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CCG > Histopathology of Cancer – Basic Concepts and Terminology > Flashcards

Histopathology of Cancer – Basic Concepts and Terminology Flashcards

1
Q

What is Neoplasia?

A

= new growth
- new growth
• Monoclonal proliferation of cells to form a tumour/ mass

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2
Q

List 3 characteristics of neoplasms

A

1) Growth exceeds stimulus and becomes autonomous
2) Neoplasms may be benign or malignant
3) Neoplasms resemble the cell of origin!

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3
Q

What is cancer?

A

malignant neoplasm

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4
Q

What is Hyperplasia?

A

increase in cell number, proportionate to stimulus

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5
Q

What is Hypertrophy?

A

increase in cell size, proportionate to stimulus

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6
Q

What is a Choristoma?

A

tumour composed of normal cells/ tissues present in an abnormal place

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7
Q

What is a hamartoma?

A

tumour composed of disorganised growth of different cell types normally present in that organ

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8
Q

What is a teratoma?

A

tumour composed of derivatives of all 3 embryological layers (ectoderm, endoderm & mesoderm) e.g. in ovary

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9
Q

What is dysplasia?

A

‘abnormal growth’; may form a benign neoplasm (e.g. adenoma); often a precursor of malignant neoplasms

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10
Q

How do benign and malignant neoplasms differ in biological potential (behaviour)?

A

MALIGNANT neoplasms have the potential to spread (metastasise);
BENIGN neoplasms do not
• Borderline (uncertain malignant potential) tumours are intermediate
• Benign neoplasms uncommonly transform into malignant neoplasms – has intermed chance of becoming worse

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11
Q

Which malignant tumors arise from these cells of origin?

  1. Epithelium
  2. Mesenchyme
  3. Primitive lymphoid/ myeloid cells (blasts)
  4. Mature lymphocytes
  5. Plasma cells
  6. Mesothelium
  7. Melanocytes
  8. Germ cells
A
  1. carcinoma
  2. sarcoma (from cartilage)
  3. leukaemia
  4. lymphoma
  5. myeloma
  6. mesothelioma
  7. melanoma
  8. teratoma, seminoma, choriocarcinoma, etc
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12
Q

Which benign tumors arise from these cells of origin?

  1. Squamous epithelium
  2. Glandular epithelium
  3. Transitional epithelium
  4. Fat
  5. Vessels
  6. Nerves
  7. Bone
  8. Cartilage
  9. Smooth muscle
  10. Skeletal muscle
A
  1. squamous papilloma
  2. adenoma
  3. transitional cell papilloma (malignant would be carcinoma)
  4. lipoma
  5. lymph/haemangioma
  6. neuroma
  7. osteoma
  8. chondroma
  9. leiomyoma
  10. rhabdomyoma
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13
Q

5 Differences between benign and malignant neoplasms

A
  • Clinical presentation (history, examination)
  • Macroscopic appearance
  • Microscopic appearance (histology)
  • Behaviour and prognosis
  • Management
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14
Q

Microscopic differences between benign and malignant neoplasms

A 
B: Close resemblance to cell of origin 
M: Poor resemblance 
B: Uniform growth pattern 
M: Irreg/haphazard growth pattern 
B: Normal nuclear size, normal cytoplasmic ratio
M: Enlarged, irreg 
B: Smooth nuclear mem
M: Irreg nuclear mem
B: Normal tumor cells in mitosis 
M: Inc tumor cells in mitosis
B: Tumor stroma - no necrosis/haemorrhage 
M: Coagulative necrosis & haemorrhage
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15
Q

List the principles of carcinogen

A

1) Initiation
2) 4 classes of normal genes are damaged in carcinogenesis
3) Clonal expansion
4) Driver mutations and epigenetic aberrations
5) Darwinian selection

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16
Q

Describe the process of initiation of carcinogen

A
  • non-lethal genetic damage to the cell:
    1) Inherited germline mutation
    2) Env damage
    3) Random
17
Q

What are the diff forms of genetic damage to the cell?

A

point mutation, translocation, deletion, gene amplifications, polysomy

18
Q

List 4 classes of normal genes are damaged in carcinogenesis

A

1) proto-oncogenes – growth promoting – mutation in proto-oncogene can prod oncogene
2) tumour suppressor genes (anti-oncogenes) – growth inhibiting e.g. p53, BRCA
3) genes that regulate apoptosis (programmed cell death)
4) genes involved in DNA repair

19
Q

Describe driver mutations and epigen aberrations (step 4)

A

Driver mutations: loss-of-function mutations in genes that maintain genomic integrity
Epigen mod: DNA methylation →↓ expression of that gene - modifications of histones (proteins which package DNA into chromatin)→↓ or ↑gene expression
Step-wise accumulation of complementary mutations and epigen mod are required for carcinogen

20
Q

Describe clonal expansion (step 3)

A

A single pre-cursor cell which has acquired non-lethal damage it its DNA undergoes clonal expansion to form a neoplasm

21
Q

Describe Darwinian selection

A
  • The tumour sub-clones which have acquired the genetic abnormalities which make them the ‘fittest’ cancer cell will out-grow the others
  • Some tumour sub-clones can acquire mutations which make them more likely to survive chemotherapy and radiotherapy
22
Q

Describe mech of spread of cancer cells

A
  • Local invasion (contiguous spread)
  • Iatrogenic implantation
  • Metastatic spread
23
Q

List the diff ways of metastatic spread

A
  • via lymphatics
  • via bloodstream (haematogenous)
  • extravascular migratory metastasis (EMM) – tumor finds blood vessel + forms a new mass
  • perineurally
  • trans-peritoneally i.e. tumor cells can travel through ascites
  • aerogenous (through lungs)
  • by fluid (eg urine)
24
Q

List types of cytology samples for cancer

A
  • naturally exfoliated, eg urine, sputum

* artificially exfoliated, eg washings, brushings, scrapings

25
Q

List types of investigations for cancer

A

• Fine Needle Aspiration (FNA) (free-hand or guided by an imaging technique)
Ancillary techniques performed on histological/ cytological samples
• Flow cytometry - Cells broken up in fluid, label with fluorescent agents + light emitted by cells in order to pick them up
• Immunohisto/cytochemistry
• Molecular diagnostics (cytogenetics, DNA analysis)

26
Q

What does management of cancer depend on?

A

1) Organ and histological type of cancer
2) Evidence for propensity to spread/ how far it has actually spread - eg microscopic lymphovascular/ perineural invasion in tumour stroma
3) Tumour GRADE & STAGE
4) Expression by tumour of targettable antigens
5) Patient’s fitness/ co-morbidities

27
Q

What is tumor stage?

A

= how far a tumour has already spread - different staging systems,
eg T – tumour (T1 → T4, increasing size/ local spread)
N – nodes (N0, N1, N2, etc, increasing number of local lymph nodes involved)
M – metastases (M0, M1, spread to distant lymph nodes and organs)

28
Q

What is tumor grade?

A
  • how closely it resembles the cell of origin (well differentiated = low grade = good prognosis) (poorly differentiated = high grade = poor prognosis)

CCG (3 decks)

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