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VBH Chaz > Blood Cancer > Flashcards

Blood Cancer Flashcards

1
Q

Describe the altered cell fate in myelodysplasia

A

Increased apoptosis
Reduced number terminally differentiated cells produced
Partial block in differentiation leDs to the accumulation of immature cells

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2
Q

List some therapeutic targets for acute myeloid leukaemia

A 
Mutations in proliferation and survival
FLT3
Oncogenic RAS
KIT alleles
PTPN11
- FLT3 inhibitors
Mutations in differentiation and self-renewal
Core binding factor
Retinoic acid receptor
MLL rearrangement
-ATRA 
Target self-renewal WNT, notch, BMI1, HOX
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3
Q

Describe the epigenetic of acute myeloid leukaemia

A

In the cancer cell DNMT, HDAC and MBP methylate

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4
Q

List some single gene molecular abnormalities in acute myeloid leukaemia

A 
FLT3
c-KIT
CEBPalpha
RUNX1
RAS
NPM1
MLL partial tandem duplication
WT1
IDH1/2
TET2
DNMT3A
BCOR
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5
Q

List the important transcription factors in blood cell differentiation

A 
RUNX1
GATA2
C/EBPalpha
DNMT3A
TET2
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6
Q

Give an example of a fusion protein in cancer and its treatment

A

PML-RARA
Produced by the t(15:17) translocation in leukaemia
Prevents transcription and therefore prevents cell differentiation
Treat with retinoic acid which binds to the Retinoic Acid Receptor and releases the conplex that prevents transcription

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7
Q

Describe core binding factor translocations in acute leukaemia

A

AML1-ETO aka RUNX1/RUNX1T1

Blocks differentiation at myeloblast stage

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8
Q

Briefly describe FLT3 in acute myeloid leukaemia

A 
Receptor tyrosine kinase
➡️RAS
➡️Akt
Mutation leads to permanent activation, and continuous proliferation
Associated with lower survival
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9
Q

Summarise myeloproliferative disease

A

Excess of myeloid cells
Primary polycythaemia- too many RBCs
Primary thrombocythaemia- too many platelets
Idiopathic myelofibrosis- too much marrow fibrosis
Chronic myeloid leukaemia (CML)- too many neutrophils

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10
Q

Summarise chronic myeloid leukaemia

A

Accumulation of myeloid progenitors
High white blood cell count
Large spleen
Can transform into acute leukaemia

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11
Q

What is the significance of Imatinib

A

BCR-Abl is a fusion protein that forms a tyrosine kinase with a markedly increased activity
Imatinib inhibits the binding of ATP to ABL tyrosine kinase
Selective for cancer cells

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12
Q

List some next gen BCR ABL inhibitors and why are they needed

A 
Nilotinib
Dasatinib
Bosutinib
Ponatinib
Needed to overcome the cancer cell mutations to overcome Imatinib, eg. Ponatinib is the only one that will work against the T315I mutation
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13
Q

Summarise classical myeloid proliferative neoplasm

A

Polycythaemia Vera- increased red cell precursors in bone marrow
Essential thrombocythaemia- increased megakaryocytes in marrow
Large spleen
Thrombosis
Haemorrhage
Itching
Gout
Clonal mutations- JAK2, CALR, MPL
Treatment- aspirin, venesection, cytoreductive agents

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14
Q

Summarise myelofibrosis

A 
Fibrotic marrow
Cytopenias
Very large spleen
-asymptomatic
-spleen pain
-fevers, sweats, back pain 
-infections
Often a poor prognosis
Blood transfusions
Treatment- thalidomide, medroxyprogesterone, Ruxolitinib-JAK inhibitor
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15
Q

Summarise myeloproliferative disease

A

Excess of myeloid cells
Primary polycythaemia- too many RBCs
Primary thrombocythaemia- too many platelets
Idiopathic myelofibrosis- too much marrow fibrosis
Chronic myeloid leukaemia (CML)- too many neutrophils

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16
Q

List some lymphoid classifications

A

Precursor B/T neoplasms- acute lymphoblastic leukaemia (ALL)
Mature B cell neoplasms- B cell lymphoma
Mature T and NK cell neoplasm- T cell lymphoma
Hodgkin lymphoma
Immune deficiency associated lymphoproliferative disease

17
Q

Summarise chronic lymphocytic leukaemia

A

Proliferation of mature B cells
Can infiltrate lymph nodes and spleen
Indolent lymphoproliferative disease
Mostly elderly

18
Q

Summarise multiple myeloma

A

Monoclonal proliferation of plasma cells
Lytic bone lesions- fractures
Paraprotein- renal failure
Marrow suppression- anaemia

19
Q

What is the significance of EBV in lymphoma?

A

EBV infection leads to a latent pool of infected B lymphocytes which if coupled with immune suppression➡️ continued growth in a sense of immune control➡️ post transplant lymphoproliferative disease
With chronic malaria➡️ chromosomal translocation and CMYC activation➡️ Burkitt lymphoma
With co-factors➡️ cellular genetic changes➡️ Hodgkin lymphoma
EBV encoded nuclear antigens (EBNA) can repress gene expression

20
Q

Name some underlying similar pathogenesis abnormalities found in lymphoproliferative diseases

A

Cytogenetic abnormalities- hyper diploid, the Philadelphia chromosome (BCR-ABL)
Translocations forming fusion proteins- t(8;14) CMYC-IGH in burkitts
Abnormalities in bone marrow microenvironment
Some bacteria and viruses with other factors like immune suppression can cause some important lymphomas

VBH Chaz (4 decks)

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