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MOD- Neoplasia 9-12 > session 9 > Flashcards

session 9 Flashcards

(72 cards)

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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
indirect systemic effects of neoplasm
- 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)
26
proto-oncogene
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).
27
oncogene
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.
28
tumour burden
total mass of tumours carried by an individual with cancer
29
for a metastasis to happed
grow and invade at site 1 enter a transport system grow at site 2 to form new tumour meanwhile--- evade the host defences
30
invasion of a carcinoma requires and the name given to this process
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
cancer niche
created when malignant cells take advantage of non-neoplastic cells to provide proteases and growth factors.
32
name the routes that malignant cells take to get to distant sites
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
extravasation
at secondary site malignant cells have to get out of the vessels and grow
34
micro-metastases
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
tumour dormancy
apparent healthy/ disease free person may harbour many micro metastases. relapse can be due to these micro metastases.
36
what determines secondary site
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
what chemicals show us about carcinogenesis
1) - long delay between exposure and malignant neoplasm 2) - risk depends on total dose of carcinogen 3) - sometimes organ specificity for carcinogens
38
procarcinogens
converted to carcinogens by cytochrome P450 enzymes in the liver
39
complete carcinogens
act as both initiators and promoters
40
how radiation causes damage...
directly damages DNA indirectly damages DNA by creating free radicals can damage bases or cause single/ double stranded breaks
41
carcinogen in cigarette smoke
polycyclic aromatic hydrocarbon
42
infections can be carcinogenic, how do they act?
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
name a natural product that acts as a carcinogen
aflatoxin- from fungus on foods such as nuts
44
what is retinoblastoma, what gene causes it
malignant retinal tumour | RB1 gene
45
outline the 2 hit hypothesis
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
tumour suppressor gene
gene that inhibits neoplastic growth
47
RAS
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
RB gene
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
xerodermapigmentosum
mutation in one of seven genes in nucleotide excision repair | sensitive to UV damage therefore cancer at a young age
50
hereditary non polyposis colon cancer (HNPCC)
autosomal dominant colon carcinoma mutation in DNA mismatch repair genes
51
familial breast carcinoma
BRAC1 / BRAC2 genes | important in repairing double stranded DNA
52
genetic instability
abnormalities that cause an accelerated mutation rate found in malignant neoplasms due to... mismatch repair, nucleotide excision repair, chromosome segregation abnormalities
53
hallmarks of cancer in malignant neoplasms
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
progression
steady increase in the number of mutations
55
most common cancers in children
leukaemia's CNS lymphomas
56
cancers with the worst outcome in men and women
pancreatic (worst) lung Oesophageal (slightly better survival)
57
4 cancers that account for the most deaths
lung cancer (most) colorectal cancer breast cancer prostate cancer
58
factors that affect the outcome of cancer
``` age general health tumour site tumour type grade stage availability of treatment ```
59
what is tumour staging
measure of the malignant neoplasms overall burden | commonest is TMN
60
outline TNM staging
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
lymphoma staging
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
colorectal carcinoma
``` dukes staging A- invasion but not through bowel B- invasion through bowel wall C- involves lymph nodes D- distant metastases ```
63
what is tumour grading
degree of differentiation of a neoplasm ``` usually--- G1-- well differentiated G2-- moderately differentiated G3-- poorly differentiated G4-- undifferentiated or anaplastic ```
64
breast cancer grading
bloom Richardson system | looks at tubule formation, nuclear variation, number of mitoses
65
Adjuvant treatment
treatment given after the removal of a primary tumour to eliminate subclinical disease
66
Neo-adjuvant treatment
given to reduce the size of a primary tumour prior to surgical excision
67
how does radiotherapy work
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
types of chemotherapy drugs that affect proliferating cells and there actions
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
outline hormone therapy used for malignant neoplasms
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
give examples including there action of targeting oncogenes in cancer therapy
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
what is an adenocarcinoma
adeno- gland carcin- cancerous oma- tumour therefore cancerous tumour of a gland
72
what is an adenoma
benign tumour formed from glandular structures in epithelial tissue

MOD- Neoplasia 9-12 (1 decks)

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