Pathology · Chapter 7

Neoplasia

The chapter question

A single cell acquires a mutation. What has to change before that cell becomes a cancer that can kill its host?

  1. basement membrane (intact)

    1. Dysplasia

    Atypia, basement membrane intact

  2. basement membrane (intact)

    2. Carcinoma in situ

    Full thickness, still contained

  3. basement membrane (breached)

    3. Invasive carcinoma

    Crosses the membrane: spread becomes possible

Teaching schematics, not micrographs.

One epithelium at three moments: dysplasia, carcinoma in situ, invasion.

Make a quick prediction

Which single change would you bet matters most in turning a contained clone into a lethal cancer?

Study path

Follow the order or jump to the concept you need. Every topic has a Deep Learning and a High-Yield view of the same facts, and ends with a short knowledge check.

0 of 7 topics studied0 of 57 questions correct
  1. 7.122 minUp nextWhat a tumor is and what it is calledA neoplasm is a clone of cells that keeps growing after the stimulus is gone. Its name records two things: the tissue it imitates and whether it behaves benignly or malignantly.Neoplasia: one clone, growing without a reasonNaming rules: -oma, carcinoma, sarcomaReading lineage under the microscopeTumor-like masses: hamartoma, choristoma, teratoma+1
  2. 7.226 minBenign or malignant: differentiation, dysplasia and invasionMalignancy is decided by behavior: invasion and metastasis. Differentiation, growth rate and the basement membrane tell you how close a tumor is to that line, and a handful of acquired capabilities explain how it crosses it.Four features that separate benign from malignantDifferentiation and anaplasiaDysplasia → carcinoma in situ → invasionTumor Pathology Case Lab+2
  3. 7.324 minInvasion and metastasisTo spread, a carcinoma cell must let go of its neighbors, cut through the basement membrane, move through matrix and enter a vessel. Which vessel it enters decides where the metastases appear.The invasion cascadeThree routes of spreadWhy liver and lung: follow the venous drainageBone metastases: blastic or lytic
  4. 7.430 minWho gets cancer, and which genes breakCancer is common, rises with age and differs between populations. Underneath, every cancer is a set of mutations in four classes of genes: accelerators, brakes, apoptosis regulators and DNA repair.Epidemiology: causes, age and populationsScreening: catching the clone earlyFour classes of cancer genesThe brakes: RB and p53+2
  5. 7.526 minCarcinogens: chemicals, viruses, radiation and bacteriaCarcinogens damage DNA directly, after metabolic activation, by inserting viral oncogenes or through chronic inflammation. Learn the few signature pairings that point to one exposure, and keep them apart from broad risk factors.Initiation and promotion; direct- and indirect-acting carcinogensChemical carcinogens: signature pairings and broad risksOncogenic virusesRadiation: ionizing and ultraviolet+1
  6. 7.624 minDiagnosis, grade and stageTissue makes the diagnosis. Grade says how abnormal the cells look; stage says how far the tumor has gone. Stains and serum markers support an answer, they do not replace the histology or the clinical picture.Getting the tissue: biopsy, FNA, frozen section, cytologyGrade versus stageImmunohistochemistry: asking the cell what it isSerum tumor markers
  7. 7.724 minEffects on the host and paraneoplastic syndromesA tumor harms its host by occupying space, by consuming and inflaming the whole body, and by secreting substances that act far from the tumor. Paraneoplastic syndromes are the third kind, and they can be the first sign of the cancer.Local effects: pressure, obstruction, bleedingCachexia and the systemic effectsEctopic hormonesNeurologic, skin, clotting and kidney syndromes

Practice

How the ideas connect

15 bridges carry one concept into the next, within this chapter and across chapters. Each is taught where you first need it.