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Pathology 3% exam weight

Neoplasia and Cancer Biology

Part of the NEET PG study roadmap. Pathology topic pathol-010 of Pathology.

Neoplasia and Cancer Biology

🟢 Lite — Quick Review (1h–1d)

Benign vs Malignant Tumors:

FeatureBenignMalignant
DifferentiationWell differentiatedPoorly/undifferentiated
Growth rateSlowRapid
MarginEncapsulated, pushingInfiltrative, irregular
Capsular involvementConfinedInvades through capsule
Necrosis/HemorrhageRareCommon
MetastasisAbsentPresent
RecurrenceRareCommon
Nuclear featuresUniformPleomorphism, ↑ N:C ratio

Grading vs Staging:

  • Grading — histological differentiation (Grade I-IV); based on microscopy
  • Staging — extent of spread (TNM: Tumor size, Nodes, Metastases); based on clinical/imaging/pathology

🟡 Standard — Regular Study (2d–2mo)

Carcinogenesis — Two-Hit Hypothesis (Knudson):

  • First hit — inherited or somatic mutation
  • Second hit — somatic mutation (loss of heterozygosis)
  • Explains familial cancers (RB, p53, BRCA1/2, APC)

Oncogenes — Common Examples:

OncogeneNormal FunctionCancer Association
RASGTPase (growth signal)Pancreatic, colorectal, lung
MYCTranscription factorBurkitt lymphoma, neuroblastoma
BCL-2Anti-apoptoticFollicular lymphoma
HER2/neu (ERBB2)Growth factor receptorBreast cancer
BCR-ABLTyrosine kinase (fusion)CML, Philadelphia chromosome
KRASGTPaseColorectal, pancreatic
EGFRGrowth factor receptorLung adenocarcinoma
ALKTyrosine kinaseLung adenocarcinoma, lymphoma
N-MYCTranscription factorNeuroblastoma

Tumor Suppressor Genes:

GeneFunctionCancer Association
RBInhibits E2F (cell cycle)Retinoblastoma, osteosarcoma
p53”Guardian of genome”; apoptosisLi-Fraumeni syndrome; most human cancers
BRCA1/BRCA2DNA repair (homologous recombination)Breast, ovarian cancer
APCInhibits Wnt signalingFamilial adenomatous polyposis (FAP)
WT1Transcription factorWilms tumor
NF1/NF2Ras GTPase regulator / cytoskeletalNeurofibromatosis 1/2
VHLUbiquitin ligase (HIF degradation)Von Hippel-Lindau disease; renal cell carcinoma
PTENPI3K/AKT inhibitorCowden syndrome

DNA Repair Genes: MSH2, MLH1 (mismatch repair) → Lynch syndrome (HNPCC)

Carcinogenic Agents:

  • Chemical: Aflatoxin B1 (liver cancer), asbestos (mesothelioma, lung cancer), vinyl chloride (angiosarcoma of liver), benzidine (bladder cancer), betel nut (oral cancer), smokeless tobacco
  • Physical: UV radiation (BCC, SCC, melanoma), ionizing radiation (leukemia, solid tumors)
  • Biological/Viral: HPV (cervical cancer — types 16, 18), HBV/HCV (hepatocellular carcinoma), EBV (Burkitt lymphoma, nasopharyngeal carcinoma), HTLV-1 (Adult T-cell leukemia/lymphoma), H. pylori (gastric MALT lymphoma), Kaposi’s sarcoma (HHV-8)

Metastasis — Routes:

  1. Direct seeding — body cavities (peritoneum, pleura)
  2. Lymphatic spread — carcinomas (most common route)
  3. Hematogenous spread — sarcomas, carcinomas (liver, lung most common secondary sites)
  4. Transcoelomic — across serosal surfaces

Metastatic Patterns:

  • Breast cancer → bone, brain, liver, lung
  • Prostate cancer → bone (osteoblastic metastases)
  • Lung cancer → adrenal glands, brain, bone, liver
  • Colon cancer → liver (portal circulation)
  • Retinoblastoma/osteosarcoma → lung (hematogenous)

Tumor Markers:

MarkerAssociated Cancer
AFPHepatocellular carcinoma, yolk sac tumor
β-hCGChoriocarcinoma, germ cell tumors
CEAColorectal carcinoma (also gastric, pancreatic, breast)
CA-125Ovarian serous carcinoma
CA 19-9Pancreatic adenocarcinoma
PSAProstate cancer
S-100Melanoma, nerve sheath tumors
ChromograninNeuroendocrine tumors
CalcitoninMedullary thyroid carcinoma
ThyroglobulinFollicular/papillary thyroid carcinoma
CA 15-3Breast cancer

🔴 Extended — Deep Study (3mo+)

Hallmarks of Cancer (Hanahan & Weinberg):

  1. Self-sufficiency in growth signals
  2. Insensitivity to growth-inhibitory signals
  3. Evasion of apoptosis
  4. Limitless replicative potential (telomerase activation)
  5. Sustained angiogenesis
  6. Invasion and metastasis
  7. Reprogramming energy metabolism (Warburg effect)
  8. Evading immune destruction
  9. Genome instability and mutation
  10. Tumor-promoting inflammation

Tumor Microenvironment:

  • Cancer-associated fibroblasts (CAFs) — secrete growth factors, remodel ECM
  • Tumor-associated macrophages (TAMs) — M2 phenotype promotes tumor growth
  • Regulatory T cells (Tregs) — suppress anti-tumor immunity
  • Myeloid-derived suppressor cells (MDSCs)
  • ECM remodeling — MMPs (matrix metalloproteinases) → invasion

Apoptosis Pathways:

Extrinsic (Death Receptor):

FasL (on cytotoxic T cells) → Fas (CD95) → FADD → Caspase 8 → Caspase 3 TNF-α → TNFR1 → TRADD → Caspase 8

Intrinsic (Mitochondrial):

DNA damage/ROS/TNF → BH3-only proteins (BIM, BAD, PUMA) → BAX/BAK → Mitochondrial outer membrane permeabilization → Cytochrome c release → Apoptosome (Apaf-1 + Caspase 9) → Caspase 3

Anti-apoptotic: BCL-2, BCL-XL, MCL-1 Pro-apoptotic: BAX, BAK, BIM, BAD, PUMA, NOXA

Tumor Invasion — Steps:

  1. Loss of E-cadherin (cell-cell adhesion)
  2. EMT (Epithelial-Mesenchymal Transition) — ↓ cytokeratin, ↑ vimentin
  3. Degradation of basement membrane (MMPs, cathepsins, uPA)
  4. Migration through ECM
  5. Intravasation → circulation → extravasation → colonization

Tumor Angiogenesis:

  • VEGF — most important pro-angiogenic factor
  • FGF — basic FGF
  • Angiopoietins — Ang-1 (maturation), Ang-2 (destabilization)
  • Tumor cells → hypoxia → HIF-1α stabilization → ↑ VEGF transcription
  • Anti-angiogenic therapy: Bevacizumab (anti-VEGF antibody), sunitinib (VEGFR inhibitor)

Telomerase and Cancer:

  • Normal somatic cells: Telomeres shorten with each division → senescence
  • Cancer cells: Telomerase reactivation → limitless replicative potential
  • hTERT (human telomerase reverse transcriptase) — re-expressed in 85-90% of cancers

Paraneoplastic Syndromes:

SyndromeAssociated CancerMechanism
Cushing syndromeSmall cell lung cancerACTH production
SIADHSmall cell lung cancerADH production
HypercalcemiaSCC lung, breast, renalPTHrP production
PolycythemiaRenal cell carcinoma, hepatocellular carcinomaEPO production
Lambert-EatonSmall cell lung cancerAnti-VGCC antibodies
Trousseau syndromePancreatic adenocarcinomaMigratory thrombophlebitis
Acanthosis nigricansGastric adenocarcinomaEGFR family activation
Peutz-JeghersOvarian sex cord tumors, Sertoli cell tumorsSTK11/LKB1 mutation

Oncogenic Viruses — Details:

  • HPV: E6 (inactivates p53), E7 (inactivates RB) → cervical, oropharyngeal, anal carcinoma
  • HBV: X protein → promotes proliferation; chronic inflammation → cirrhosis → HCC
  • HCV: Chronic inflammation → cirrhosis → HCC
  • EBV: LMP-1 (constitutive NF-κB activation) → Burkitt lymphoma, Hodgkin lymphoma, nasopharyngeal carcinoma, post-transplant lymphoproliferative disorder
  • HHV-8 (Kaposi’s sarcoma herpesvirus): vFLIP → activates NF-κB → Kaposi sarcoma, primary effusion lymphoma

Chemotherapy — Mechanism-Based Classification:

ClassMechanismExamples
Alkylating agentsCrosslink DNACyclophosphamide, cisplatin, nitrosoureas
Anti-metabolitesMimic substratesMethotrexate, 5-FU, cytarabine, mercaptopurine
Microtubule inhibitorsMitosis arrestVincristine, paclitaxel
Topoisomerase inhibitorsDNA replication stressEtoposide, irinotecan, doxorubicin
DNA crosslinkersPlatinum-basedCisplatin, carboplatin
AntibioticsIntercalation/free radicalDoxorubicin, bleomycin
CorticosteroidsLymphocyte apoptosisPrednisone
Biological/TargetedKinase inhibitors, antibodiesImatinib, rituximab, trastuzumab

Special Considerations:

  • Bleomycin — pulmonary fibrosis (↑ risk with O₂ supplementation)
  • Doxorubicin — cardiotoxicity (free radical generation); cumulative dose limit
  • Cisplatin — nephrotoxicity, ototoxicity, peripheral neuropathy
  • Cyclophosphamide — hemorrhagic cystitis (acrolein toxicity); prevent with MESNA
  • Methotrexate — mucositis, myelosuppression; antidote: leucovorin (folinic acid)
  • Vincristine — neurotoxicity (peripheral neuropathy); don’t give intrathecally (fatal)

Carcinoid Syndrome:

  • Secretory product: Serotonin (5-HT), histamine, bradykinin
  • Features: Flushing, diarrhea, wheezing, right-sided heart disease (carcinoid heart disease — tricuspid/pulmonic stenosis/regurgitation)
  • Usually indicates liver metastases (because hepatic metabolism normally inactivates serotonin before systemic circulation)
  • Urinary 5-HIAA — serotonin metabolite; diagnostic marker

Key NEET-PG Clinical Pearls:

  • Philadelphia chromosome = t(9;22) BCR-ABL fusion → CML, ALL
  • Li-Fraumeni syndrome = germline p53 mutation → multiple cancers (breast, sarcoma, brain, adrenocortical)
  • Xeroderma pigmentosum = defective nucleotide excision repair → UV-induced skin cancers
  • Ataxia telangiectasia = ATM mutation → ↑ sensitivity to ionizing radiation; lymphoid malignancies
  • Bloom syndrome = BLM helicase defect → ↑ sister chromatid exchanges; AML, lymphomas
  • BRCA1/BRCA2 = defective homologous recombination repair → breast, ovarian, pancreatic cancer
  • MEN syndromes: MEN1 (pituitary, parathyroid, pancreatic tumors; menin gene), MEN2A/2B (medullary thyroid carcinoma, pheochromocytoma, parathyroid; RET proto-oncogene)
  • Lynch syndrome (HNPCC) = mismatch repair defects → colorectal, endometrial, ovarian cancer
  • Gardner syndrome = APC mutation → FAP + desmoid tumors, osteomas, sebaceous cysts
  • Turcot syndrome = APC or MMR mutations → colorectal + brain tumors

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