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Neoplasia > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

What is neoplasia

A

Uncontrolled cell growth that persists in absence of stimuli

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2
Q

What do cdks do?

A

activate downstream proteins by phosporylation

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3
Q

What happens to cells at G0 phase?

A

Are dormant and will only move onto differentiation, proliferation or cell death if they detect signals (eg ligands such as growth factors) from other cells

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4
Q

Permanent cells

A

Cannot duplicate (eg neurones, cardiac myocytes)

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5
Q

Conditionally-renewing cells

A

Will proliferate and differentiate to repair injury (eg hepatocytes)

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6
Q

Labile tissue

A

Constantly dividing in health (eg epithelia and bone marrow)

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7
Q

Hypertrophy

A

Increase in cell size and hence organ size

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8
Q

Hyperplasia

A

Increase in cell number and hence organ size (eg lactating breasts, prostate enlargement with age)

Organ architecture maintained and proliferation stops when stimulus removed

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9
Q

Metaplasia

A

One differentiated cell becomes another due to persistent injury, but reverses once injury removed (eg bronchus due to tar)

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10
Q

Dysplasia

A

descriptive appearance, not stage

Irreversible cytological changes in neoplasia

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11
Q

Invasion

A

Neoplasm infiltrates surrounding tissue and/or organs

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12
Q

Metastasis

A

Neoplasm spreads to other parts of the body via the blood, lymph or body spaces and proliferates

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13
Q

Benign

A

Neoplasm proliferates but does not invade or metastasise

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14
Q

Benign tumour classifications

A 
Surface epithelia=papilloma
Glandular epithelia= adenoma
Fat= lipoma
Fibrocytes=fibroma
Cartilage=chondroma
Smooth muscle= leiomyoma
Skeletal muscle= rhabdomyoma
Bone=osteoma
Germ cells/gonads= teratoma
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15
Q

Malignant tumour classifications

A 
Surface epithelia= squamous cell carcinoma
Glandular= adenocarcinoma
Germ cells/gonads= teratocarcinoma
Skin= melanoma
Lymph nodes= lymphoma
Astrocytes= glioma
WBC= leukaemia
Connective tissue= sarcoma
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16
Q

How can tumours cause death

A

Destruction of vital tissue, haemorrhage, opportunistic infection

17
Q

Carcinoma in situ

A

Neoplasm just before stage of invasion

18
Q

Carcinoma vs sarcoma

A

Carcinoma= forms in skin or tissue cells that line body’s internal organs (most common)6

Sarcoma= grows in body’s connective tissue cells

19
Q

What is TNM?

A

Cancer staging system (stands for tumour, node, metastasis)

Scores tumour size, lymph node involvement and extent of distant metastases

20
Q

Cancer grading

A

1-3, graded by degree of tissue differentiation (3=worst)

21
Q

Oncogenesis

A

Development of a tumour

Also carcinogenesis

22
Q

Oncogenes

A

Normal genes which, if mutated, cause cancer (often regulatory genes)

23
Q

Mechanisms of oncogene activation

A
  • retrovirus inserts oncogenes into host cell genome or introduce viral promoters (so transcription factors express host genes inappropriately)
  • Ras genes can become oncogene through point mutation (causing Ras molecular switch to be permanently active)
  • epidermal growth factor receptor (EGFR) can become overly active by amplification or truncation
  • growth factors (eg sis) can be altered
24
Q

Tumour suppressor genes (TSGs)

A
  • Retinoblastoma (Rb) codes for pRb protein which must be phosphorylated in cell cycle by CDK for cell to pass from G1 to S phase, Rb blocks progression through cell cycle by binding to transcription factor E2F
  • p53 protects genome, conc. of p53 increases when DNA is damaged, acts as transcription factor for CDK inhibitor (p21), meaning p21 can’t phosphorylate Rb (resulting in cell cycle arrest), if damage irreparable then apoptosis occurs
  • APC is regulatory protein in Wnt ligand pathway, regulates B-catenin which acts as transcription factor for growth promoting genes
25
Q

Stroma

A

Supporting vascular connective tissue surrounds organs and sarcinomas

26
Q

Angiogenesis

A

Blood vessel growth (essential for tumour growth)

27
Q

In which condition are nucleotide excision proteins mutated?

A

Xeroderma pigmentosum (damaged DNA results in skin cancer)

28
Q

What happens when viral oncogenes activate telomerase?

A

Cells become immortal as telomerase enzymes make new repeat sequences on telomere

29
Q

Hallmarks of cancer

A
  • self sufficiency in growth signals
  • insensitivity to growth inhibition signals
  • evasion of apoptosis
  • immortality
  • angiogenesis
  • invasion and metastasis
30
Q

Pleomorphism

A

Larger cell nuclei

31
Q

How to identify cancerous cells on pathology slides

A

Lesions, cells crowded (sometimes with mucus), hyperchromasia (darker staining nuclei), variation in cell size/shape, reduced differentiation, loss of cell polarity, abnormal and increased mitosis

32
Q

Causes of cancer

A
  • viral transduction transforming DNA using oncogene (RAS switch)
  • deletion of TSG (proliferation no longer inhibited/ apoptosis no longer promoted, oncogene activated)
  • defects in DNA repair gene (eg. those coding for mismatch repair proteins)
  • electrophiles activated from chemical carcinogens
  • tar metaplasia from smoking
  • radiation: eg. UV rays may cause DNA strand breaks or thymine dimers (disrupting base pairing)
33
Q

Cancer Risk factors

A

Increased age, smoking, genetic predisposition, environment (incl. carcinogen exposure) radiation exposure, infectious agents (viruses), parasites

34
Q

Cancer treatment

A
  • Surgery
  • chemotherapy (metastasised)
  • radiotherapy
  • bone marrow transplants
  • angiostatic agents
  • pain relief
  • palliative care
  • immunotherapy
35
Q

What is immunotherapy?

A

Treatment used to stimulate immune system to recognise cancer cells as foreign and attack them

36
Q

How to tell difference between benign and malignant tumour

A

Benign: clearly circumscribed, not extended into tissue but into lumen (exophytic growth)

Malignant: messy, crab-like spread into affected tissue (endophytic growth)

37
Q

Polyps

A

Abnormal outgrowths connected to affected tissue by a stalk

Neoplasia (1 decks)

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