SET4 Flashcards

1
Q

These tend to be CD13+, CD33+, MPO+, and CD116+

A

Myeloid Cells

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2
Q

Name 3 drugs or situations that increase a patients risk of HBV reactivation

A

Anti-CD20 drugs (Rituximab, Obinutuzumab), Alemtuzumab (Anti-CD52), and Allo-HSCT; should be on HBV ppx at least 6 months after last cycle

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3
Q

This drug is an anti-CD22 immunoconjugate carrying calicheamicin used in relapsed or refractory B ALL?

A

Inotuzumab ozogamicin

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4
Q

This is when a person develops fever during neutrophil recovery after allo-HSCT

A

Engraftment Syndrome; fever, skin rash, and pulmonary capillary leak can occur

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5
Q

What drug has been shown to cause atypical fractures of the diaphyseal femoral shaft? MOA?

A

Denosumab, RANKL inhibitor

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6
Q

True or false: CNS ppx is not needed for T-ALL presenting with mediastinal Dz

A

False, CNS ppx is needed for all pts with any ALL

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7
Q

What is the best drug for HBV reactivation ppx in pts on Rituximab or Obinutuzumab, or Alemtuzumab?

A

Entacavir is best (others are Tenofovir, Lamivudine, Adofovir, and Telbivudine)

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8
Q

This drug showed a statistically significant improvement in the treatment of chemotherapy-induced peripheral neuropathy

A

Duloxetine

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9
Q

The molecular weight of BCR-ABL depends on where the chromosome breakpoint occurs: What is the MC transcript in ALL and what is the MC transcript in CML?

A

ALL most commonly has p190 and CML most often has p210

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10
Q

What can you say about the endometrial cancers that occur due to tamoxifen use?

A

They occur often after 5 years of use and are usually well-differentiated and early stage

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11
Q

If ALL has CD20+ what effect does this have on prognosis? What do you do about it in Tx?

A

Worse prognostic indicatior; add rituximab i.e. R-HyperCVAD

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12
Q

The greatest cumulative risk of endometrial CA occurs after how long of exposure to tamoxifen?

A

5- years, the cancers are usually well-differentiated and occur at early stage

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13
Q

Explain the two signalling events required for T Cell Activation

A

1) TCR binds to antigent on APC via MHC 1 and MHC 2; CD28 on T cell (Co-stimulatory receptor) binds to B7 ligand on B cell (B7-1 = CD80, B7-2 = CD86); these events lead to T cell proliferation and cytokine release; this process is checked by CTLA upregulation on T cells which tries to downregulate CD28

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14
Q

Although 5-FU overdose can occur for a number of reasons due to human error, deficiency of what enzyme can lead to 5-FU overdose? What drug can tx?

A

Dihydropyridine Dehydrogenase; Uridine Triacetate

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15
Q

What ALL medications allergic reaction can be Tx with Erwinia chrysanthem?

A

Allergies to Pegasparaginase

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16
Q

How frequently does Philadelphia positivity occur in ALL pts? General mgmt?

A

20-30% they should get a TKI in addition to multiagent chemo and since it confers poor prognosis would do allo HSCT in first remission

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17
Q

What are two cytogenetic abnormalities associated with favorable prognosis in ALL?

A

Hyperdiploidy and TEL-AML1 gene mutation t(12;21)(p13;q22)

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18
Q

These tend to be CD2+, CD3+, CD5+, CD7+, and CD30+

A

T cells

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19
Q

A patient with MM on denosumab complains of hip pain, what should you do and why?

A

Image hip as the denosumab causes atypical femoral neck fx so the pain may be due to denosumab and not dz progression

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20
Q

Explain why Ph + ALL has aggressive biology (of note it is usually L2 morphology and CD10+ and CD20+)

A

Often has many epigenetic changes downstream of BCR-ABL that contribute to its aggressive biology

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21
Q

How does T cell ALL often present?

A

Can present with marked leukocytosis, mediastinal dz given that T cells mature in thymus and CNS dz

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22
Q

Which drug is a BiTE?

A

Blinatumumab (Blincyto) BiTE = Bispecific T cell Engager; it works by directing CD8+ T cells to CD19 expressing B cells and so is used in refractory or relapsed ALL

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23
Q

What is the mechanism of action of Inotuzumab ozogamicin and what is its clinical use?

A

Anti-CD22 immunoconjugate carrying calicheamicin (ozogamicin) and is internalized by B-Cell ALL cells and causes double stranded DNA breaks and apoptosis

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24
Q

What is the most common AE of Cladribine when used to Tx Hairy Cell Leukemia?

A

Fever, thought to be due to release of cytokines from the apoptotic hairy cells; NSAIDs good for these fevers

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25
Q

What drug is a peptide thrombopoetin mimetic? Non-peptide thrombopoeitin mimetic?

A

Romiplostin consists of IgG Fc fragment with thrombopoeitin (TPO) peptides attached; Eltrombopag is non-peptide thrombopoeitin mimetic

26
Q

What drug is approved for 5-FU and capecitabine overdoses?

A

Uridine Triacetate

27
Q

What is the mechanism of action of Blinatumumab? Clinical use?

A

It is a Bispecific T-cell Engager that directs CD8+ T cells to CD19 which is expressed on B cells; used in relapsed or refractory B-cell ALL

28
Q

When anticoagulation needed in setting of DVT in cancer most clinical practice guidelines say to continue AC for how long?

A

As long as the cancer is active; LMWH (lovenox) preferred

29
Q

Cancer cells that overexpress folate carrier type 1 susceptible to this

A

Praletrexate, enters via folate carrier type 1

30
Q

All pts with ALL need ppx for what sanctuary site?

A

CNS (intrathecal MTX or Ara-C OR HD MTX given systemically)

31
Q

How do you treat engraftment syndrome?

A

Steroids

32
Q

Name two agents that have shown shown single agent activity in relapsed or refractory B-cell ALL

A

Inotuzumab ozogamicin and Blinatumumab

33
Q

These tend to be CD34+, CD117+, CD123+, and HLA-DR +

A

Blasts

34
Q

This tends to be CD11c + and CD103+

A

Hairy Cell Leukemia

35
Q

When doing allo-HSCT, is it better to have a CMV + donor or CMV -

A

CMV + because the donor will be able to mount a more robust immune response should a CMV reactivation occur

36
Q

How is Hypodiploidy defined in ALL? Effect on prognosis?

A

Less than 44 chromosomes; poor prognosis

37
Q

What are the most common toxicities of asparaginase?

A

Hepatic and Pancreatic (pancreatitis very common, monitor); I saw a pt die of hepatic failure

38
Q

Why do patients with Hairy Cell Leukemia on Cladribine get febrile?

A

Cladribine leads to apoptosis of the Hairy Cells and this can cause fevers; should still work up for infectious cause

39
Q

What is Romiplostin?

A

A peptide based Thrombopoetin analog consisting of IgG Fc fragment with 4-14 amino acid TPO peptides attached; in contrast to Eltrombopag which is non-peptide TPO analog

40
Q

B7 ligand is present on APCs and interacts with CD28 (costimulatory signal on T cell) what are the two subtypes of B7 ligand

A

B7-1 is CD80, B7-2 is CD86

41
Q

When does VZV most commonly occur following a allo-HSCT?

A

It is a common late phase infection i.e. after 100 days

42
Q

What is the drug Uridine Triacetate approved for?

A

5-FU and Capecitabine overdose

43
Q

What setting is Nelaribine used in ALL?

A

Sometimes used in relapsed T-cell ALL

44
Q

Routine prophylaxis of ambulatory cancer is not generally recommended except in what situation?

A

When thalidomide or lenalidomide are being used, very high DVT risk; LMWH (lovenox) preffered

45
Q

Explain how CTLA-4 inhibitors “unleash” the immune system

A

Basically when a T cell binds an antigen the CD28 receptor on T cell and B7 on the APC (2 subtypes) interact and lead to T cell proliferation; in response to this CTLA is upregulated on the T cell and competes for CD28 to prevent overactivation of the immune system but ipilimumab blocks CTLA-4 allowing the immune system to go nuts

46
Q

What are the 6 poor risk groups in ALL?

A

Hypodiploidy, t(v;11q23) MLL rearranged; t(11:14), t(4;11), t(9;22), complex karyotype (more than 5 chromosomal abnormalities)

47
Q

What are the treatment options for PD-1 and Ipilimumab related GI toxicity?

A

GI toxicity is autoimmune mediated so it is autoimmune colitis; tx is with steroids and in refractory cases infliximab

48
Q

The studies showing that Ph + ALL need allo-HSCT in first remission were done before what “era”?

A

The imatinib era, they probably still need allo HSCT but just keep in mind they were not on TKIs in these studies

49
Q

True or False: TEL-AML1 gene rearrangements t(12;21)(p13;q22) is a good cytogenetic risk in ALL

A

True, as is hyperdiploidy i.e. 51-65 chromosomes

50
Q

These tend to be CD19+, CD20+, CD22+, CD79+, and PAX5+

A

B-Cells

51
Q

BCR-ABL p190 most commonly occurs in this setting ____ whereas p210 is most common here ______

A

p190 more common in ALL though p210 possible; p210 more common in CML though p190 still possible

52
Q

What two drugs have been implicated in Transplant Associated Thrombotic Microangiopathy

A

Cyclosporine and Tacrolimus

53
Q

What is Eltrombopag?

A

A non-peptide thrombopoeitin analog; in contrast to Romiplostin which is a peptide based thrombopoetin mimetic

54
Q

What is CD45

A

The Leukocyte common antigen

55
Q

What is Engraftment Syndrome?

A

A condition in which a person develops a febrile syndrome during neutrophil recovery following a transplant; fever and skin rash in addition to pulmonary leak are common

56
Q

How is complex karyotype defined in ALL

A

More than 5 cytogenetic abnormalities

57
Q

Thymic T-ALL confers a better prognosis and often expresses this _____

A

CD1a

58
Q

What are some ways that CMV reactivation can present in the transplant setting?

A

Hepatitis, Pneumonitis, Retinitis, and Encephalitis

59
Q

What is true of TEL-AML1 gene rearrangements in childhood ALL and adult ALL?

A

Both associated with favorable prognosis, occurs in 20% of childhood ALL but only 2% of adult ALL

60
Q

How does praletrexate (anti-folate drug) enter the cancer cell

A

Via folate carrier type 1

61
Q

Maintenance therapy with this regiment is common in ALL

A

POMP