Pathology · Short notes

Neoplasia: Short Notes & Cheat Sheet

Benign versus malignant tumours, nomenclature, dysplasia and metaplasia, grading and staging, spread, oncogenes and tumour suppressors, carcinogens and tumour markers.

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Short notes

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What causes cancer

ChemicalsTobacco, naswar, aflatoxin,asbestosVirusesHPV, HBV, HCV, EBV, HHV-8Bacteria and parasitesH. pylori, SchistosomaRadiationUV (skin), ionising (leukaemia)OncogenesRAS, MYC, HER2, BCR-ABLTumour suppressorsTP53, RB, BRCA1/2, APCCarcinogenesis
Most cancers need several hits, combining inherited risk with chemical, viral or radiation exposure.

Definitions and naming

  • Benign tumours are well differentiated, grow slowly, are often encapsulated and do not metastasise. Metastasis is the one feature that proves malignancy.
  • Benign tumours end in -oma (adenoma, lipoma, leiomyoma). Malignant epithelial tumours are carcinomas; malignant mesenchymal tumours are sarcomas.
  • Exceptions: lymphoma, melanoma, seminoma and hepatoma are malignant despite the -oma ending.
  • Metaplasia is replacement of one adult cell type by another (Barrett's oesophagus; squamous metaplasia in smokers' bronchi). Dysplasia is disordered growth and is precancerous.
  • Carcinoma in situ has not crossed the basement membrane. Anaplasia means lack of differentiation.

Grading, staging and spread

  • Grading describes how differentiated the tumour looks; staging (TNM: tumour, nodes, metastasis) describes how far it has spread and predicts outcome better.
  • Carcinomas usually spread by lymphatics; sarcomas usually by blood. Renal, liver and follicular thyroid carcinomas and choriocarcinoma also spread through blood.
  • Transcoelomic spread seeds body cavities (e.g. ovarian cancer to the peritoneum).
  • Paraneoplastic syndromes: small-cell lung cancer (SIADH, ACTH); squamous lung cancer (PTHrP, high calcium).

Causes

  • Oncogenes gain function (RAS, MYC, HER2, BCR-ABL); tumour suppressor genes lose function (TP53, RB, BRCA1/2, APC). TP53 is the most commonly mutated gene in cancer.
  • Knudson's two-hit hypothesis: both copies of a tumour suppressor gene must be lost.
  • Chemicals: tobacco (lung, mouth, bladder), aflatoxin (liver), asbestos (mesothelioma), benzene (leukaemia), and chewed tobacco such as naswar, gutka and betel (mouth cancer, common in Pakistan).
  • Viruses: HPV 16/18 (cervix, oropharynx), HBV and HCV (liver cancer; HCV is very common in Pakistan), EBV (Burkitt, nasopharyngeal, Hodgkin), HHV-8 (Kaposi). H. pylori causes gastric cancer and MALT lymphoma.
  • Breast cancer is the commonest cancer in Pakistani women; mouth cancer is among the commonest in men.

Cheat sheet

High-yield facts in one place. Cover the right-hand column and test yourself.

Tumour markers

MarkerTumour
AFPHepatocellular carcinoma, yolk sac tumour
CEAColorectal cancer
CA-125Ovarian cancer
CA 19-9Pancreatic cancer
PSAProstate cancer
β-hCGChoriocarcinoma, germ cell tumours
CalcitoninMedullary thyroid carcinoma

Carcinogen → cancer

CarcinogenCancer
Tobacco smokeLung, bladder, mouth
Naswar, gutka, betelOral cavity
AflatoxinLiver
AsbestosMesothelioma
HPV 16/18Cervix
HBV, HCVHepatocellular carcinoma
H. pyloriGastric adenocarcinoma, MALT lymphoma
Schistosoma haematobiumBladder squamous carcinoma

Memory aids

Carcinoma = Covering (epithelium), Sarcoma = Supporting tissue
Epithelial cancers are carcinomas; connective tissue cancers are sarcomas.

Exam traps

  • Lymphoma and melanoma are malignant despite ending in -oma.
  • Metaplasia is reversible and not itself cancer; dysplasia is precancerous.
  • Staging predicts prognosis better than grading.
  • Oncogenes need one activated copy; tumour suppressors usually need both copies lost.

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