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Flashcards in tumour pathology Deck (94):
1

what is a tumour (neoplasm)?

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

2

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

it will continue

3

is tumour growth irreversible?

true

4

what two types of tumour are there?

benign
malignant

5

what separates malignant (cancer) tumours from benign ones?

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

6

what are the 3 most common cancers for males?

prostate
lung
colon

7

what are the 3 most common cancers for females?

breast
lung
colon

8

what are the 3 most common overall cancers?

breast
lung
colon

9

how are tumours classified?

based on tissue of origin
benign vs malignant

10

what are the names for benign and malignant glandular tumours?

benign: adenoma
malignant: adenocarcinoma

11

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

benign: squamous papilloma
malignant: squamous carcinoma

12

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

benign: osteoma
malignant: osteosarcoma

13

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

benign: lipoma
malignant: lipo-sarcoma

14

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

benign: fibroma
malignant: fibro-sarcoma

15

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

leukaemia

16

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

lymphoma

17

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

CNS: astrocytoma
PNS: schwannoma

18

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

ovarian usually benign, testicular usually malignant

19

what are the features of benign tumours?

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

20

what are the features of malignant tumours?

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

21

what are some properties of cancer cells?

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

22

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

loss of tumour suppressor genes
increased function of oncogenes

23

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

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

24

what are some biomarkers indicative of cancer cells?

onco-fetal proteins
oncogene products
growth factors and receptors

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