Tumour Pathology Flashcards
What is haemoptysis?
Coughing up blood
Epithelium glandular benign
Adenoma
Epithelium glandular malignant
Adenocarcinoma
Epithelium squamous benign
Squamous papilloma
Epithelium squamous malignant
Squamous carcinoma
Tissue, Bone benign
Osteoma
Tissue, Bone, malignant
Osteo- sarcoma
Tissue, fat, benign
Lipoma
Tissue, fat, malignant
Lipo-sarcoma
Tissue, fibrous-tissue, benign
Fibroma
Tissue, Fibrous-tissue, malignant
Fibro-sarcoma
Blood, white blood cells, malignant
Leukaemia
Lymphoid tissue, malignant
Lymphoma
Melanocytes, benign
Naevus
Melanocytes, malignant
Melanoma
Neural tissue, central nervous system, malignant
Astrocytoma
Neural tissue, peripheral nervous system, malignant
Schwannoma
What is dysplasia?
Presence of cells of an abnormal type within a tissue
No invasion but can progress to cancer
Intraepithelial neoplasia
Development of a benign neoplasia or high-grade dysplasia in epithelium
Properties of cancer cells?
Loss of tumour suppressor genes - e.g Rb, APC
Gain of function of oncogenes
Altered cellular function
Abnormal morphology
Cells capable of independent growth
Tumour biomarkers
What are tumour biomarkers?
Alpha - feta protein
Carcino-embryonic antigen
Oestrogen receptor
Prostate specific antigen
What can biomarkers be used for?
Screening, diagnosis, prognostic, or predictive
What is retinoblastoma?
Tumour in eyes
Normally found in children
Around 40-50 children each year
High cure level
2 forms of retinoblastoma
Inherited - younger, more tumours (both eyes),
2 abnormal copies (one from birth, then another mutation)
Sporadic - older, just one eye
Just 1 abnormal copy (point mutations)
What are anti-oncogenes?
Tumour suppressor genes
Follows ‘2 hit hypothesis’ - needs two mutations
Genes that Normally regulate cell cycle.
Inherited cancer syndromes
Account for just 5 -10%
Genetic predispositions to develop cancer
Earlier onset and multiple tumours
Inherited to predisposition of cancer
Familial retinoblastoma
Familial adenomatous polyposis of colon - 100% risk of invasive colon cancer by 50 (bowel removal)
Hereditary breast and ovarian cancer syndrome
Hereditary non-polyposis colorectal cancer syndrome
Li-fragment syndrome
Multiple endocrine neoplasia
Van hipped-Linda syndrome
List of tumour suppressor genes
APC - colon cancer
P53
Rb - retinoblastoma
P16
What is another name for a tumour suppressor gene?
Anti - oncogene
What are proto-oncogenes?
Normal genes coding for normal growth regulating proteins
Abnormal - GAIN of function (one abnormal copy) activated
Tumour suppressor genes (antioncogenes)
Abnormal = loss of function
Proto-oncogenes
GAIN of function = abnormal
List of Porto-oncogenes
Growth factors
Growth factor receptors
Signal transducers
Regulatory proteins
Cell cycle regulators - cyclins/ cyclin dependant kinases
Example of oncogenes activation
HER2 and breast cancer
What are translocations?
Chromosomal rearrangements
Burritos lymphoma (malignancy of B cells)
Chemical carcinogenesis
Carcinogens react with DNA - purine and pyridimine bases in DNA are critical targets for radiation damage.
Activation of oncogenes and loss of anti-oncogenes
Radiation carcinogenesis
Purine and my ride mine bases in DNA -critical targets
UVB present in sunlight
CT scans
Viral carcinogenesis
Oncoviruses
Virus inserts oncogene into host DNA causing cell division
HPV (genital, throat and anal cancers)
Hep B (liver cancer)
EBV (lymphoma)
HPV
Human papilloma virus
Causes cervical cancer
Multi step carcinogenesis hypothesis
Mutations accumulate with time
Mutations of many oncogenes and anti-oncogenes to cause cancer
With age - Repair less effective
Bronchial mucosa bad cigarettes
(Chemical carcinogenesis - multi step carcinogenesis)
Progressive accumulation of mutations: cyclins, p53.
Cyclins = cell cycle control P53 = apoptosis and cell cycle control
Colorectal adenoma-carcinoma sequence
Dysplastic cells - adenoma, losing cell cycle control
Normal —— adenoma ———- carcinoma
Summary of molecular basis of cancer
Mutations can be inherited or sporadic
Mutations accumulate over time - explains cancer being very prominent in the elderly
Loss of cell cycle control key to malignant transformation
Key regulators include p16, cyclin D, CDK4, Rb - mutated in MAJORity of cancers
Loss mutations of p53 allow genetically damaged cells to proliferate, forming malignant neoplasms
