Lymphoma/Leukemia Flashcards
Follicular lymphoma and >15centroblasts/hpf and solid sheets of centrolblasts
3B - treat as if DLBCL
CD20
b cell marker except Hodgkin
Treatment for Hodgkin Lymphoma early stage unfavorable not bulky
abvd x 3 and PET neg then no further (RAPID trial)
abvd x 4 and 30 gy
small/medium CD5+, CD10-
MCL or SLL
MCL is CD23-
SLL is CD23+
Treatment for Hodgkin Lymphoma early stage favorable
ABVD x 2 PET then XRT x 20gray
or ABVD x 3
bilateral breast implants
ALCL
Hodgkin Lymphoma
CD15+,CD30+, CD20- CD45+
ALCL also same pattern
Second line therapy HL
chemo f/b HDT/ASCT
CD45
lymphoid marker
small/medium CD5-, CD10+ (t8:14)
BL
small/medium CD5-, CD10+, BCL6+ (t14:18)
Follicular
4th line HL
NIvolumab
Third line for Hodgkin
Brentuximab
small/medium CD5-, CD10-
MZL unless MYD88+ the LPL
CD10+
follicular and burkitts
follicular and ritux
stop after four doses and retreat when develops progression. No need to give maintenance.
follow-up for DLBCL
no scans!
Hodgkin late stage treatment
dont radiate
unfavorable risk factors for HL
3 sites, ESR 50, bulky is greater than 10cm
CD23+
CLL if CD5+
mycosis fungoides with sezary cells - first line treatment not getting better with topicals
HDAC inhibitor
primary mediastinal DLBCL
REPOCH x 6
Pregnant woman hodgkin
ABVD second trimester
Treatment for Hodgkin Lymphoma early stage bulky
abvd 4 - 6 + 30 gy XRT
PTLD
he tumors that occur early are generally of B cell origin and uniformly positive for EBV, and the tumors that occur late may be negative for EBV and of T-cell origin. The early-occurring tumors often regress following withdrawal of immunosuppression. In contrast, withdrawal of immunosuppression for the monoclonal tumors may result in resolution of the tumor, but that is generally short-term. In general, tumors that develop late require treatment with aggressive chemotherapy. Additional treatment strategies currently being studied include the use of rituximab alone or in combination with chemotherapy, and EBV-specific cytotoxic T-lymphocytes.
PTLD most frequently originates from donor lymphocytes following an allogeneic transplant and occurs more frequently with T-cell depletion. There is also an association of increased risk when the donor is EBV or CMV positive and the recipient is EBV or CMV negative.
Following a solid organ transplant, PTLDs typically originate from host lymphocytes, and, following an allogeneic stem cell transplant, the cells originate from donor lymphocytes. There are four types of PTLDs: (1) early lesions with plasmacytic hyperplasia and infectious mononucleosis-like changes, (2) polymorphic PTLD, which are polyclonal or monoclonal lymphoid infiltrates with evidence of malignant transformation but do not meet all the criteria for one of the B-cell or T-cell lymphomas recognized in the immunocompetent patient, (3) monomorphic PTLD has monoclonal lymphoid proliferations satisfying criteria for a B-cell or T-cell lymphoma in an immunocompetent patient, and (4) classic Hodgkin lymphoma type, which is less common and almost always associated with EBV.
Staging and diagnosis of active myeloma
clonal population of plasma cells greater than 10% on biopsy or extramedullary plasmacytoma with any one of the following: elevated calcium greater than 11 mg/dL, renal insufficiency creatinine greater than 2.0 mg/dL or glomerular filtration rate (GFR) less than 40 mL/min/1.73m^2; anemia hemoglobin less than 10 g/dL or 2 g/dL below the lower limit; one or more osteolytic bone lesions; clonal marrow plasma cells greater than 60% and an abnormal free light chain ratio of greater than 100; or one focal lesion on MRI greater than 5 mm.
According to the ISS, stage III disease is classified as beta-2 microglobulin at greater than 5.5 ug/mL and stage I disease is classified as beta-2 microglobulin at less than 3.5 ug/mL with albumin greater than 3.5 g/dL. Stage II disease is the area in between. For the R-ISS, stage I disease is defined by standard-risk cytogenetics and normal LDH, stage III is high-risk cytogenetics with elevated LDH, and stage II falls in between. At present, high risk indicates the presence of del(17p) and/or translocation t(4;14) and/or translocation t(14;16). It is true that our understanding of smoldering myeloma is evolving with a subset of patients who need earlier intervention. In this case, it is also of note that certain cytogenetics, such as t(11;14), may portend a better prognosis, but this is still not established.
adult ALL
There is no such thing as low risk in adult ALL, and standard risk includes a low WBC count at presentation (<30.0 × 10^9/L [<30 000/μL] for B-lineage and 100.0 × 10^9/L [<100 000/μL] for T-lineage ALL) and age younger than 35 years. While patients with Ph-chromosome positivity have a targeted agent that can be used as an adjunct to chemotherapy, these patients have a worse prognosis compared to Ph-negative patients. Platelets count at presentation does not affect outcome.
Accelerated phase of CML
The two criteria often used to define accelerated phase are the MD Anderson and WHO criteria. Most clinical trials incorporate the modified MD Anderson criteria. Peripheral blasts are between 15% and 30% or peripheral blasts + promyelocytes are over 30%, basophils are 20%, platelets are <100 X 10^9/L , and there may be clonal evolution.
Treatment options for accelerated phase per NCCN guidelines employ a higher doses of typical upfront tyrosine kinase inhibitors (TKIs) either imatinib 600 mg, dasatanib 140 mg, nilotinib 400mg twice a day. For those who have failed or were intolerant to imatanib or other first line TKI, bosutinib 500 mg daily or omacetexine (after two or more prior therapies) can be used. If patient has a known T315I mutation, ponatanib or omacetaxine have demonstrated clinical activity in this resistant clone.
CLL brain toxicity
Think PML from JC virus
del(17p) in CLL
poor response to chemoimmunotherapy
Mycosis fungoides is
CD4+ and CD5
hair cell leukemia patients
Vemurafenib is an oral BRAF inhibitor and interrupts the B-Raf/MEK/ERK pathway if a V600E mutation is present. This mutation has been identified in 95 to 100% of classical hairy cell leukemia.
symptomatic hairy cell leukemia (HCL). The initial therapy of HCL should be a purine analog. The efficacy of a single cycle of infusional cladribine has been established in multiple reports. All other options listed are not appropriate therapy for a patient with symptomatic HCL.
LCL (anaplastic large cell lymphoma
here is an important distinction between primary cutaneous CD30+ ALCL (anaplastic large cell lymphoma) and CD30 + ALCL with systemic disease. ALK+ portends a better prognosis for systemic ALCL when treated with anthracycline based therapy such as CHOP or CHOEP (cyclophosphamide, doxorubicin, vincristine, etoposide, prednisone). In contrast to this; primary cutaneous ALCL is usually ALK negative and typically follows a more indolent course. For this reason it is typically preferable to pursue either surgical excision or radiation even at times when there is limited nodal involvement. Lesions do due tend to recur overtime, but the consensus is to not overtreat these. According to the International T cell Lymphoma Project the 5 year failure-free survival and overall survival rates among patients with primary ALCL were 55% and 90%, respectively.Methotrexate, brentuximab vedoitin (a toxin linked anti CD30 antibody) and pralatrexate, although highly active agents, are reserved for multifocal, systemic or relapsed disease. CHOP based therapy is typically only used for systemic ALCL.
treatment of treatment induced MDS after autoHCT
allo
fever, weight gain, respiratory distress, pulmonary infiltrates, episodic hypotension, and renal failure in treatment for APL
The syndrome is thought to be related to the sudden maturation of promyelocytes. If untreated, the syndrome can be fatal. However, if treated with dexamethasone most disease will rapidly respond within 1 to 3 days. Development of the retinoic acid syndrome is not a contraindication to further therapy with all-trans retinoic acid.
6MP testing
for TPMT!
AML and FLTD3, NPM1
if FLTD3 mutationpositive than alloHCT, if both lacking mutation then transplant. If only NPM1, good prognosis and just do chemo.
Low risk MDS treatment
lenolidamide
High MDS
acatizdine
chromosome 5,7 shortest survival
low counts
blasts
Old pt with AML
acatizidine or decitabine
CML first line TKI, second line
1st: imatinib,
2nd: dasatinib, bosutinib
mutation ponanitn
Hairry cell leukemia
B cell markers and CD103 and TRAP staining
Bilobed
Treatment is often with nucleoside like pentostatin or cladaribine.
Second line is CD20 antibody, BRAF inhibitor, or ibrutinib
MPNs poor prognostic
> 60 or thrombotic complications. Then add hydroxyurea.
