes
Episome genome, doesn’t integrate
Hepatitis B
DNA oncogenic virus
Chronic persistent infection
HBx protein binds to p53, disrupts growth control of liver cells leading to cirrhosis
Human T cell leukaemia
RNA oncogenic retrovirus
Infection by transmission of infected T cells by fluid exchange
