neoplasias Flashcards
1
Q
basic components of all tumors
A
- neoplastic cells (parenchyma)
- supporting stroma
2
Q
supporting stroma of tumor cells
A
- CT
- blood vessels
- adaptive/ innate immunity cells
3
Q
tumor microenviornment
A
- hematopoietic cells
- cells with mesenchymal origin
- non-cellular components
4
Q
heatompoietic cells in tumor microenviornment
A
- cells arise in bone marrow
- consist of T and B cells, NK cells, macrophages, and neutrophils
5
Q
cells with mesenchymal origin in tumor microenviornment
A
- fibroblasts
- myofibroblasts
- mesenchymal stem cells
- adipocytes
- endothelial cells
6
Q
non-cellular components of microenviornment
A
- ECM
- proteins
- glycoproteins
- proteoglycans
7
Q
significance of tumor microenviornment
A
- protects cancer cells
- important influence on malignancy outcome and treatment responses
8
Q
differentiation
A
- how closely tumor cells histologically and functionally resemble their normal cell counterpart
- lack of differentiation= anaplasia
9
Q
metaplasia
A
replacement of one cell type with another cell type
10
Q
dysplasia
A
loss of ceulluar uniformity and architectural organization
11
Q
carcinoma in situ
A
marked dysplastic changes involving the entire thickness of epithelium
12
Q
invasive carcinoma
A
basement membrane is not intact so abnormal cells can escape and metastasize
13
Q
local invasion of neoplasms
A
- most benign tumors don’t invade locally
- malignant tumors cause local invasion
14
Q
metastasis of neoplasms
A
- single most important features distinguishing benign from malignant
- can metastasize due to dislodged cells
15
Q
pathways of tumor spread
A
- seeding of body cavities and surfaces
- lymphatic spread
- hematogenous spread
16
Q
what tumors commonly spread hematogenously
A
- sarcoma
- some carcinomas
17
Q
what tumors commonly spread in lymphatics
A
carcinomas
18
Q
tropism
A
- tumors tendency to metastasize to specific organs
- indicates ability to adopt and colonize
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
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
21
Q
environmental factors in cancer
A
- infectious agent
- smoking
- alcohol consumption
- diet
- obesity
- reproductive history
- environmental carcinogens
- age
22
Q
acquired predisposing factors in cancer
A
- chronic inflammation
- precursor lesions
- immunodeficiency states
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
oncogenes
promote autonomous/ abnormal cell growth
26
tyrosine kinase
- family of receptors that phosphorylate target protein using ATP
- causes cellular growth, apoptosis, and cell migration
27
tyrosine kinase mutations
- cause inappropriate activation of signaling pathways
| - leads to neoplastic growth
28
MYC oncogene
- most commonly involved in human tumors
| - causes over-expression of growth factor receptors
29
main cause of MYC oncogene mutation
- causes burkitt lymphoma
| - is an aggressive b cell lymphoma
30
tumor suppressor genes
- slow cell divisions
- repair DNA mistakes
- activate apoptosis
- cancer arises due to inactivation
- i.e. RB and P53
31
loss of heterozygosity
- mutation of both alleles of tumor suppressor genes needed for carcinogenesis
32
RB
- tumor suppressor gene
- causes persistent cell cycling
- mutation causes pathogenesis of childhood tumor retinoblastoma
33
P53 gene
- 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
cell mediated immunity
- cytotoxic T cells (CD8+)
- NK cells
- macrophages
35
role of telomeres
- protect end of chromosomes
- when shorten, cell undergoes senescence and/or apoptosis
- telomerase builds telomeres
36
role of telomerase in tumor cells
- is active in tumor cells
| - prevents apoptosis
37
metastatic cascade
- invasion of ECM
| - vascular dissemination and homing of tumor cells
38
invasion of ECM
- detachment and loosening of intracellular junctions
- ECM degraded by proteases
- migration of tumor cells
39
theories about how metastasis occurs
- clonal evolution model -> rare variant clones
- metastasis signature
- metastatic variants exist in a tumor with metastatic signature
- role of tumor stroma
40
genomic instability
- DNA repair pathways act indirectly by correcting spontaneous DNA errors
- inherited mutations increase risk of carcinogenesis
41
mutations that cause breast cancer
- BRCA1
| - BRCA2
42
mutations that cause ovarian, prostate, pancreas and stomach cancers
mutations in BRCA2
43
angiogenesis
- creation of new blood vessels
- stimulates tumor growth through endothelial cell production of GF
- influences metastatic potential
44
result of hypoxia in tumorgenesis
- causes upregulation of VEGF
| - leads to angiogenesis
45
proapoptotic proteins
- considered primed for apoptosis
| - occurs in normal cells
46
antiapoptotic proteins
- considered unprimed for apoptosis
| - occurs in tumor cells
47
do cancer cells utilize aerobic or anaerobic metabolism?
- anaerobic respiration
| - able to complete anaerobic respiration 100 times faster than aerobic respiration
48
steps involved in chemical carcinogenesis
- initiation
| - promotion
49
initiation of chemical carcinogenesis
- induction of irreversible changes/ mutations in the genome
- direct acting agents- no metabolic conversion
- indirect acing agents- metabolic conversion
50
promotion of chemical carcinogenesis
- can induce tumors in previously initiated cells by stim cell proliferation
- short lived, reversible and nontumorigenic
51
UVA radiation
- creates ROS
| - gets through all clothes and sunscreen
52
UVB radiation
- most prominent UV damage
- causes t dimers
- t dimers distort DNA
53
radiation carcinogenesis
- damage the nucleotides or DNA sugar moieties
- strand breaks in DNA
- indirect DNA damage by increasing ROS
54
benign and malignant tumors can cause problems due to:
- location
- functional activity like hormones produced
- bleeding and infection
- sx from tumor rupture or infection
- cachexia
55
cachexia
- profound muscle loss
- possible fat loss
- staged as precachexia, cachexia, refractor cachexia
56
pathophys of cachexia
- cytokines, inflammation and hypermetabolic state
- lipolysis and lipid mobilization
- genomics
- cancer treatments
- reduced dietary intake or absorption
