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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
TNM system
-T: 0-4 -N: 0-3 -M: 0-1 ex: T3N1M0
26
Principles of carcinogenesis
-mutations target either oncogenes or tumor suppressor genes -multiple genes involved
27
oncogenes
genes that encode proteins that promote cancer
28
Retinoblastoma
-mutation of single gene -childhood retinal cancer -cells don't stop dividing = tumors -hereditary carriers have mutation in gene RB1 -can be nonhereditary
29
Two-hit hypothesis
-assumes retinoblastoma requires 2 mutations -predicts number of cases of cancer over time in non/hereditary retinoblastoma
30
RBI
-tumor suppressor -2 mutations on both alleles required for retinoblastoma
31
Retinoblastoma carriers
-have one recessive mutation in one RBI allele -one hit
32
Noncarriers of retinoblatoma require what to develop cancer?
-2 mutations on both RBI alleles -2 hits
33
Oncogenes
-altered genes that drive cancer -DOMINANT in a single allele -normal version is "protooncongnee"
34
Oncogene translocation
-makes protein with new function -ex BCR-ABL
35
BCR-ABL protein
-results as chromosomal translocation -produces kinase that drives proliferation in leukemia
36
Oncogene mutation
-makes more active version of protein -ex: k-ras
37
Oncogene duplication
-overexpression of normal protein involved in cell growth
38
Pediatric Cancers
-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
39
Adult cancers
-rarely just a single mutation -tend to be more heterogeneous -patients have different combinations of mutations
40
Risk factors of cancers
-age -environment -genetics -inflammation -viruses
41
Age
-cancers often require multiple mutations -can take 20+ years -accumulation of mutations -decline in immune function
42
Environmental factors
-increased mutation rate -smokers -carcinogens -UV radiation -Xray radiation
43
Carcinogens
-agents that can induce tumors -most react with DNA -mustard gas -nitroso in meat -chemo -benzo[a]pyrene from smoke
44
Genetics
-inherited mutations in tumor suppressor genes -many in DNA repair genes
45
BRCA1/2 mutation
-ds break repair -ovarian cancer -breast cancer
46
XP (xeroderma pigmentosum) mutation
-nucleotide excision repair -skin cancer
47
ATM (ataxia telangiectasia) mutation
-ds break repair -lymphoma -leukemia
48
BLM (bloom's syndrome) mutation
-DNA helicase -various cancers
49
Chronic Inflammation
-results in persistent regenerative proliferation (hyperplasia) -DNA damage by oxygen and nitrogen species from immune cells -unhealed skin wounds can lead to cancer
50
Cancers from inflammation
-skin cancer -hepatocellular carcinoma -gastric cancer -colorectal cancer
51
hepatocellular carcinoma cause
-cirrhosis of liver -inflammation
52
gastric cancer cause
-inflammation -chronic gastritis due to long term infection
53
colorectal cancer cause
-inflammation -chronic ulcerative colitis -villous adenomas (polyps) of the colon
54
Virus mechanisms of causing cancer
-integration into genome -chronic inflammation increases risk of liver cancer -may alter cell pathways to inactivate tumor suppressors or disrupt cell cycle control
55
Oncogenic viruses
-Epstein Barr -Kaposis -HPV -Hep B -Hep C (RNA) -HTLV1 (RNA)
56
human papillomaviruses (HPV)
-cervical cancer -2 viral proteins inactivate tumor suppressors
57
HPV proteins
-E6 and E7 that inactivate tumor suppressors p53 and pRb
58
Hallmarks of cancers
-growth signals -insensitive to anti-growth signals -invasion and metastasis -limitless replication -angiogenesis -evading apoptosis
59
Cell Cycle
-G0/G1: cell duplicates contents -S: replicates DNA -G2: preps and repairs DNA -M: mitosis -cytokinesis
60
Cell cycle clock
-determines when cells move phases -driven by cyclins -R point
61
cyclins
-paired with cyclin-dependent kinases (CDKs) -drive cell cycle clock
62
R point
-restriction point -time point when cells decide whether to enter cell cycle
63
G1 checkpoint
-cell size -nutrients -DNA damage -growth factors
64
S phase checkpoint
-DNA damage -DNA replication
65
G2 phase checkpoint
-cell size -DNA replication
66
Mitosis checkpoint
-chromosome attachment to spindle
67
#1 self-sufficiency in growth signals
-activation of kinase transduction pathways that respond to growth factors -activation of receptor tyrosine kinase
68
Growth factor receptors
-receptor tyrosine kinases (RTKs)
69
Activation of receptor tyrosine kinase
-gain of function mutation in RTK -amplification of RTK
70
Activation of RTK signaling pathways
-cancer mutations common -activate oncogenes -inactivate tumor suppressors
71
RTK activation of oncogenes by:
-RTK kinase -Ras GTPase -B-Raf kinase -PI3K kinase -AKT kinase
72
inactivation of tumor suppressors by:
-PTEN phosphatase -TSC GTPase activator
73
#2 Resistance to growth inhibitory signals
-loss of expression of growth inhibitory proteins (tumor suppressors)
74
Growth inhibitors
-TGF-B -p53 -p16 -RB inhibits E2f transcription factor -effects G1/S transition
75
#3 Evading Apoptosis
-prevents cell death upon DNA damage -tumor suppressors -p53, p21, BAX
76
p53
transcription factors -tumor suppressor
77
p21
CDK inhibitor -cell cycle checkpoint -tumor suppressor
78
BAX
-pro apoptotic regulator -tumor suppressor
79
#4 Limitless replicative potential
-telomere shortening leads to chromosome abnormalities = cell death -tumor cells overexpress telomerase = immortal
80
Hayflick limit
-normal cells can only divide 40-60 times
81
#5: sustained angiogenesis
-triggered by tumor cells -neovascularization -tumor cells produce VEGF to get blood supply -hypoxia signaling pathway
82
HIFa
-transcription factor for hypoxia genes (VEGF)
83
VHL (von-Hippel-Lindau)
-tumor suppressor -E3 ligase for HIFa
84
#6 tissue invasion/Metastasis
-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
Multistep carcinogenesis
-initiation -promotion -progression
86
Initiation step of carcinogenesis
-exposure of cells to carcinogen -irreversible changes in genome -amount of exposure matters
87
Promotion step of carcinogenesis
-unregulated growth of mutated cells -growth factors and chemicals -may occur after long latency periods
88
Progression step of carcinogenesis
-acquisition of malignant characteristics -invasive and metastatic ability
89
Tumor microenvironment
-sometimes phenotype of cancer can normalize when it is removed from tumor environment and placed in normal environment
90
Components of tumor microenvironment
-macrophages, fibroblasts, endothelial cells, immune and inflammatory cells -EC matrix and signaling substances likes cytokines and hormones
91
Systemic manifestations of cancer
-wasting syndrome -fatigue and sleep disorder -anemia -apin
92
wasting syndrome (cancer anoreacia-cahexia syndrome)
-anoreaxia -cachexia (wasting body fat and muscle tissue) -nutrition does not reverse cachexia -cause of morbidity and mortality
93
Fatigue and Sleep disorder
-tiredness, lack of energy not relieved by sleep -poor sleep
94
Anemia
-blood loss, hemolysis, impaired blood production -drugs in treatment may also decrease RBC production
95
Pain of cancer
-common in late stage -pain management necessary even when incurable
96
Molecular diagnosis
-identify molecular causes of cancer -FISH, IHC, DNA sequencing -Targeted cell therapy
97
Fluorescence in situ hybridization (FISH)
-estimate gene copy number
98
Immunochemistry (IHC)
-assess protein expression and tissue distribution
99
Targeted cancer therapy
-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
Cancer biomarkers
-proteins overexpressed in cancer tissues -not good for diagnosis bc high false positive rate -useful in monitoring treatment response and recurrence
101
Common biomarkers
-PSA - prostate cancer -AFP - liver and testis cancer -CA 125 - ovarian cancer

PATHO (31 decks)

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