tumour pathology Flashcards

1
Q

what is a tumour (neoplasm)?

A

abnormal growing mass of tissue, the growth of which is uncoordinated with normal tissue

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2
Q

what will happen to the tumour growth if any stimulus which may have caused the tumour to form is removed?

A

it will continue

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3
Q

is tumour growth irreversible?

A

true

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4
Q

what two types of tumour are there?

A

benign

malignant

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5
Q

what separates malignant (cancer) tumours from benign ones?

A

malignant tumours have the ability to invade adjacent tissue and to metastasise to other sites within the body

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6
Q

what are the 3 most common cancers for males?

A

prostate
lung
colon

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7
Q

what are the 3 most common cancers for females?

A

breast
lung
colon

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8
Q

what are the 3 most common overall cancers?

A

breast
lung
colon

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9
Q

how are tumours classified?

A

based on tissue of origin

benign vs malignant

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10
Q

what are the names for benign and malignant glandular tumours?

A

benign: adenoma
malignant: adenocarcinoma

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11
Q

what are the names for benign and malignant tumours of squamous epithelium?

A

benign: squamous papilloma
malignant: squamous carcinoma

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12
Q

what are the names for benign and malignant tumours of the bone?

A

benign: osteoma
malignant: osteosarcoma

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13
Q

what are the names for benign and malignant tumours affecting fat tissue?

A

benign: lipoma
malignant: lipo-sarcoma

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14
Q

what are the names for benign and malignant tumours affecting fibrous tissue?

A

benign: fibroma
malignant: fibro-sarcoma

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15
Q

what is the name given to malignant cancer of the blood?

A

leukaemia

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16
Q

what is the name given to malignant cancer of the lymphoid tissue?

A

lymphoma

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17
Q

what are the names of tumours of the central and peripheral nervous system

A

CNS: astrocytoma
PNS: schwannoma

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18
Q

what is the difference between ovarian and testicular teratomas? (germ cell tumours)

A

ovarian usually benign, testicular usually malignant

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19
Q

what are the features of benign tumours?

A
non invasive growth pattern
usually encapsulated
no evidence of invasion
no metastases
cells similar to normal cells
cells function similarly to normal tissues
well differentiated
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20
Q

what are the features of malignant tumours?

A
invasive growth pattern
no capsule or capsule breached by tumour cells
cells are abnormal
poor differentiation
loss of normal function
evidence of spread of cancer
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21
Q

what are some properties of cancer cells?

A

altered genetics
altered cellular function
abnormal morphology
cells are capable of independent growth

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22
Q

what are some examples of the altered genetics of cancer cells?

A

loss of tumour suppressor genes

increased function of oncogenes

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23
Q

what are the examples of altered cellular function of cancer cells?

A

production of tumour related proteins
loss of cell-cell adhesion
altered cell-matrix adhesion

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24
Q

what are some biomarkers indicative of cancer cells?

A

onco-fetal proteins
oncogene products
growth factors and receptors

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25
what is alpha-fetoprotein indicative of?
teratoma of testis | hepatocellular carcinoma
26
what is carcino-embryonic antigen (CEA) indicative of?
colon cancer
27
what is oestrogen receptor indicative of?
breast cancer
28
what is her2 indicative of?
breast cancer
29
what is prostate specific antigen indicative of?
prostate cancer
30
what is the histological appearance of cancer cells?
cellular and nuclear pleomorphism (marked variation in size and shape) mitoses are present and often abnormal
31
what are the two processes relating to cell growth and cell death that occur in tumour growth?
angiogenesis | apoptosis
32
what is the pathology of tumour angiogenesis?
new blood vessel formation by tumours required to sustain tumour growth new blood vessels provide a route for release of tumour cells into circulation the higher the number of blood vessels in a tumour the poorer the prognosis
33
what is apoptosis and what is its role in tumour pathology?
programmed single cell death regulates tumour growth involved in the reponse to chemo/radiotherapy
34
what is the major clinical problem associated with cancer?
formation of metastatic tumours
35
what are some modes of cancer spreading?
local spread lymphatic spread blood spread trans-coelomic spread
36
how would a tumour manage to spread into the blood/lymphatic system?
invasion into the connective tissue is followed by invasion into the lymphatic system/bloodstream
37
describe the process of tumour metastasis via lymphatics
tumour cells adhere to lymph vessels tumours invade lymphatic system and then invade lymph nodes formation of metastasis in lymph node clinical evidence of metastasis
38
describe the process of tumour metastasis via blood?
adherence of tumour cells to blood vessels, followed by invasion into blood vessels invasion of tumour cells into tissue formation of metastasis clinical evidence of metastasis
39
what happens in trans-coelomic spread?
spread of tumour cells across body cavities
40
what are some example of tumours that show trans-coelomic spread?
lung stomach colon ovary
41
what are some common sites of metastasis?
``` liver lung brain bone (axial skeleton) adrenal gland ```
42
what are some uncommon sites of metastasis?
spleen kidney skeletal muscle heart
43
where do tumours of breast tissue commonly metastasis do?
bone and lung
44
where do tumours of the prostate commonly metastasis to?
bone
45
where do tumours of the colon commonly metastasise to?
liver
46
what are some local effects of benign tumours?
pressure and obstruction
47
what are some local effects of malignant tumours?
``` pressure obstruction tissue destruction bleeding (anaemia, haemorrhage) pain adverse effects of treatment ```
48
why can malignant tumours cause pain?
pressure on nerves perineural infiltration bone pain from pathological fractures
49
what are systemic effects of malignant tumours?
secretion of hormones ( can be normal or abnormal) weight loss- cachexia paraneoplastic syndromes effects of treatments
50
what are paraneoplastic syndromes?
a syndrome that is the consequence of cancer in the body but is not due to the local presence of cancer cells (such as inappropriate hormone secretion)
51
what is "normal" hormone production from tumours?
when hormones are produced by tumours of endocrine organs (however there is abnormal control of hormone production/secretion)
52
what is abnormal/inappropriate hormone production from tumours?
when hormones are produced by tumours of an organ that does not normally produce hormones (such as ACTH being produced in lung cancer)
53
what is dysplasia?
pre malignant change which is the earliest stage that the process of malignancy can be visualised
54
what are some features of dysplasia?
it is identified in the epithelium no invasion can progress to cancer disorganisation of cells
55
what would you see at a cellular level in dysplasia?
increased nuclear size increased mitotic activity abnormal mitoses
56
what is the cell cycle?
time interval between mitotic divisions
57
what are some external factors that control the cell cycle?
hormones, growth factors, cytokines, stroma
58
what are some intrinsic factors that control the cell cycle?
critical checkpoints- restriction point (R)
59
what is the significance of the restriction point?
prior to the restriction point progress through G1 depends on external stimuli after the restriction point the cell cycle progresses autonomously
60
what are the phases of the cell cycle?
quiescent - G0 interphase - G1, S, G2 cell division - mitosis (M)
61
when would the cell cycle be arrested in G1?
if the cell size is inadequate if the nutrient supply is inadequate if an essential external stimulus is lacking if DNA damage is detected
62
when would the cell cycle be arrested in G2?
if the cell size is inadequate | if DNA damage is detected
63
when would the cell cycle be arrested in S?
if the DNA is not replicated
64
when would the cell cycle be arrested in M phase?
chromosome mis-alignment
65
what are the checkpoints in the cell cycle composed of?
system of cyclically active and inactive enzymes | catalytic sub unit activated by a regulatory sub unit
66
what are catalytic subunits of checkpoints called?
cyclin dependent kinases
67
what are the regulatory units of checkpoints called?
cyclins
68
what is the name given to the active enzyme complex at a cell cycle checkpoint?
CDK/cyclin complex
69
what do active CDK/cyclin complexes do?
phosphorylate target proteins
70
what effect does phosphorylation of target proteins by CDK/cyclin complexes have?
activates/inactivates the substrate, substrates regulate events in the next cycle phase
71
what form are CDKs expressed in?
inactive form
72
what other group of compounds regulates CDK activity apart from cyclins?
CDK inhibitors
73
what family of CKIs bind to CDK 4 and 6?
INK4A
74
what is carcinogenesis caused by?
mutation of genetic material that upsets the normal balance between proliferation and apoptosis
75
mutations of what can cause a cell to lose control of proliferation?
cell division, apoptosis and DNA repair
76
formation of what causes cancer at chromosome sites?
adducts
77
what is a DNA aduct?
covalently bound product formed from when chemical carcinogens or their active metabolites react with DNA
78
what is the primary defect in cancer?
uncontrolled cell proliferation via cell cycle dysregulation
79
what are the two regulatory pathways that are frequently disrupted to cause cancer?
cyclin D-pRb-E2F pathway | p53 pathway
80
what is the function of the retinoblastoma gene (pRb)
to activate or inactivate the E2F transcription factor
81
what is the function of E2F?
potent stimulator of cell cycle entry
82
what is the effect of absent or inactive pRb?
releases the "brake" on the cell cycle
83
where are virtually all cancers dysregulated?
G1-S
84
what are the 4 genes that mutate to cause cancer dysregulation at G1-S?
Rb, CDK4, cyclin D p16
85
what is the function of p53?
maintains genomic integrity:
86
what is the effect of increased p53 in damaged cells?
induces cell cycle arrest at G1 facilitates DNA repair in severe damage - p53 induced apoptosis
87
what is the effect of mutated p53?
no G1 arrest and no repair of damaged DNA - leads to the proliferation of genetically damaged cells and the formation of malignant neoplasms
88
what do Rb gene mutations favour?
cell proliferation
89
what mutations can mimic the effect of pRb loss?
mutational activation of cyclin D or CDK4 | mutational inactivation of CDKIs
90
what are some genetic inherited characteristics of inherited retinoblastoma?
one defective copy inherited | somatic point mutation of the other copy
91
what are some genetic characteristics of sporadic retinoblastoma?
both hits occur in a single cell
92
what are some examples of inherited cancer syndromes?
familial retinoblastoma familial adenomatous polyposis of colon multiple endocrine neoplasia
93
what are some characteristics of familial cancers?
family clustering of cancers but individual presdisposition unclear multifactorial inheritance early age of onset multiple/bilateral tumours
94
what are some examples of familial cancers?
some breast and ovarian cancers