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x 6102 Final > cancer > Flashcards

cancer Flashcards

(64 cards)

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1
Q

benign tumors general characteristics

A

Grow slowly
Have a well-defined capsule
Are well differentiated (look like the tissue from which they arose)
Low mitotic index (dividing cells are rare)
Do not metastasize
Suffix “-oma”

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2
Q

malignant tumors general characteristics

A

Grow rapidly
Are not encapsulated
Are poorly differentiated (may not be able to determine tissue of origin)
High mitotic index (many dividing cells)
Can spread distantly, often through blood vessels and lymphatics

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3
Q

carcinoma

A

cancers arising from epithelial tissue

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4
Q

adenocarcinoma

A

cancers arising from ductal or glandular structures

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5
Q

sarcoma

A

cancers arising from connective tissue (ex. cancer of skeletal muscle are called rhabdomyosarcomas)

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6
Q

lymphoma

A

cancers of lymphatic tissue

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7
Q

leukemia

A

cancers of blood forming cells

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8
Q

carcinoma in situ

A

early stage cancers

preinvasive epithelial tumors of glandular or squamous cell

  • localized to epithelium
  • haven’t penetrated local basement membrane or invaded surrounding stroma (functional /connective tissue)

often found: cervix, skin, oral cavity, esophagus, bronchus, stomach, endometrium, breast, large bowel

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9
Q

tumor markers

A

substances produced by both benign & malignant cells

  • present in/on tumor cells or are found in blood, spinal fluid, or urine
  • substrates including hormones, enzymes, genes, antigens, antibodies
  • screen/identify individuals at high risk for cancer
  • help diagnose specific types of tumors
  • used to follow clinical course of cancer
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10
Q

paraneoplastic syndrome

A

symptom complexes triggered by a cancer; not caused by direct local effects of tumor mass

caused by biologic substances released from the tumor (e.g., hormones/tumor markers) or by immune response triggered by the tumor
- ex: pheochromocytoma

may be the earliest symptom of a cancer

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11
Q

anaplasia

A

the absence of differentiation; characterized as a loss of organization and marked increase in nuclear size with evidence of ongoing proliferation

cancer cells don’t acquire specialized function

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12
Q

most common genetic mutation in cancers

A

point mutation (alteration of one or a few nucleotide base pairs)

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13
Q

chromosomal translocations activate oncogenes 2x ways

A
  • excess production of a proliferative factor

- production of novel proteins with growth promoting properties

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14
Q

point mutation

A

alteration of one or few nucleotide base pairs → converts from proto-oncogene to unregulated oncogene

= accelerates cell proliferation

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15
Q

gene amplication

A

over duplication of a gene that increases expression of oncogene

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16
Q

tumor suppressor genes

A

encode proteins that in their normal state halt proliferation

takes 2 hits to inactivate 2 alleles of tumor-suppressor gene bc alleles act in recessive manner at cellular level

inherited mutations are almost always found in these d/t loss of heterozygosity or epigenetic silencing

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17
Q

epigenetic silencing

A

normal phenomenon where whole regions of chromosomes are shut off so the pattern of gene expression is different than that seen in other cells with the same genes

  • can silence tumor suppressing genes
  • contribute to inappropriate expression of oncogenes
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18
Q

caretaker genes

A

responsible for maintenance of genomic integrity, encode proteins involved in repairing damaged DNA during:

  • DNA replication
  • mutations d/t ultraviolet or ionizing radiation
  • mutations caused by chemicals & drugs
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19
Q

inherited mutations are almost always found where & how

A

in tumor-suppressor genes by loss of heterozygosity or epigenetic silencing

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20
Q

mutant protein RAS

A

stimulates cell growth even when growth factors missing

up to 1/3 of all cancers have activating mutation in in gene for intracellular signaling protein RAS

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21
Q

angiogenesis + factors x3

A

aka neovascularization – ability to secrete factors that stimulate new blood vessel growth

Vascular endothelial growth factor (VEGF)
Platelet derived growth factor (PDGF)
Basic fibroblast growth factor (bFGF)

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22
Q

6 pathways/hallmarks of cancer

A
  • sustained angiogenesis
  • tissue invasion and metastasis
  • evading apoptosis
  • self-sufficiency in growth signal
  • insensitivity to anti-growth signals
  • limitless replicative potential
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23
Q

HPV + cancer

A

cervical cancer

vaccines protect against HPV 16 & 18 (causes 70% of cervical cancers) + HPV 6 & 11 (causes 90% of genital warts)

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24
Q

Epstein Barr + cancer

A

development of B-cell lymphomas (Hodgkin/non-Hodgkin), cancers of nasopharynx

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25
Kaposi sarcoma
occurs in a significantly more virulent form in individuals who are immunocompromised
26
Hep B + Hep C + cancer
together = liver cancer Hep B = vaccine, none for C
27
chronic inflammation + cancer
predisposes to cancer because it stimulates a wound-healing response that includes proliferation and new blood vessel growth more susceptible to this: GI tract, prostate, thyroid gland, pancreas, bladder, pleura, skin
28
metastasis process
invasion or local spread is a prerequisite - recruitment of macrophages - cell-cell adhesion changes: slippery and mobile - increased motility of individual tumor cells - ability to invade local blood/lymphatic vessels - must be able to survive in the circulation (bloodstream) and proliferate
29
mechanisms of metastasis x2
spread via vascular and lymphatic pathways via neovascularization → regional lymph nodes selectivity of different cancers for different sites (poorly understood) - ex: breast cancer to bone but not kidney, spleen
30
cancer staging criteria x3
size of the tumor (T) degree to which it has locally invaded (N)odes extent to which it has spread: (M)etastasis
31
cancer stages x4
Stage 1 – confined to its organ or origin Stage 2 – locally invasive Stage 3 – has advanced to regional structures Stage 4 – has spread to distant sites
32
pain + cancer
little to no pain in early stages of malignancy; significant pain in late stages
33
most frequently reported symptom of cancer and cancer treatment
fatigue
34
induction chemotherapy
shrinks or causes tumors to disappear (may improve symptoms without providing a cure)
35
adjuvant chemotherapy
given after surgical excision of a cancer to eliminate micrometastases
36
neoadjuvant chemotherapy
given before localized (surgical or radiation) treatment of cancer – may shrink a cancer so that surgery may spare normal tissue
37
radiation therapy
kills cancer cells while minimizing damage to normal structures; best for treating localized disease in areas that are hard to reach surgically (Ex. brain, pelvis)
38
ionizing radiation
damages DNA in cancer cells – rapidly renewing cells are more radiosensitive
39
brachytherapy
capsules (I-125) of radiation that are temporarily placed into body cavities (Ex. cervical, prostate, head/neck cancers)
40
epigenetic
non-genetic influences on gene expression
41
epigenetic alterations for cancer x3
heritable changes in gene and non–coding RNA expression that do not involve changes in DNA sequence - DNA methylation (addition of methyl group) - microRNA silencing = gene silencing (muted) - histone modification = loss of function which facilitates tumor initiation/progression
42
developmental plasticity
degree to which development is contingent on its environment - requires stable gene expression partly modulated by epigenetic processes (DNA methylation, histone modification) - sensitivity to environmental-lifestyle factors influences the mature phenotype; is dependent of interactions genome/epigenome.
43
multigenerational phenotypes
Exposure: Direct Definition: Simultaneous exposure of multiple generations to an environmental factor
44
transgenerational phenotypes
Exposure: Initial germline exposure (ancestral) Definition: Transgenerational phenotype is transmitted to future generations through germline inheritance
45
somatic cell inheritance in cancer
Biologic Response: Critical for adult-onset disease in exposed individual; not transmitted to future generations as transgenerational effect
46
germ cell inheritance in cancer
Biologic Response: Allow transmission between generations; promote transgenerational phenotype
47
dietary sources of methylation
folate, methionine, betaine, serine, choline, B vitamins
48
choline deficiency in pregnancy linked to
hypermethylation
49
microRNAs (miRs)
human genome encodes more than 1000 - regulate diverse signaling pathways - decrease the stability/expression of other genes by pairing with mRNA in process that involves RNA-induced silencing complex (RISC) - single miR can have multiple mRNA targets - oncomirs: stimulate cancer development/ progression
50
xenobiotics & enzymes x2
toxic, mutagenic, carcinogenic chemicals in food activated: phase I enzymes - Cyp450 family (primary) defense mechanisms: phase II detoxification enzymes - compound clearance through portal circulation & antioxidant system - expression induced by isothiocyanates (cruciferous vegetables)
51
Glutathione-S-transferases (GSTs)
enzyme housekeepers that metabolize environmental carcinogens & reactive oxygen species (ROS) if lacking = higher risk for cancer d/t ↓ ability to dispose of activated carcinogens
52
Warburg effect
tumors consume large quantities of glucose (aerobic glycolysis NOT ox phos) → make cellular-building blocks = rapid proliferation (there are some tumors that use ox phos)
53
hyperinsulinemia + cancer
increased risk: colon, endometrium, possibly kidney and pancreas
54
insulin-like growth factor 1 + cancer
promoted by insulin - increased risk: prostate cancer
55
reverse Warburg effect
some tumors use oxidative stress to extract recycled nutrients from cancer-associated fibroblasts in stromal tissue
56
Human herpes virus type 8 + cancer
Kaposi sarcoma
57
Human T-cell lymphotropic virus type 1
leukemia and lymphoma
58
ionizing radiation + cancer
associated with: acute leukemias, ↑ frequencies: thyroid & breast carcinomas, lung, stomach, colon, esophageal, urinary tract cancers, multiple myeloma random energy deposition into cell tissue = - oncogene activation - tumor-suppressor genes deactivation - chromosomal aberrations/DNA damage - genomic instability - bystander effects
59
ultraviolet radiation + cancer
- squamous cell carcinoma (TP53 gene mutation) - basal cell carcinoma (patched gene mutation) - melanoma (p16 gene mutation) principal source: sunlight - ultraviolet A (UVA) & ultraviolet B (UVB) promotes inflammation & ROS
60
electromagnetic radiation + cancer
type of non-ionizing, low-frequency radiation = induced electromagnetic field with associated currents inside tissue microwaves, radar, cell phones, mobile telephone base stations, appliances, power frequency radiation associated with electricity and radio waves, fluorescent lights, computers, other electric equipment
61
cancer cells grow in what kind of environments?
hypoxic and acidic
62
cancer cell metabolism
even in the presence of O2, cancer cells perform glycolysis (aerobic glycolysis) this allows lactate and its metabolites to be used for efficient production of lipids and other molecular building blocks needed for rapid cell growth
63
clonal proliferation/expansion
mutant cell may have selective advantage neighbors progeny accumulate faster than those of nonmutant neighbors. tumor development is a form of Darwinian evolution – cells with a genetic change conferring survival advantage out-compete neighbors
64
alpha fetoprotein (AFP)
tumor cell marker produced by liver and germ cell tumors

x 6102 Final (3 decks)

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