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PATHO > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

Neoplasia

A

-dysregulated cell proliferation
-abnormal growth of cells/tissues

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2
Q

Cancer tumors

A

-less differentiated
-invasive
-metastatic
-larger
-rapidly growing

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3
Q

Nomenclature of benign tumor

A

-add -oma to the parenchymal tissue type

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4
Q

carcinoma

A

-canver of epithelial tissue origin

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5
Q

sarcoma

A

cancer of connective, muscle, endothelial tissues

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6
Q

leukemia

A

-cancer of blood cells

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7
Q

blastoma

A

-cancer of neural tissues

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8
Q

Characteristics of cancer cells

A

-anaplasia
-genetic instability
-growth factor independence
-loss of cell-density dependent inhibition
-anchorage independence
-faulty cell-cell communication
-unlimited life span
-antigen expression
-abnormal production of protiens/hormones
-cytoskeletal changes

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9
Q

anaplasisa

A

-loss of cell differentiation
-resemblance to undifferentiated cells

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10
Q

Genetic instability of cancer cells

A

-aneuploidy (loss or gain chromosomes)
-intrachromosomal instability (insertions, deletions, amplifications)
-microsatellite instability (short repetitive sequences of DNA)
-point mutations

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11
Q

cell-density-dependent inhibition

A

-contact inhibition
-growth regards adjacent tissue

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12
Q

anchorage independence

A

-cells remain viable without normal attachments to other cells and matrix
-needed for metastasis

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13
Q

Faulty cell-cell communication of cancer cells

A

-formation of intercellular connections and responsiveness to membrane signals are interfered

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14
Q

Cancer cells can divide how many times?

A

unlimited

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15
Q

Tumor antigens

A

-cancer cells that express cell surface antigens that are recognized as foreign
-ex: fetal proteins that are not expressed by comparable cells in adult
-used as cancer biomarkers

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16
Q

Cancer cell protein/hormone production

A

-secrete enzymes that enable invasion and spread
-may synthesize own growth hormones (like estrogen in breast cancer)
-secrete procoagulant substances that affect clotting

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17
Q

Cytoskeletal changes of cancer cells

A

-change in intermdiate and actin filaments, and microtubules
-abnormal morphology
-facilitate invasion and metastasis

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18
Q

Grading of cancer

A

-determined by tumor cell morphology
-smaple from biopsy/pap smear
-based on differentiation state and number of mitoses of the tumor

-Grades X, I, II, III, IV

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19
Q

Grade X

A

-grade cannot be assessed

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20
Q

Grade I

A

-well differentiated
-low grade

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21
Q

Grade II

A

-moderately differentiated
-intermediate grade

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22
Q

Grade III

A

-poorly differentiated
-high grade

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23
Q

Grade IV

A

-undifferentiated
-high grade

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24
Q

Staging based on:

A

-size of primary lesion (T)
-extent of spread to lymph nodes (N)
-presence/absence of metastases (M)

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25
Q

TNM system

A

-T: 0-4
-N: 0-3
-M: 0-1

ex: T3N1M0

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26
Q

Principles of carcinogenesis

A

-mutations target either oncogenes or tumor suppressor genes
-multiple genes involved

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27
Q

oncogenes

A

genes that encode proteins that promote cancer

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28
Q

Retinoblastoma

A

-mutation of single gene
-childhood retinal cancer
-cells don’t stop dividing = tumors
-hereditary carriers have mutation in gene RB1
-can be nonhereditary

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29
Q

Two-hit hypothesis

A

-assumes retinoblastoma requires 2 mutations
-predicts number of cases of cancer over time in non/hereditary retinoblastoma

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30
Q

RBI

A

-tumor suppressor
-2 mutations on both alleles required for retinoblastoma

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31
Q

Retinoblastoma carriers

A

-have one recessive mutation in one RBI allele
-one hit

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32
Q

Noncarriers of retinoblatoma require what to develop cancer?

A

-2 mutations on both RBI alleles
-2 hits

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33
Q

Oncogenes

A

-altered genes that drive cancer
-DOMINANT in a single allele
-normal version is “protooncongnee”

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34
Q

Oncogene translocation

A

-makes protein with new function
-ex BCR-ABL

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35
Q

BCR-ABL protein

A

-results as chromosomal translocation
-produces kinase that drives proliferation in leukemia

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36
Q

Oncogene mutation

A

-makes more active version of protein
-ex: k-ras

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37
Q

Oncogene duplication

A

-overexpression of normal protein involved in cell growth

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38
Q

Pediatric Cancers

A

-tend to be single genetic events important at developmental times
-if carriers of RBI mutation dont develop cancer as kids they wont get it at all but will pass it on

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39
Q

Adult cancers

A

-rarely just a single mutation
-tend to be more heterogeneous
-patients have different combinations of mutations

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40
Q

Risk factors of cancers

A

-age
-environment
-genetics
-inflammation
-viruses

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41
Q

Age

A

-cancers often require multiple mutations
-can take 20+ years
-accumulation of mutations
-decline in immune function

42
Q

Environmental factors

A

-increased mutation rate
-smokers
-carcinogens
-UV radiation
-Xray radiation

43
Q

Carcinogens

A

-agents that can induce tumors
-most react with DNA
-mustard gas
-nitroso in meat
-chemo
-benzo[a]pyrene from smoke

44
Q

Genetics

A

-inherited mutations in tumor suppressor genes
-many in DNA repair genes

45
Q

BRCA1/2 mutation

A

-ds break repair
-ovarian cancer
-breast cancer

46
Q

XP (xeroderma pigmentosum) mutation

A

-nucleotide excision repair
-skin cancer

47
Q

ATM (ataxia telangiectasia) mutation

A

-ds break repair
-lymphoma
-leukemia

48
Q

BLM (bloom’s syndrome) mutation

A

-DNA helicase
-various cancers

49
Q

Chronic Inflammation

A

-results in persistent regenerative proliferation (hyperplasia)
-DNA damage by oxygen and nitrogen species from immune cells
-unhealed skin wounds can lead to cancer

50
Q

Cancers from inflammation

A

-skin cancer
-hepatocellular carcinoma
-gastric cancer
-colorectal cancer

51
Q

hepatocellular carcinoma cause

A

-cirrhosis of liver
-inflammation

52
Q

gastric cancer cause

A

-inflammation
-chronic gastritis due to long term infection

53
Q

colorectal cancer cause

A

-inflammation
-chronic ulcerative colitis
-villous adenomas (polyps) of the colon

54
Q

Virus mechanisms of causing cancer

A

-integration into genome
-chronic inflammation increases risk of liver cancer
-may alter cell pathways to inactivate tumor suppressors or disrupt cell cycle control

55
Q

Oncogenic viruses

A

-Epstein Barr
-Kaposis
-HPV
-Hep B
-Hep C (RNA)
-HTLV1 (RNA)

56
Q

human papillomaviruses (HPV)

A

-cervical cancer
-2 viral proteins inactivate tumor suppressors

57
Q

HPV proteins

A

-E6 and E7 that inactivate tumor suppressors p53 and pRb

58
Q

Hallmarks of cancers

A

-growth signals
-insensitive to anti-growth signals
-invasion and metastasis
-limitless replication
-angiogenesis
-evading apoptosis

59
Q

Cell Cycle

A

-G0/G1: cell duplicates contents
-S: replicates DNA
-G2: preps and repairs DNA
-M: mitosis
-cytokinesis

60
Q

Cell cycle clock

A

-determines when cells move phases
-driven by cyclins
-R point

61
Q

cyclins

A

-paired with cyclin-dependent kinases (CDKs)
-drive cell cycle clock

62
Q

R point

A

-restriction point
-time point when cells decide whether to enter cell cycle

63
Q

G1 checkpoint

A

-cell size
-nutrients
-DNA damage
-growth factors

64
Q

S phase checkpoint

A

-DNA damage
-DNA replication

65
Q

G2 phase checkpoint

A

-cell size
-DNA replication

66
Q

Mitosis checkpoint

A

-chromosome attachment to spindle

67
Q

1 self-sufficiency in growth signals

A

-activation of kinase transduction pathways that respond to growth factors
-activation of receptor tyrosine kinase

68
Q

Growth factor receptors

A

-receptor tyrosine kinases (RTKs)

69
Q

Activation of receptor tyrosine kinase

A

-gain of function mutation in RTK
-amplification of RTK

70
Q

Activation of RTK signaling pathways

A

-cancer mutations common
-activate oncogenes
-inactivate tumor suppressors

71
Q

RTK activation of oncogenes by:

A

-RTK kinase
-Ras GTPase
-B-Raf kinase
-PI3K kinase
-AKT kinase

72
Q

inactivation of tumor suppressors by:

A

-PTEN phosphatase
-TSC GTPase activator

73
Q

2 Resistance to growth inhibitory signals

A

-loss of expression of growth inhibitory proteins (tumor suppressors)

74
Q

Growth inhibitors

A

-TGF-B
-p53
-p16
-RB inhibits E2f transcription factor

-effects G1/S transition

75
Q

3 Evading Apoptosis

A

-prevents cell death upon DNA damage
-tumor suppressors
-p53, p21, BAX

76
Q

p53

A

transcription factors
-tumor suppressor

77
Q

p21

A

CDK inhibitor
-cell cycle checkpoint
-tumor suppressor

78
Q

BAX

A

-pro apoptotic regulator
-tumor suppressor

79
Q

4 Limitless replicative potential

A

-telomere shortening leads to chromosome abnormalities = cell death
-tumor cells overexpress telomerase = immortal

80
Q

Hayflick limit

A

-normal cells can only divide 40-60 times

81
Q

5: sustained angiogenesis

A

-triggered by tumor cells
-neovascularization
-tumor cells produce VEGF to get blood supply
-hypoxia signaling pathway

82
Q

HIFa

A

-transcription factor for hypoxia genes (VEGF)

83
Q

VHL (von-Hippel-Lindau)

A

-tumor suppressor
-E3 ligase for HIFa

84
Q

6 tissue invasion/Metastasis

A

-adhesion and invasion of basement membrane
-pass thru EC matrix
-intravasation (enter)
-travel by vasculature
-adhesion to membrane at destination
-extravasation (exit)
-metastatic deposit
-angiogenesis and growth

85
Q

Multistep carcinogenesis

A

-initiation
-promotion
-progression

86
Q

Initiation step of carcinogenesis

A

-exposure of cells to carcinogen
-irreversible changes in genome
-amount of exposure matters

87
Q

Promotion step of carcinogenesis

A

-unregulated growth of mutated cells
-growth factors and chemicals
-may occur after long latency periods

88
Q

Progression step of carcinogenesis

A

-acquisition of malignant characteristics
-invasive and metastatic ability

89
Q

Tumor microenvironment

A

-sometimes phenotype of cancer can normalize when it is removed from tumor environment and placed in normal environment

90
Q

Components of tumor microenvironment

A

-macrophages, fibroblasts, endothelial cells, immune and inflammatory cells
-EC matrix and signaling substances likes cytokines and hormones

91
Q

Systemic manifestations of cancer

A

-wasting syndrome
-fatigue and sleep disorder
-anemia
-apin

92
Q

wasting syndrome (cancer anoreacia-cahexia syndrome)

A

-anoreaxia
-cachexia (wasting body fat and muscle tissue)
-nutrition does not reverse cachexia
-cause of morbidity and mortality

93
Q

Fatigue and Sleep disorder

A

-tiredness, lack of energy not relieved by sleep
-poor sleep

94
Q

Anemia

A

-blood loss, hemolysis, impaired blood production
-drugs in treatment may also decrease RBC production

95
Q

Pain of cancer

A

-common in late stage
-pain management necessary even when incurable

96
Q

Molecular diagnosis

A

-identify molecular causes of cancer
-FISH, IHC, DNA sequencing
-Targeted cell therapy

97
Q

Fluorescence in situ hybridization (FISH)

A

-estimate gene copy number

98
Q

Immunochemistry (IHC)

A

-assess protein expression and tissue distribution

99
Q

Targeted cancer therapy

A

-BCR-ABL translocation - inhibtiors
-estrogen receptor in breast cancer - antihormone therapy
-HER2 overexpression - anti HER2 antibodies
-EGFR mutations - EGFR inhibitors
-Ras mutations - targeted inhibitors

100
Q

Cancer biomarkers

A

-proteins overexpressed in cancer tissues
-not good for diagnosis bc high false positive rate
-useful in monitoring treatment response and recurrence

101
Q

Common biomarkers

A

-PSA - prostate cancer
-AFP - liver and testis cancer
-CA 125 - ovarian cancer

PATHO (31 decks)

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