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Oncology - Sheet1 Flashcards

1
Q

Epidemiology of Cancer

A

Epidemiology of cancer

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2
Q

Epstein Barr virus

A

Burkitts lymphoma

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3
Q

human papillomavirus

A

cervical cancer

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4
Q

Hepatitis B virus

A

Liver cancer

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5
Q

Human T-cell lymphotrophic virus

A

Adult T cell leukemia

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6
Q

Kaposi’s sarcoma- associated herpes virus

A

Kaposi’s sarcoma

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7
Q

pleomorphis

A

nucleus becoming more irregular in shape

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8
Q

2 distinctions of malignant tumor

A

infiltration of surrounding normal tissue and metastasis

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9
Q

Epithelial origin malignant

A

carcinoma

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10
Q

epithelial originan benign

A

papilloma, adenoma

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11
Q

mesenchymal origin malignant

A

sarcoma

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12
Q

mesenchymal origina benign

A

fibroma, lipoma

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13
Q

hematopoietic origin malignant

A

lymphoma, leukemia

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14
Q

well differentiated =

A

benign

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15
Q

undifferentiated =

A

malignant

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16
Q

carcinoma in situ

A

pre-invasive cancer. dysplastic changes in full epithelium but no invasion

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17
Q

6 initial cancer hallmarks

A

growth factor independence, no response to anti-growth, resistance to apoptosis, limitless replicative, recruitment blood, invasion and metastasis

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18
Q

PI3K

A

kinase involved in intracellular signaling

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19
Q

PI3K function

A

converts PIP2 to PIP3

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20
Q

What activates PI3K

A

various receptor tyrosine kinases including EGF

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21
Q

PIP3 function

A

docking site for plecksrin homology domains. Main function is activation of AKT

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22
Q

Warburg effect

A

high glycolytic rate in many cancer cells

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23
Q

AKT ajor effect

A

increases glucose transport and glycolysis = warburg effect

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24
Q

PTEN

A

antagonist to PIK3, dephosphorylates PIP3

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25
Q

Li-Fraumeni syndrome

A

only one germ-linke copy of p53 so succeptible to a number of cancers. Loss of Heterozygosity

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26
Q

p53 regulates

A

p21, GADD45, Bax,puma,noxa, DM2

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27
Q

p21

A

cyclin/CDK inhibtor. cell cycle arrest

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28
Q

CGADD45

A

DNA repair pathways protects genome

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29
Q

Bax, Puma, Noxa

A

pro-apoptotic protein inducing cell death

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30
Q

MDM2

A

ubiquilates p53, for degredation

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31
Q

ATM, ATR, CHK2

A

activators of p53

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32
Q

what transcribes MDM2

A

p53 transcribes it - form of negative feedback inhibition

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33
Q

Two protein classes important in apoptosis

A

caspases and nucleases

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34
Q

Caspase basic mechanism

A

use conserved cystein to cleave after aspartate. Makes the CASP part.

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35
Q

Intrinsic apoptotic pathway

A

cytochrome c binds Apaf-1 recruits initiator procaspase 9

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36
Q

cytochrome c

A

molecule in mitochondria critical for intrinsic apoptotic pathway

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37
Q

caspase 9 activates

A

initiator caspase activating 3,6,7 for execution

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38
Q

Cytochrome C release promoters

A

Bax and Bak

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39
Q

Cytochrome C release inhibit

A

Bcl-2 inhibits BAK pore formation

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40
Q

BAK function

A

sits in outer membrane to make pores.

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41
Q

BAX function

A

when activated goes to BAK and helps make a pore

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42
Q

Extrinsic pathway

A

Fas receptor activated by FasL. Recruits FADD - procaspases8 or 10 - caspases 3,6,7

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43
Q

Fas receptor

A

death signaling receptor responding to FasL

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44
Q

FADD

A

Fas associated death domain protein recruiting initator caspases

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45
Q

Family of death receptors

A

DR4,5 TNFR1, DR3

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46
Q

hTERT function

A

can surpress senescence of human cells. it extends and stabilizes chromosomes

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47
Q

breakage fusion bridge cycles

A

cycles that occur with no telomeres involving DNA damage

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48
Q

VEGF

A

stimulates EC division, master regulator of antiogenesis. VEGF-A most prominent

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49
Q

VEGF activates

A

specific receptor tyrosine kinases on ECs

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50
Q

Avastin (bevacizumab)

A

antibody against VEGF. late stage colon and renal cancer

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51
Q

Sunitinib and sorafenib

A

small molecule based inhibitors. block VEGFR2

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52
Q

seed and soil concept

A

cancer will lodge in areas that have appropriate growth factors for it to survive

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53
Q

Avastin problem

A

successful inhibition of VEGF makes tumor more invasive and metastatic

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54
Q

Cancer Diagnostics

A

Cancer Diagnostics

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55
Q

philadelphia chromosome

A

translocation from 22 to 9

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56
Q

philadelphia chromosome encodes

A

BCR-ABL

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57
Q

BcrABL

A

has abnormal tyrosine kinase activity

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58
Q

FFPE

A

formalin fixed paraffin embedded

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59
Q

Imatinib

A

Prevents ADP bidning to CL enzyme

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60
Q

BRAF mutation

A

40-60% of melanoma lesions. mutation predicts response to vemurafenib. most common mutation = V600E

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61
Q

BRAF in papillary thryoid carcinoma

A

benign never have mutation. 40-70 have mutation

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62
Q

BRAF in colorectal

A

predicts poorer prognosis

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63
Q

Ilumina sequencing

A

real time sequencing by synthesis

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64
Q

Sequencing read length

A

nuber of sequential images taken

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65
Q

sequencing read depth

A

number of DNA fragments sequenced for any position

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66
Q

One test at a time paradigm

A

only test for utation in cancers where it is signifiant and has a certain rate

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67
Q

bcr abl hallmark

A

growth-factor independence

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68
Q

Leukemai vs Lymphoblast

A

Leukemia generally of cells native to marrow. generally more immature cells

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69
Q

acute neoplasm

A

early undifferentiated state

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70
Q

chronic neoplasm

A

mature, differentiated states

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71
Q

germinal center B cell markers

A

CD10+, BCL6+, BCL2-

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72
Q

Mantle B cell markers

A

CD10-, BCL6-, BCL2+

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73
Q

CD 21 marker

A

follicular dendritic meshwork

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74
Q

Burkitt lymphoma translocation

A

t(8:14). overexpress MYC

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75
Q

Follicular lymphoma translocation

A

t14:18 overexpress BCL2

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76
Q

reason for more B cell NHL

A

because B cells go through multiple rounds of genetic rearrangement

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77
Q

Small B cell NHLs (3)

A

SLL/CLL, Follicular lymphoma, marginal zone lymphoma

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78
Q

FL common organ involvement

A

Spleen and liver. Rarely to bone marrow

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79
Q

FL pathology

A

centrocytes and centroblasts. follicles close together

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80
Q

centrocytes

A

small, cleaved low grade germinal center B cells

81
Q

centroblasts

A

large transformed noncleaved germainl b cells

82
Q

FL bone marrow growth

A

grows in a paratrabelcular pattern. Don’t grow freely in space but pay attention to the trabeculae

83
Q

FL immunophenotype

A

CD19,20 - B cell + CD10,6,2. CD5-

84
Q

FL Ki67 levels

A

Low because proliferation low

85
Q

CLL/SLL male to female ratio

86
Q

CLL/SLL clinical

A

BM involvement, spleen, liver, peripheral blood, chance of immune dysregulation

87
Q

Richter’s transformation

A

CLL/SLL transforming to diffuse large B cell lymphoma

88
Q

CLL/SLL morphology

A

difffuse effacement of architecture, proliferation centers in pseudofollicles. prolymphocytes paraimmunoblasts

89
Q

CLL./SLL classic morphologic feature (2)

A

Lymphocytosis and smudge cells

90
Q

Lymphocytosis

A

composed of small mature lymphocytes. Not larger than blood cells

91
Q

CLL/SLL bone marrow infiltration

A

generally in forms of diffuse sheets. nodular pattern means better prognosis

92
Q

CLL/SLL important markers

A

CD5+ and BCL2+ CD19,20+

93
Q

CLL/SLL genetics

A

13q = better prognosis. Others (trisomy 12, 11q dleetion, worse), 17p bad

94
Q

Zap70 indicates

A

positive zap70 indicates no somatic hypermutation

95
Q

Zap70 positive CLL/SLL

A

naive B cell, more aggressive. unmutated variable

96
Q

Zap70 negative CLL/SLL

A

mature B cell. indolent ones

97
Q

Most common adult leukemia

98
Q

Marginal Zone lymphoma types

A

3 separatate disease, extranodal, nodal, splenic

99
Q

Extranodal marginal zone lymphoma of mucosa associated lymphoid tissue

A

MZ lymphoma of extranodal sites

100
Q

MALT lymphoma unique association

A

with chronic inflammation. Also from infectious agent

101
Q

MZ lymphoma phenotype

A

nothign unusual. CD19,20+ CD10,6-, CD2+. Restricted light chain

102
Q

MALT lymphoma mechanism

A

stimulation of cell growth through NF-kappaB activation

103
Q

MALT lymphoma spread

A

spread from mucosal site to mucosal site. Require multiple hits to become cancerous

104
Q

MALT cytogenic hallmark

A

t(11:18). mostlikely fully independent

105
Q

Plasma cell morphology

A

clumped clockface nuclear chromatin. perinuclear clear zone, gray cytoplasm

106
Q

multiple myeloma epi

A

most common in african americans, second most common caucasians

107
Q

Multiple myeloma clinical

A

weakens bone. accumulate in areas of hematopoiesis

108
Q

Multiple myeloma morphology variants

A

flame cell, mott cell, plasma cell atypia

109
Q

flame cell

A

plasma cell with IgA and pink border

110
Q

Mott Cell

A

cell filled with globules of intracytoplasmic monoclonal Ig

111
Q

Bence Jones proteins

A

excess light chain in multiple myeloma. come out in urine. Only light chains pass through kidney

112
Q

Multiple myeloma paraprotein detection

A

detect with electrophoresis. Most are IgG or IgA

113
Q

Multiple myeloma paraprotein effects

A

immunodeficiency bc no normal IgG. Renal failure

114
Q

Cast nephropathy

A

Multiple myeloma caused - excess light chains in distal form tubular cast.

115
Q

Multiple myeloma renal failure mechanisms

A

cast nephropathy, proximal tubulopathy, hypercalcemia, amyloidosis

116
Q

proximal tubulopathy MM

A

the light chains are toxic to proximal tubule in which they are being reabsorbed

117
Q

hypercalcemia MM

A

impair renal concentration. lood volume.

118
Q

Amyloidosis MM

A

light chains settle as amyloid deposits. light chain settle in beta pleated sheets to form tissue deposits

119
Q

Multipe Myeloma blood smear

A

serum hyperviscoscity. get blood cells to line up in rouleaux

120
Q

MM paraprotein effects blood

A

beleding bc interfere w platelets and clotting. cryoglobulinema

121
Q

Multiple myeloma cytogenetics

A

13q more aggressive.

122
Q

Multiple Myeloma bone destruction

A

infiltration of neoplastic cells. osteoclast activation and osteoblast inhibiition. weak trabecular bone and hypercalcemia

123
Q

DLBCL presentation

A

rapidly enlarging single mass

124
Q

EBV DLBCL mechanism

A

no immune surveilance allows B cell proliferation getting genetic accidents and forming aggressive lesion

125
Q

DLBCL marcoscopy

A

Fish-flesh replacement. hemorrhage, necrosis, fibrosis

126
Q

DLBCL pathology

A

centroblastic or immunoblastic apperance. diffuse architectural effacement and large cells. often necrosis

127
Q

International Prognostic index DLBCL

A

a way to estimate outcomes. uses LDH etc. to measure extent of disease

128
Q

DLBCL genetic subtypes

A

There are germianl center types GCB and activated B cell types ABC

129
Q

GBC DLBCL outcome

A

generally better survival

130
Q

ABC DLBCL

A

worse outcome

131
Q

3 variants Burkitt Lymphoma

A

endemic, sporadic, immunodeficiency associated

132
Q

Endemic BL epi

A

2:1 males, associated with EBV.

133
Q

Sporadic BL epi

A

3:1 males. rare in adults

134
Q

Immunodeficient BL

A

association with HIV infection

135
Q

Endemic BL common site

A

facial bone.

136
Q

Sporadic BL common site

A

abdominal, ileocecal

137
Q

Immunodef BL site

A

lymph nodes or bone marrow

138
Q

BL morphology

A

Starry sky pattern. very basophilic cells. lipid vacuoles

139
Q

BL immunophenotype

A

germinal center B cell. CD10,6+ and BCL2-

140
Q

BL Ki67

A

almost 100% rapid proliferation

141
Q

Burkitt lymphoma central event

A

activation of cMYC

142
Q

Burkitt Lymphoma translocation

A

t(8:14) exrpress cMYC with IgH

143
Q

Hodgkin diagnostic cell

A

reed-sternberg cell

144
Q

Hodgkin cell origin

A

germinal center B cell=

145
Q

Hodgkin staging

A

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

146
Q

WBC Disorders

A

WBC Disorders

147
Q

Radiation

148
Q

Radiation basic mechanism

A

damage DNA so that proliferating cells with damaged DNA and no check points will die

149
Q

Damage to DNA by ionization facilitated by

150
Q

direct ionization

A

directly damage DNA strand

151
Q

indirect ionization

A

damage DNA through reactive intermediates

152
Q

Main methods of radiation delivery

A

External beam radiation therapy, internal radiation therapy

153
Q

radiosensitivity

A

in vitro sensitivity. Favorable cell survival curves.

154
Q

radioresponsiveness

A

clinical reponse of tumor during or after treatment.

155
Q

radiation therapeutic index

A

degree of effect on tumor compared to normal tissue

156
Q

radiation acute toxicity

A

skin, oral mucosa, small bowel bc rapid turnover

157
Q

radiation late toxicity

A

damage from cell loss and fibrosis. spine, lung, heart, brain

158
Q

4 R’s radiobiology

A

reassortmetn of cells within cell c ycle, reoxygenation, repair of sublethal damage in normal tissue, repopulation

159
Q

concurrent chemoRT mechanism

A

direct enhancement of DNA damage, inhibit cellular repair, accumulate cells in radiosensitive phase, work against radioresistant cells, inhibit repopulation of tumor cells

160
Q

RT GTV

A

gross tumor volume, macroscopic cancer

161
Q

RT CTV

A

clinical target volume

162
Q

RT PTV

A

planning target volume = internal margin + setup margin

163
Q

Bragg Peak effect

A

peak radiation that is applied to the actual tumor

164
Q

Proton therapy benefit

A

no exit radiation. Can get higher Bragg peak effect

165
Q

Cervical Cancer screening guidelines

A

Pap every 3 years until 65. then every 5 years

166
Q

CT scans for non smokers

A

Not recommended. CT annually for selected smokers/former smokers

167
Q

Cancer staging solid tumors

A

TNM, T relates to size etc of primary tumor. N relates to nodal invovlmenet. M relates to metastatic disease.

168
Q

Effect of bone mestases

A

causes osteolysis or bone formation = pain

169
Q

cachexia syndrome

A

fatigue, weight loss, from inflammatory factors like TNF w/ cancer

170
Q

paraneoplastic syndromes

A

tumor produces hormones causing changes.

171
Q

Cancer performance status

A

ECOG system. 4 is completely disabled

172
Q

HPV types for cervical cancer

173
Q

HPV types for genital warts

174
Q

HPV types in anal cancer

175
Q

Bone marrow cellularity percent

A

%cellularity = 100-age

176
Q

Inherited bone marrow failure syndromes

A

Fanconi anemia, dyskeratosis congenita, diamond blackfan anemia

177
Q

G-CSF, GM-CSF

A

stimulate proliferation of myeloid progenitor cells. speeds differentiation to neutrophils

178
Q

TPO mimetics

A

stimulate megakaryocyte prliferationa dn differentiation causing rise in platelet counts. includes romiplostim and eltrombopag

179
Q

Romiplostim

A

peptide TOP mimetic. activate TPO receptor by binding to external domain

180
Q

Eltrombopag

A

nonpeptide TOP. binds to transmembrane site on receptor and activates

181
Q

Aged HSC differentiate preferentially into

A

myeloid typpe over lympho and erythro

182
Q

pancytopenias

A

fanconi anemia adn dyskeratosis congenita

183
Q

single lineage cytopenia RBC

A

diamond blackfan anemia

184
Q

single lineage cytopenia myeloid

A

schwachman diamon syndrome, sever congenital neutropenia

185
Q

single lineage cytopenia platelets

A

congenital amegakaryocytic thrombocytopenia. thrombocytopenia and absent radii, familial platelet disorder

186
Q

Fanconi anemia presentation

A

congenitcal anomolies, progressive bone maorrow failure.

187
Q

Fanconi anemia screening test

A

DEB/MMC hypersensitivity

188
Q

Dyskeratosis congenita classic feautres

A

hyper/hypo pigmentation, leukoplakia, nail dysrotphy, bone marrow failure

189
Q

Diamond blackfan anemia features

A

red cell aplasia, congenital anomolies, osteosarcoma.

190
Q

Diamond blackfan anemia cause

A

defect in ribosome synthesis

191
Q

acute leukemia presentation

A

abrupt pancytopenia

192
Q

myelodysplastic syndromes

A

acquired persistent reduction in circulating myeloid blood cell counts, not due to nutriotion or othe illnesses

193
Q

Myelodysplastic syndrome morphology

A

hypercellular marrow. megaloblastoid RBC precursors

194
Q

t(15:17)

A

fuses PML transcription factor with retinoic acid receptor. in AML

195
Q

Leukemia signs

A

pallor, rashes, lymph node enlargement, swollen gumjs

196
Q

Leukostasis

A

abnormal blood circulation, extreme circulatin gtumor burden.

197
Q

Defining pathology AML

198
Q

Auer rods

A

aggregates of myeloperoxidase

MDTI (10 decks)

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