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MOD- Neoplasia 9-12 > session 9 > Flashcards

session 9 Flashcards

1
Q

neoplasm

A

abnormal growth of a cell that persists after the initial stimulus is removed

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2
Q

malignant neoplasm

A

abnormal growth of a cell that persists after the initial stimulus is removed, it invades surrounding tissue with the potential to spread to distant sites

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3
Q

tumour

A

clinically detectable lump or swelling

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4
Q

cancer

A

malignant neoplasm

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5
Q

metastasis

A

malignant neoplasm that has spread from its original site to a new non-contiguous site

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6
Q

dysplasia

A

pre-neoplastic alteration in which tissues have disordered cellular organisation, cells often show variation in size and shape. non neoplastic because it is reversible

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7
Q

what is an initiator/ promoter and explain their combined effect

A

initiators are mutagenic agents that cause mutation in somatic cells. promoters cause cell proliferation. together they expand the monoclonal population of mutant cells. overtime becomes a neoplasm known as progression.

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8
Q

monoclonal

A

collection of cells that originate from a single founding cell

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9
Q

behavioural differences between benign and malignant neoplasms

A

benign- confined, don’t metastasise

malignant- metastasise

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10
Q

differences visible to the naked eye between benign and malignant neoplasms

A

benign- confined, pushing outer margin, compress the surrounding tissue
malignant- irregular margin and shape, necrosis and ulceration, invasive and destroy

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11
Q

microscopic differences between malignant and benign neoplasms

A

both can show dysplasia (enlargement of an organ or tissue by the proliferation of cells of an abnormal type, as a developmental disorder or an early stage in the development of cancer)
benign- cells are differentiated
malignant- vary. low grade has cells with a higher degree of differentiation. high grade has cells with a lower degree of differentiation. no resemblance to any tissue is known as anaplastic.

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12
Q

pleomorphic

A

level of differentiation of cells. there can be variation in the cells size and shape. with worsening differentiation cells have:

  • increased nuclear size
  • increased nucleus: cytoplasm ratio
  • increased mitotic figures
  • increased variation in size, shape and nuclei
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13
Q

oma—is the ending of what type of neoplasm

A

benign neoplasm

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14
Q

malignant neoplasms end in…

A

carcinoma- epithelial cells

sarcoma- if stromal (CT cells)

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15
Q

in situ

A

no invasion of epithelial basement membrane

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16
Q

invasive

A

penetrates basement membrane

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17
Q

leukaemia

A

malignant neoplasm of blood forming cells arising in the bone marrow

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18
Q

lymphoma

A

malignant neoplasm of lymphocytes, mainly effect lymph nodes

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19
Q

germ cell neoplasm

A

from pluripotent cells in testis/ ovary

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20
Q

blastoma

A

found in children as forms from immature precursor cells. e.g. nephroblastoma

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21
Q

describe the general rules of malignant neoplasm spread

A

carcinoma- via lymphatic’s

sarcoma- via blood stream

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22
Q

places most likely to spread to the bone

A 
breast
lung
thyroid
prostate
kidney
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23
Q

most likely to spread via the blood

A

brain
lung
bone
liver

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24
Q

direct local effects of neoplasms

A

direct invasion and destruction of normal tissue
ulcers at surface- bleed
compress adjacent structures
block tubes and orifices

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25
Q

indirect systemic effects of neoplasm

A
  • increased tumour burden has parasitic effects as well as the effects of secreted factors (e.g. cytokines), leads to decreased appetite, cachexia, malaise, immunosuppression, thrombosis
  • benign neoplasm of endocrine gland glands are well differentiated so produce hormones/ malignant tumours may also cause tumours
  • neuropathies effect brain, peripheral nerves, skin (pruritis, abnormal pigmentation, pyrexia, dermato-myositis)

paraneoplastic syndrome (disease and set of symptoms as a consequence of cancer)

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26
Q

proto-oncogene

A

proto-oncogenes are normal genes that control cell division and differentiation they do this by producing proteins that transduce mitogenic signals (signals in the body that cause mitosis).

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27
Q

oncogene

A

proto-oncogenes can become an oncogene either if mutated or if their expression is increased. oncogenes cause increased mitosis and so the formation of tumours, ie are cancerous.

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28
Q

tumour burden

A

total mass of tumours carried by an individual with cancer

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29
Q

for a metastasis to happed

A

grow and invade at site 1
enter a transport system
grow at site 2 to form new tumour

meanwhile— evade the host defences

30
Q

invasion of a carcinoma requires and the name given to this process

A

adhesion alteration- cell to cell- decrease E Cadherin expression which usually binds cells, cell to stroma- decrease integrins expression

alter motility- change actin cytoskeleton

degrade basement membrane and stroma- altered protease expression, matrix metalloproteinases.

NAME OF PROCESS- epithelial to mesenchymal transition (EMT)

31
Q

cancer niche

A

created when malignant cells take advantage of non-neoplastic cells to provide proteases and growth factors.

32
Q

name the routes that malignant cells take to get to distant sites

A

blood- via capillaries and venules
lymphatic’s
transcoelomic (fluid in body cavities)

(NOTE- cancer cells can cause angiogenesis- new cells are leaky so aid metastasis)

33
Q

extravasation

A

at secondary site malignant cells have to get out of the vessels and grow

34
Q

micro-metastases

A

surviving microscopic deposits that fail to grow. they may have lodged at a secondary site, the cells then die or fail to grow to a clinically noticeable tumour. a hostile environment can also stop growth. cells are known as dormant.

35
Q

tumour dormancy

A

apparent healthy/ disease free person may harbour many micro metastases. relapse can be due to these micro metastases.

36
Q

what determines secondary site

A

1) regional drainage of blood, lymph, coelomic fluid
2) seed and soil- explains unpredictable spread of blood borne metastases. the sells will travel everywhere but only in specific conditions/ niche will they grow.

37
Q

what chemicals show us about carcinogenesis

A

1) - long delay between exposure and malignant neoplasm
2) - risk depends on total dose of carcinogen
3) - sometimes organ specificity for carcinogens

38
Q

procarcinogens

A

converted to carcinogens by cytochrome P450 enzymes in the liver

39
Q

complete carcinogens

A

act as both initiators and promoters

40
Q

how radiation causes damage…

A

directly damages DNA
indirectly damages DNA by creating free radicals

can damage bases or cause single/ double stranded breaks

41
Q

carcinogen in cigarette smoke

A

polycyclic aromatic hydrocarbon

42
Q

infections can be carcinogenic, how do they act?

A

directly– effect genes that control cell growth
indirectly– through chronic tissue injury, the regeneration acts as a promoter for pre-existing mutations or can lead to new mutations due to replication errors

43
Q

name a natural product that acts as a carcinogen

A

aflatoxin- from fungus on foods such as nuts

44
Q

what is retinoblastoma, what gene causes it

A

malignant retinal tumour

RB1 gene

45
Q

outline the 2 hit hypothesis

A

explains the difference between tumours in families and general population
1st hit- inheritance- appears in every cell
2nd hit- somatic mutation
therefore for a non-inherited cancer, both hits have to be in the same somatic cell.

46
Q

tumour suppressor gene

A

gene that inhibits neoplastic growth

47
Q

RAS

A

proto-oncogene
encodes small G proteins that relay signals into the cells that eventually push the cells past the cell cycle restriction point
mutant RAS produces a protein that is always active therefore the cell always continues past the cell cycle restriction point

48
Q

RB gene

A

tumour suppressor gene.
usually inhibits passage through the cell cycle restriction point
therefore if both alleles are mutated then continuous passage through the restriction point

49
Q

xerodermapigmentosum

A

mutation in one of seven genes in nucleotide excision repair

sensitive to UV damage therefore cancer at a young age

50
Q

hereditary non polyposis colon cancer (HNPCC)

A

autosomal dominant
colon carcinoma
mutation in DNA mismatch repair genes

51
Q

familial breast carcinoma

A

BRAC1 / BRAC2 genes

important in repairing double stranded DNA

52
Q

genetic instability

A

abnormalities that cause an accelerated mutation rate found in malignant neoplasms
due to… mismatch repair, nucleotide excision repair, chromosome segregation abnormalities

53
Q

hallmarks of cancer in malignant neoplasms

A

1) self sufficient in growth signals
2) resistant to stop growth signals
3) immortalisation (no limit to the number of times cell can divide)
4) angiogenesis- sustained ability for new vessel production
5) resist apoptosis
6) invade and metastasise

54
Q

progression

A

steady increase in the number of mutations

55
Q

most common cancers in children

A

leukaemia’s
CNS
lymphomas

56
Q

cancers with the worst outcome in men and women

A

pancreatic (worst)
lung
Oesophageal (slightly better survival)

57
Q

4 cancers that account for the most deaths

A

lung cancer (most)
colorectal cancer
breast cancer
prostate cancer

58
Q

factors that affect the outcome of cancer

A 
age
general health
tumour site
tumour type
grade
stage
availability of treatment
59
Q

what is tumour staging

A

measure of the malignant neoplasms overall burden

commonest is TMN

60
Q

outline TNM staging

A

T- size of the primary tumour, (usually T1- T4)
N- extent of regional node metastases (e.g. N0 - N3)
M- extent of distant metastases spread (M0 or M1)

used to convert to a 1 to 4 scale
varies between cancers but generally----
1- early local disease
2- advanced local disease
3- regional metastases
4- advanced disease with distant metastasis
61
Q

lymphoma staging

A

ann arbor
1- single node
2- 2 separate regions one side of the diaphragm
3- both sides of diaphragm
4- diffuse/disseminated one 1+ extra-lymphatic organs (bone or lungs)

62
Q

colorectal carcinoma

A 
dukes staging
A- invasion but not through bowel
B- invasion through bowel wall
C- involves lymph nodes
D- distant metastases
63
Q

what is tumour grading

A

degree of differentiation of a neoplasm

usually---
G1-- well differentiated
G2-- moderately differentiated
G3-- poorly differentiated
G4-- undifferentiated or anaplastic
64
Q

breast cancer grading

A

bloom Richardson system

looks at tubule formation, nuclear variation, number of mitoses

65
Q

Adjuvant treatment

A

treatment given after the removal of a primary tumour to eliminate subclinical disease

66
Q

Neo-adjuvant treatment

A

given to reduce the size of a primary tumour prior to surgical excision

67
Q

how does radiotherapy work

A

kills proliferating cells by triggering apoptosis or interfering with mitosis.
direct or free radical induced DNA damaged, detected at the cell cycle checkpoints triggering apoptosis

68
Q

types of chemotherapy drugs that affect proliferating cells and there actions

A

antimetabolites- mimic normal substrate in DNA replication
Alkylating/ Platinum drugs- cross link the 2 strands of the DNA helix
Antibiotics-
plant derived drugs- blocks microtubule assembly and interferes with mitotic spindle formation

69
Q

outline hormone therapy used for malignant neoplasms

A

selective oestrogen receptor modulators (SERM’s) bind to oestrogen receptors preventing oestrogen from binding. e.g. tamoxifen
used to treat hormone receptor positive breast cancer

androgen blockade is used for prostate cancer

70
Q

give examples including there action of targeting oncogenes in cancer therapy

A

Herceptin- blocks Her 2 signalling (her-2 genes are over expressed in a quarter of cancers)
Imatinib- chronic myeloid leukaemia has an abnormal chromosomal rearrangement (Philadelphia chromosome) that codes for an oncogenic fusion pore (BCR-ABL) imatinib inhibits fusion proteins

71
Q

what is an adenocarcinoma

A

adeno- gland
carcin- cancerous
oma- tumour

therefore cancerous tumour of a gland

72
Q

what is an adenoma

A

benign tumour formed from glandular structures in epithelial tissue

MOD- Neoplasia 9-12 (1 decks)

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