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Patho 2 > neoplasias > Flashcards

neoplasias Flashcards

1
Q

basic components of all tumors

A
  • neoplastic cells (parenchyma)

- supporting stroma

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2
Q

supporting stroma of tumor cells

A
  • CT
  • blood vessels
  • adaptive/ innate immunity cells
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3
Q

tumor microenviornment

A
  • hematopoietic cells
  • cells with mesenchymal origin
  • non-cellular components
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4
Q

heatompoietic cells in tumor microenviornment

A
  • cells arise in bone marrow

- consist of T and B cells, NK cells, macrophages, and neutrophils

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5
Q

cells with mesenchymal origin in tumor microenviornment

A
  • fibroblasts
  • myofibroblasts
  • mesenchymal stem cells
  • adipocytes
  • endothelial cells
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6
Q

non-cellular components of microenviornment

A
  • ECM
  • proteins
  • glycoproteins
  • proteoglycans
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7
Q

significance of tumor microenviornment

A
  • protects cancer cells

- important influence on malignancy outcome and treatment responses

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8
Q

differentiation

A
  • how closely tumor cells histologically and functionally resemble their normal cell counterpart
  • lack of differentiation= anaplasia
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9
Q

metaplasia

A

replacement of one cell type with another cell type

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10
Q

dysplasia

A

loss of ceulluar uniformity and architectural organization

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11
Q

carcinoma in situ

A

marked dysplastic changes involving the entire thickness of epithelium

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12
Q

invasive carcinoma

A

basement membrane is not intact so abnormal cells can escape and metastasize

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13
Q

local invasion of neoplasms

A
  • most benign tumors don’t invade locally

- malignant tumors cause local invasion

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14
Q

metastasis of neoplasms

A
  • single most important features distinguishing benign from malignant
  • can metastasize due to dislodged cells
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15
Q

pathways of tumor spread

A
  • seeding of body cavities and surfaces
  • lymphatic spread
  • hematogenous spread
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16
Q

what tumors commonly spread hematogenously

A
  • sarcoma

- some carcinomas

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17
Q

what tumors commonly spread in lymphatics

A

carcinomas

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18
Q

tropism

A
  • tumors tendency to metastasize to specific organs

- indicates ability to adopt and colonize

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19
Q

mechanisms of tumors tropisms

A
  • adhesion molecules with preferential expression of ligands in specific organs
  • chemokine receptors in particular organs
  • microenviornment of organ might not be suitable
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20
Q

where is the primary site of metastasize for colon cancer and why?

A
  • metastasizes to liver

- due to portal vein drainage from colon directly to liver

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21
Q

environmental factors in cancer

A
  • infectious agent
  • smoking
  • alcohol consumption
  • diet
  • obesity
  • reproductive history
  • environmental carcinogens
  • age
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22
Q

acquired predisposing factors in cancer

A
  • chronic inflammation
  • precursor lesions
  • immunodeficiency states
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23
Q

hallmarks of cancer

A
  • sustaining proliferative signaling
  • avoiding immune destruction
  • evading growth suppressors
  • enabling replicative immortality
  • tumor promoting inflammation
  • activating invasion and metastasis
  • genomic instability
  • inducing angiogenesis
  • resisting cell death
  • deregulating cellular energetics
24
Q

normal cell proliferation

A
  • growth factor binding to cell surface receptor
  • activation of signal transduction proteins
  • initiating DNA transcription
25
Q

oncogenes

A

promote autonomous/ abnormal cell growth

26
Q

tyrosine kinase

A
  • family of receptors that phosphorylate target protein using ATP
  • causes cellular growth, apoptosis, and cell migration
27
Q

tyrosine kinase mutations

A
  • cause inappropriate activation of signaling pathways

- leads to neoplastic growth

28
Q

MYC oncogene

A
  • most commonly involved in human tumors

- causes over-expression of growth factor receptors

29
Q

main cause of MYC oncogene mutation

A
  • causes burkitt lymphoma

- is an aggressive b cell lymphoma

30
Q

tumor suppressor genes

A
  • slow cell divisions
  • repair DNA mistakes
  • activate apoptosis
  • cancer arises due to inactivation
  • i.e. RB and P53
31
Q

loss of heterozygosity

A
  • mutation of both alleles of tumor suppressor genes needed for carcinogenesis
32
Q

RB

A
  • tumor suppressor gene
  • causes persistent cell cycling
  • mutation causes pathogenesis of childhood tumor retinoblastoma
33
Q

P53 gene

A
  • normally prevents growth of genetically defective cells
  • senses DNA damage
  • if DNA can be repaired, cell undergoes S phase
  • if DNA cant be repaired, induces apoptosis
  • mutated in more than 50% of all cancers
34
Q

cell mediated immunity

A
  • cytotoxic T cells (CD8+)
  • NK cells
  • macrophages
35
Q

role of telomeres

A
  • protect end of chromosomes
  • when shorten, cell undergoes senescence and/or apoptosis
  • telomerase builds telomeres
36
Q

role of telomerase in tumor cells

A
  • is active in tumor cells

- prevents apoptosis

37
Q

metastatic cascade

A
  • invasion of ECM

- vascular dissemination and homing of tumor cells

38
Q

invasion of ECM

A
  • detachment and loosening of intracellular junctions
  • ECM degraded by proteases
  • migration of tumor cells
39
Q

theories about how metastasis occurs

A
  • clonal evolution model -> rare variant clones
  • metastasis signature
  • metastatic variants exist in a tumor with metastatic signature
  • role of tumor stroma
40
Q

genomic instability

A
  • DNA repair pathways act indirectly by correcting spontaneous DNA errors
  • inherited mutations increase risk of carcinogenesis
41
Q

mutations that cause breast cancer

A
  • BRCA1

- BRCA2

42
Q

mutations that cause ovarian, prostate, pancreas and stomach cancers

A

mutations in BRCA2

43
Q

angiogenesis

A
  • creation of new blood vessels
  • stimulates tumor growth through endothelial cell production of GF
  • influences metastatic potential
44
Q

result of hypoxia in tumorgenesis

A
  • causes upregulation of VEGF

- leads to angiogenesis

45
Q

proapoptotic proteins

A
  • considered primed for apoptosis

- occurs in normal cells

46
Q

antiapoptotic proteins

A
  • considered unprimed for apoptosis

- occurs in tumor cells

47
Q

do cancer cells utilize aerobic or anaerobic metabolism?

A
  • anaerobic respiration

- able to complete anaerobic respiration 100 times faster than aerobic respiration

48
Q

steps involved in chemical carcinogenesis

A
  • initiation

- promotion

49
Q

initiation of chemical carcinogenesis

A
  • induction of irreversible changes/ mutations in the genome
  • direct acting agents- no metabolic conversion
  • indirect acing agents- metabolic conversion
50
Q

promotion of chemical carcinogenesis

A
  • can induce tumors in previously initiated cells by stim cell proliferation
  • short lived, reversible and nontumorigenic
51
Q

UVA radiation

A
  • creates ROS

- gets through all clothes and sunscreen

52
Q

UVB radiation

A
  • most prominent UV damage
  • causes t dimers
  • t dimers distort DNA
53
Q

radiation carcinogenesis

A
  • damage the nucleotides or DNA sugar moieties
  • strand breaks in DNA
  • indirect DNA damage by increasing ROS
54
Q

benign and malignant tumors can cause problems due to:

A
  • location
  • functional activity like hormones produced
  • bleeding and infection
  • sx from tumor rupture or infection
  • cachexia
55
Q

cachexia

A
  • profound muscle loss
  • possible fat loss
  • staged as precachexia, cachexia, refractor cachexia
56
Q

pathophys of cachexia

A
  • cytokines, inflammation and hypermetabolic state
  • lipolysis and lipid mobilization
  • genomics
  • cancer treatments
  • reduced dietary intake or absorption

Patho 2 (15 decks)

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