Oncology - Sheet1 Flashcards
(198 cards)
1
Q
Epidemiology of Cancer
A
Epidemiology of cancer
2
Q
Epstein Barr virus
A
Burkitts lymphoma
3
Q
human papillomavirus
A
cervical cancer
4
Q
Hepatitis B virus
A
Liver cancer
5
Q
Human T-cell lymphotrophic virus
A
Adult T cell leukemia
6
Q
Kaposi’s sarcoma- associated herpes virus
A
Kaposi’s sarcoma
7
Q
pleomorphis
A
nucleus becoming more irregular in shape
8
Q
2 distinctions of malignant tumor
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infiltration of surrounding normal tissue and metastasis
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Q
Epithelial origin malignant
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carcinoma
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Q
epithelial originan benign
A
papilloma, adenoma
11
Q
mesenchymal origin malignant
A
sarcoma
12
Q
mesenchymal origina benign
A
fibroma, lipoma
13
Q
hematopoietic origin malignant
A
lymphoma, leukemia
14
Q
well differentiated =
A
benign
15
Q
undifferentiated =
A
malignant
16
Q
carcinoma in situ
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pre-invasive cancer. dysplastic changes in full epithelium but no invasion
17
Q
6 initial cancer hallmarks
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growth factor independence, no response to anti-growth, resistance to apoptosis, limitless replicative, recruitment blood, invasion and metastasis
18
Q
PI3K
A
kinase involved in intracellular signaling
19
Q
PI3K function
A
converts PIP2 to PIP3
20
Q
What activates PI3K
A
various receptor tyrosine kinases including EGF
21
Q
PIP3 function
A
docking site for plecksrin homology domains. Main function is activation of AKT
22
Q
Warburg effect
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high glycolytic rate in many cancer cells
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Q
AKT ajor effect
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increases glucose transport and glycolysis = warburg effect
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Q
PTEN
A
antagonist to PIK3, dephosphorylates PIP3
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Li-Fraumeni syndrome
only one germ-linke copy of p53 so succeptible to a number of cancers. Loss of Heterozygosity
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p53 regulates
p21, GADD45, Bax,puma,noxa, DM2
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p21
cyclin/CDK inhibtor. cell cycle arrest
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CGADD45
DNA repair pathways protects genome
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Bax, Puma, Noxa
pro-apoptotic protein inducing cell death
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MDM2
ubiquilates p53, for degredation
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ATM, ATR, CHK2
activators of p53
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what transcribes MDM2
p53 transcribes it - form of negative feedback inhibition
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Two protein classes important in apoptosis
caspases and nucleases
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Caspase basic mechanism
use conserved cystein to cleave after aspartate. Makes the CASP part.
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Intrinsic apoptotic pathway
cytochrome c binds Apaf-1 recruits initiator procaspase 9
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cytochrome c
molecule in mitochondria critical for intrinsic apoptotic pathway
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caspase 9 activates
initiator caspase activating 3,6,7 for execution
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Cytochrome C release promoters
Bax and Bak
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Cytochrome C release inhibit
Bcl-2 inhibits BAK pore formation
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BAK function
sits in outer membrane to make pores.
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BAX function
when activated goes to BAK and helps make a pore
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Extrinsic pathway
Fas receptor activated by FasL. Recruits FADD - procaspases8 or 10 - caspases 3,6,7
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Fas receptor
death signaling receptor responding to FasL
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FADD
Fas associated death domain protein recruiting initator caspases
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Family of death receptors
DR4,5 TNFR1, DR3
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hTERT function
can surpress senescence of human cells. it extends and stabilizes chromosomes
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breakage fusion bridge cycles
cycles that occur with no telomeres involving DNA damage
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VEGF
stimulates EC division, master regulator of antiogenesis. VEGF-A most prominent
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VEGF activates
specific receptor tyrosine kinases on ECs
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Avastin (bevacizumab)
antibody against VEGF. late stage colon and renal cancer
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Sunitinib and sorafenib
small molecule based inhibitors. block VEGFR2
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seed and soil concept
cancer will lodge in areas that have appropriate growth factors for it to survive
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Avastin problem
successful inhibition of VEGF makes tumor more invasive and metastatic
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Cancer Diagnostics
Cancer Diagnostics
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philadelphia chromosome
translocation from 22 to 9
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philadelphia chromosome encodes
BCR-ABL
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BcrABL
has abnormal tyrosine kinase activity
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FFPE
formalin fixed paraffin embedded
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Imatinib
Prevents ADP bidning to CL enzyme
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BRAF mutation
40-60% of melanoma lesions. mutation predicts response to vemurafenib. most common mutation = V600E
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BRAF in papillary thryoid carcinoma
benign never have mutation. 40-70 have mutation
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BRAF in colorectal
predicts poorer prognosis
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Ilumina sequencing
real time sequencing by synthesis
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Sequencing read length
nuber of sequential images taken
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sequencing read depth
number of DNA fragments sequenced for any position
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One test at a time paradigm
only test for utation in cancers where it is signifiant and has a certain rate
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bcr abl hallmark
growth-factor independence
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Leukemai vs Lymphoblast
Leukemia generally of cells native to marrow. generally more immature cells
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acute neoplasm
early undifferentiated state
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chronic neoplasm
mature, differentiated states
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germinal center B cell markers
CD10+, BCL6+, BCL2-
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Mantle B cell markers
CD10-, BCL6-, BCL2+
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CD 21 marker
follicular dendritic meshwork
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Burkitt lymphoma translocation
t(8:14). overexpress MYC
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Follicular lymphoma translocation
t14:18 overexpress BCL2
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reason for more B cell NHL
because B cells go through multiple rounds of genetic rearrangement
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Small B cell NHLs (3)
SLL/CLL, Follicular lymphoma, marginal zone lymphoma
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FL common organ involvement
Spleen and liver. Rarely to bone marrow
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FL pathology
centrocytes and centroblasts. follicles close together
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centrocytes
small, cleaved low grade germinal center B cells
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centroblasts
large transformed noncleaved germainl b cells
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FL bone marrow growth
grows in a paratrabelcular pattern. Don't grow freely in space but pay attention to the trabeculae
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FL immunophenotype
CD19,20 - B cell + CD10,6,2. CD5-
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FL Ki67 levels
Low because proliferation low
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CLL/SLL male to female ratio
2:01:00
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CLL/SLL clinical
BM involvement, spleen, liver, peripheral blood, chance of immune dysregulation
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Richter's transformation
CLL/SLL transforming to diffuse large B cell lymphoma
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CLL/SLL morphology
difffuse effacement of architecture, proliferation centers in pseudofollicles. prolymphocytes paraimmunoblasts
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CLL./SLL classic morphologic feature (2)
Lymphocytosis and smudge cells
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Lymphocytosis
composed of small mature lymphocytes. Not larger than blood cells
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CLL/SLL bone marrow infiltration
generally in forms of diffuse sheets. nodular pattern means better prognosis
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CLL/SLL important markers
CD5+ and BCL2+ CD19,20+
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CLL/SLL genetics
13q = better prognosis. Others (trisomy 12, 11q dleetion, worse), 17p bad
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Zap70 indicates
positive zap70 indicates no somatic hypermutation
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Zap70 positive CLL/SLL
naive B cell, more aggressive. unmutated variable
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Zap70 negative CLL/SLL
mature B cell. indolent ones
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Most common adult leukemia
CLL/SLL
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Marginal Zone lymphoma types
3 separatate disease, extranodal, nodal, splenic
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Extranodal marginal zone lymphoma of mucosa associated lymphoid tissue
MZ lymphoma of extranodal sites
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MALT lymphoma unique association
with chronic inflammation. Also from infectious agent
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MZ lymphoma phenotype
nothign unusual. CD19,20+ CD10,6-, CD2+. Restricted light chain
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MALT lymphoma mechanism
stimulation of cell growth through NF-kappaB activation
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MALT lymphoma spread
spread from mucosal site to mucosal site. Require multiple hits to become cancerous
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MALT cytogenic hallmark
t(11:18). mostlikely fully independent
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Plasma cell morphology
clumped clockface nuclear chromatin. perinuclear clear zone, gray cytoplasm
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multiple myeloma epi
most common in african americans, second most common caucasians
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Multiple myeloma clinical
weakens bone. accumulate in areas of hematopoiesis
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Multiple myeloma morphology variants
flame cell, mott cell, plasma cell atypia
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flame cell
plasma cell with IgA and pink border
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Mott Cell
cell filled with globules of intracytoplasmic monoclonal Ig
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Bence Jones proteins
excess light chain in multiple myeloma. come out in urine. Only light chains pass through kidney
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Multiple myeloma paraprotein detection
detect with electrophoresis. Most are IgG or IgA
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Multiple myeloma paraprotein effects
immunodeficiency bc no normal IgG. Renal failure
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Cast nephropathy
Multiple myeloma caused - excess light chains in distal form tubular cast.
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Multiple myeloma renal failure mechanisms
cast nephropathy, proximal tubulopathy, hypercalcemia, amyloidosis
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proximal tubulopathy MM
the light chains are toxic to proximal tubule in which they are being reabsorbed
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hypercalcemia MM
impair renal concentration. lood volume.
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Amyloidosis MM
light chains settle as amyloid deposits. light chain settle in beta pleated sheets to form tissue deposits
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Multipe Myeloma blood smear
serum hyperviscoscity. get blood cells to line up in rouleaux
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MM paraprotein effects blood
beleding bc interfere w platelets and clotting. cryoglobulinema
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Multiple myeloma cytogenetics
13q more aggressive.
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Multiple Myeloma bone destruction
infiltration of neoplastic cells. osteoclast activation and osteoblast inhibiition. weak trabecular bone and hypercalcemia
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DLBCL presentation
rapidly enlarging single mass
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EBV DLBCL mechanism
no immune surveilance allows B cell proliferation getting genetic accidents and forming aggressive lesion
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DLBCL marcoscopy
Fish-flesh replacement. hemorrhage, necrosis, fibrosis
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DLBCL pathology
centroblastic or immunoblastic apperance. diffuse architectural effacement and large cells. often necrosis
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International Prognostic index DLBCL
a way to estimate outcomes. uses LDH etc. to measure extent of disease
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DLBCL genetic subtypes
There are germianl center types GCB and activated B cell types ABC
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GBC DLBCL outcome
generally better survival
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ABC DLBCL
worse outcome
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3 variants Burkitt Lymphoma
endemic, sporadic, immunodeficiency associated
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Endemic BL epi
2:1 males, associated with EBV.
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Sporadic BL epi
3:1 males. rare in adults
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Immunodeficient BL
association with HIV infection
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Endemic BL common site
facial bone.
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Sporadic BL common site
abdominal, ileocecal
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Immunodef BL site
lymph nodes or bone marrow
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BL morphology
Starry sky pattern. very basophilic cells. lipid vacuoles
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BL immunophenotype
germinal center B cell. CD10,6+ and BCL2-
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BL Ki67
almost 100% rapid proliferation
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Burkitt lymphoma central event
activation of cMYC
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Burkitt Lymphoma translocation
t(8:14) exrpress cMYC with IgH
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Hodgkin diagnostic cell
reed-sternberg cell
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Hodgkin cell origin
germinal center B cell=
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Hodgkin staging
stage 1 = 1 site. Stage 2 - 2 regions one side of diaphragm, stage 3 - both sides of diaphragm lymph system only, stage 4 - out of lymphatic. Type A if no symptoms
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WBC Disorders
WBC Disorders
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Radiation
Radiation
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Radiation basic mechanism
damage DNA so that proliferating cells with damaged DNA and no check points will die
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Damage to DNA by ionization facilitated by
oxygen
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direct ionization
directly damage DNA strand
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indirect ionization
damage DNA through reactive intermediates
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Main methods of radiation delivery
External beam radiation therapy, internal radiation therapy
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radiosensitivity
in vitro sensitivity. Favorable cell survival curves.
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radioresponsiveness
clinical reponse of tumor during or after treatment.
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radiation therapeutic index
degree of effect on tumor compared to normal tissue
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radiation acute toxicity
skin, oral mucosa, small bowel bc rapid turnover
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radiation late toxicity
damage from cell loss and fibrosis. spine, lung, heart, brain
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4 R's radiobiology
reassortmetn of cells within cell c ycle, reoxygenation, repair of sublethal damage in normal tissue, repopulation
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concurrent chemoRT mechanism
direct enhancement of DNA damage, inhibit cellular repair, accumulate cells in radiosensitive phase, work against radioresistant cells, inhibit repopulation of tumor cells
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RT GTV
gross tumor volume, macroscopic cancer
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RT CTV
clinical target volume
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RT PTV
planning target volume = internal margin + setup margin
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Bragg Peak effect
peak radiation that is applied to the actual tumor
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Proton therapy benefit
no exit radiation. Can get higher Bragg peak effect
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Cervical Cancer screening guidelines
Pap every 3 years until 65. then every 5 years
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CT scans for non smokers
Not recommended. CT annually for selected smokers/former smokers
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Cancer staging solid tumors
TNM, T relates to size etc of primary tumor. N relates to nodal invovlmenet. M relates to metastatic disease.
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Effect of bone mestases
causes osteolysis or bone formation = pain
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cachexia syndrome
fatigue, weight loss, from inflammatory factors like TNF w/ cancer
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paraneoplastic syndromes
tumor produces hormones causing changes.
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Cancer performance status
ECOG system. 4 is completely disabled
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HPV types for cervical cancer
16 and 18
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HPV types for genital warts
6 and 11
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HPV types in anal cancer
16 and 18
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Bone marrow cellularity percent
%cellularity = 100-age
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Inherited bone marrow failure syndromes
Fanconi anemia, dyskeratosis congenita, diamond blackfan anemia
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G-CSF, GM-CSF
stimulate proliferation of myeloid progenitor cells. speeds differentiation to neutrophils
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TPO mimetics
stimulate megakaryocyte prliferationa dn differentiation causing rise in platelet counts. includes romiplostim and eltrombopag
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Romiplostim
peptide TOP mimetic. activate TPO receptor by binding to external domain
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Eltrombopag
nonpeptide TOP. binds to transmembrane site on receptor and activates
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Aged HSC differentiate preferentially into
myeloid typpe over lympho and erythro
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pancytopenias
fanconi anemia adn dyskeratosis congenita
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single lineage cytopenia RBC
diamond blackfan anemia
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single lineage cytopenia myeloid
schwachman diamon syndrome, sever congenital neutropenia
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single lineage cytopenia platelets
congenital amegakaryocytic thrombocytopenia. thrombocytopenia and absent radii, familial platelet disorder
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Fanconi anemia presentation
congenitcal anomolies, progressive bone maorrow failure.
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Fanconi anemia screening test
DEB/MMC hypersensitivity
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Dyskeratosis congenita classic feautres
hyper/hypo pigmentation, leukoplakia, nail dysrotphy, bone marrow failure
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Diamond blackfan anemia features
red cell aplasia, congenital anomolies, osteosarcoma.
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Diamond blackfan anemia cause
defect in ribosome synthesis
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acute leukemia presentation
abrupt pancytopenia
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myelodysplastic syndromes
acquired persistent reduction in circulating myeloid blood cell counts, not due to nutriotion or othe illnesses
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Myelodysplastic syndrome morphology
hypercellular marrow. megaloblastoid RBC precursors
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t(15:17)
fuses PML transcription factor with retinoic acid receptor. in AML
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Leukemia signs
pallor, rashes, lymph node enlargement, swollen gumjs
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Leukostasis
abnormal blood circulation, extreme circulatin gtumor burden.
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Defining pathology AML
auer rods
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Auer rods
aggregates of myeloperoxidase
