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x 6102 Final > cancer > Flashcards

cancer Flashcards

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
Q

Kaposi sarcoma

A

occurs in a significantly more virulent form in individuals who are immunocompromised

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26
Q

Hep B + Hep C + cancer

A

together = liver cancer

Hep B = vaccine, none for C

27
Q

chronic inflammation + cancer

A

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
Q

metastasis process

A

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
Q

mechanisms of metastasis x2

A

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
Q

cancer staging criteria x3

A

size of the tumor (T)

degree to which it has locally invaded (N)odes

extent to which it has spread: (M)etastasis

31
Q

cancer stages x4

A

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
Q

pain + cancer

A

little to no pain in early stages of malignancy; significant pain in late stages

33
Q

most frequently reported symptom of cancer and cancer treatment

A

fatigue

34
Q

induction chemotherapy

A

shrinks or causes tumors to disappear (may improve symptoms without providing a cure)

35
Q

adjuvant chemotherapy

A

given after surgical excision of a cancer to eliminate micrometastases

36
Q

neoadjuvant chemotherapy

A

given before localized (surgical or radiation) treatment of cancer – may shrink a cancer so that surgery may spare normal tissue

37
Q

radiation therapy

A

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
Q

ionizing radiation

A

damages DNA in cancer cells – rapidly renewing cells are more radiosensitive

39
Q

brachytherapy

A

capsules (I-125) of radiation that are temporarily placed into body cavities (Ex. cervical, prostate, head/neck cancers)

40
Q

epigenetic

A

non-genetic influences on gene expression

41
Q

epigenetic alterations for cancer x3

A

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
Q

developmental plasticity

A

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
Q

multigenerational phenotypes

A

Exposure: Direct
Definition: Simultaneous exposure of multiple generations to an environmental factor

44
Q

transgenerational phenotypes

A

Exposure: Initial germline exposure (ancestral)
Definition: Transgenerational phenotype is transmitted to future generations through germline inheritance

45
Q

somatic cell inheritance in cancer

A

Biologic Response: Critical for adult-onset disease in exposed individual; not transmitted to future generations as transgenerational effect

46
Q

germ cell inheritance in cancer

A

Biologic Response: Allow transmission between generations; promote transgenerational phenotype

47
Q

dietary sources of methylation

A

folate, methionine, betaine, serine, choline, B vitamins

48
Q

choline deficiency in pregnancy linked to

A

hypermethylation

49
Q

microRNAs (miRs)

A

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
Q

xenobiotics & enzymes x2

A

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
Q

Glutathione-S-transferases (GSTs)

A

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
Q

Warburg effect

A

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
Q

hyperinsulinemia + cancer

A

increased risk: colon, endometrium, possibly kidney and pancreas

54
Q

insulin-like growth factor 1 + cancer

A

promoted by insulin - increased risk: prostate cancer

55
Q

reverse Warburg effect

A

some tumors use oxidative stress to extract recycled nutrients from cancer-associated fibroblasts in stromal tissue

56
Q

Human herpes virus type 8 + cancer

A

Kaposi sarcoma

57
Q

Human T-cell lymphotropic virus type 1

A

leukemia and lymphoma

58
Q

ionizing radiation + cancer

A

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
Q

ultraviolet radiation + cancer

A
  • 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
Q

electromagnetic radiation + cancer

A

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
Q

cancer cells grow in what kind of environments?

A

hypoxic and acidic

62
Q

cancer cell metabolism

A

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
Q

clonal proliferation/expansion

A

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
Q

alpha fetoprotein (AFP)

A

tumor cell marker produced by liver and germ cell tumors

x 6102 Final (3 decks)

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