properties of cancer (W13) Flashcards

1
Q

epithelial malignancy name?

A

carcinoma

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2
Q

which part of an ulcer should you biopsy

A

the edge

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3
Q

appearances of surface neoplasms?

A

plaque, ulcerated, annular, pedunculated polyp, papillary, exophytic/mass forming

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4
Q

difference between polyp and papillary

A

polyp - epithelium covers raised core
papillary - epithelium covers thin branches. greater surface area but same size

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5
Q

name for neoplasm with connective tissue stalk?

A

pedunculated

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6
Q

name for neoplasm without connective tissue stalk?

A

sessile

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7
Q

benign neoplasms - how do they cause problems?

A

compression
obstruction/intussusception
haemorrhage, infarction
secreted products
progression to malignancy
cosmetic
local trauma/irritation

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8
Q

problems with neoplasms which are tubes/ducts/surfaces

A

perforation, occlusion, ulceration

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9
Q

problems with neoplasms which are space -occupying

A

spinal cord compression

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10
Q

problems with neoplasms - organ destruction?

A

liver failure from carcinomatosis, CNS invasion

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11
Q

problems with neoplasms - organ encasement?

A

respiratory failure (pleural mesothelioma)

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12
Q

cachexia?

A

muscle goes into catabolic mode, ‘cannibalises itself’, not reversable with nutritional support

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13
Q

paraneoplastic meaning?

A

usually secretion of factors from neoplasms that the tissue wouldn’t usually secrete

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14
Q

paraneoplastic complications

A

venous thrombosis
hypercalcaemia
neuropathies
dermatomycosis
finger clubbing
nephrotic syndrome

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15
Q

field cancerisation?

A

expanded collections of cells that express some positively selected phenotypic changes needed for malignancy

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16
Q

clonal mosaicism?

A

cells with genes with a survival advantage in a tissue expands a the expense of others resulting in a less diverse cell population in a tissue.

17
Q

what does mutation count and clone size increase with

A

chronic inflammation
carcinogens (sun exposure, smoking, alcohol)

18
Q

how does chronic inflammation cause an increase in mutation count and clone size

A

more regeneration, more DNA damage

19
Q

how do carcinogens cause an increase in mutation count and clone size

A

many chemical carcinogens do not mutate, but enable clonal expansion

20
Q

how many altered driver genes is needed to convert a normal cell to an early invasive cancer cell

A

around 3 - varies with cancer type and individuals

21
Q

what many cancerous tissues look like?

A

normal
hyperplastic (too many cells)
metaplastic
dysplastic (cells look weird - highest risk)

22
Q

clonal haematopoiesis?

A

driver gene mutations in bone marrow favour growth of bone marrow cells. cases white blood cells produced to be more inflammatory

23
Q

clonal haematopoiesis is a risk factor for which diseases

A

coronary heart disease, stroke, chronic liver disease

24
Q

where are vessels present in a cancer? what does this cause?

A

only on the outer parts, at some point as you get deeper the tissue pressure is too high. This causes tissue fluid to seep to the surface towards lymphatics (allowing any detached cancer cells to easily spread)

25
Q

acidity of a cancer tumor

A

pretty acidic as there is not much glucose or oxygen

26
Q

why is the outwards movement of tissue fluid in a cancer problematic for treatment

A

drugs aren’t likely to diffuse in, will only effect the surface of the cancer

27
Q

characteristic of fast growing cancer

A

viable cells around blood vessels and necrosis in-between

28
Q

what does chaotic angiogenesis create

A

chaotic blood flow (so silly so goofy)
pooling, eddies, flow reversals, leakiness etc. creates regional differences within a cancer

29
Q

what happens when cancer driver genes are multiply copied? what does this mean?

A

copies tend to detach from the chromosome and form a ring (similar to a bacterial chromosome)
this causes it not to be picked up in whole gene sequencing

30
Q

universal cancer tasks

A

division, accumulation of biomass, lipogenesis, immune interaction, invasion and tissue remodelling

31
Q

cancer trade off between conflicting tasks causes what?

A

cancers have to have plasticity to alter trade-offs between tasks

32
Q

mesenchymal plasticity?

A

carcinoma can reversibly take on characteristics of fibroblasts

33
Q

what does epithelial mesenchymal plasticity (EMP) allow cancer cells to do

A

move and therefore invade
downregulate proliferation therefore resist therapy that targets proliferating cells

34
Q

how do metabolic conditions in cancer impair the immune system

A

antigen signalling under metabolic stress causes CD8 T cell exhaustion. cancer cells very good at stealing all the glucose.

35
Q

what eliminates most circulating cancer cells

A

NK cells

36
Q

how do cancer cells subvert immune activation

A

release immunosuppressive factors. repress antigen processing and presentation. reduce MHC 1
display immune inhibitors

37
Q

how do cancer cells survive treatment

A

cancer treatments leave residual cells - reservoir for relapse
active resistant of treatment
genetic resistance - new clone develops