Lutz CA
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CNS Lymphoma | AIDS
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Carribean, Japan | HTLV
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Nasopharyngeal T cell lymphoma | EBV Asia, South America
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B cell lymphoma | Hep C
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MALT of stomach | H. Pylori
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cutaneous MALT | Borrelia burgdorferi
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t11;14 Mantle Cell Lphoma | BCL-1, prevent apoptosis
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t14;18 Follicular Center Cell Lphoma | BCL-2, upreg prolif
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stage determined CA | Hodgkins
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CD 20+, 45+ | Lcyte Predominance Hodgkins
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Females, mediastinum involved | Nodular sclerosis, 20-70% Hodgkins
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CD 5, 20, 23 | SLL/CLL
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CD 5, 20 | Mantle cell
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CD 10, 20, 23 | Follicular cell
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CD 20, 23 | Marginal zone, malt
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t11;18 | Marginal zone, malt
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lethal midline granuloma, Asia Central America | NK/T cell Lphoma; EBV CD56+
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erythroderma+ blood involvement | Sezary Sx
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cerebriform nuclei, Pautrier uabscess | Mycosis fungoides
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aggressive, children, mediastinum, CD3, Tdt | Lblastic Lphoma
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CD 30+, ALK+, t2;5 | Anaplastic large T cell Lphoma
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<10% plasma cell, no lytic bone lesion | MGUS
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m/c 1* bone CA, M protein, Bence-Jones, OAF | Mult Myeloma
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B-pleated sheet, Congo red stain | Amyloid
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Ig light chain | AL
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SAA acute phase reactant | AA
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m/c systemic amyloid, <60% PC, free light chain | AL
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arthritis, RA, Chronic sepsis, slower>AL | AA
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high SAA, elderly, ESRD, Crohn's, Chronic sepsis | poor prognosis
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TB, mycobacteria, fungal, sarcoid | granuloma
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monoclonal | CA causing virus
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polyclonal | DNA methylation
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CA causing viruses | HPV, EBV, HTLV
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predicts clinical outcome well | stage
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wt of detectable CA | 1g
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cell # of detectable CA | 1 billion, 30 cell division
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cell # to kill the pt | 1 kg, 1000 billion cell
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CD 133+, blast crisis | CA stem cell
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size of blood supply | 1mm req bl supply
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dominant negative mutation | p53 tumor suppressor, one loss=CA
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sis protooncogene | PDGF
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autocrine cell growth w/ PDGF | astrocytoma, osteosarcoma
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HER2/neu | EGF-R
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breast CA, ovarian CA | HER2/neu R
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ineffective EGF-R inhibitor | KRAS mutation
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ret oncogene | thyroid carcinoma, MEN
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loss of inhibitory abl domain | abl-bcr, CML
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signal transduction in 15-20% of CA | ras
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codon 12 13 | ras-GTP always active
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GTPase Activating Protein, tumor suppressor | NF-1, degrade GTP->GDP
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melanoma, NF | NF-1
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lung CA, downregulate ras | LET7microRNA
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transcription factors | C-myc, L-myc, N-myc
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tumor suppressor, cell cycle regulator | Rb
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bind E2F transcription factor | Rb
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suppress cell cycle | Rb-E2F recruit HDACs
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inc cyclin | inc prolif thru CDK->Rb-po4 + E2F
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Rb inactivated in | retinoblastoma, osteosarcoma
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Rb inactivated by | HPV
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Knudson's hypothesis | 1 defective allele inherited, 1 more for CA
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cyclin D1 activation | bcl-1 Mantle cell, t11;14
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ATM | ataxia telangectasia
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DNA repair proteins recruited by RAP80 | BRCA1, ABRA1
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NER UV light | Xeroderma Pigmentosum
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BER | smoking, reactive O2, bases go 1st
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MMR | MSH2, MLH1; hi MSI-> Lynch Sx
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HR | BRCA1, BRCA2 in breast, ovarian CA
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prevent rasGTP-x->rasGDP | pt mut in codon 12 13 and NF-1
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Ig heavy chain next to C-myc | t8;14 Burkitt Lphoma
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acetylation of histone H3 H4 | activation
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histone H3 Lys 4 methylation | active transcription
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histone H3 Lys 9 methylation | inactive transcription
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ALL1/MLL | Lys 4 methylator in ALL AML
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Molec Mech #1 | APC/MUTYH loss, Kras mut, p53 loss
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Molec Mech #1 | adenomatous polyp, M>F, Lt>rt, 60% spor, FAP
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molec Mech #2 | CIMP, BRAF1 mut, hi MSI, methylated promoter, MGMT loss
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molec Mech #2 | serrated polyp, F>M, Rt>lt, 20% spor
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molec mech #3 | mut MSH2, 6, MLH1, PMS2, HNPCC/Lynch sx
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FAP APC loss | benign polyp, 42 yo, Tx- proctolectomy
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Lynch Sx | init adenoma, 48yo, Tx- colonoscopy
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Apoptos Extrinsic pathway | TNF, Fas bind Init caspases-> Effector caspase
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Apoptos Intrinsic pathway | Bak, Bax, Bim
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anti- apop | Bcl-2 Bcl-x
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Bcl-> cytC-> | Apaf-1-> Init caspase-> effector caspase
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telomere sequence | TTAGGG
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melanoma | neural crest origin, Slug TF.
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sarcomas [bone] metastasize to | lung
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lung carcinoma metastasize to | brain
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colorectal CA metastasize to | liver
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