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Double hit diffuse large b cell lymphoma

Double hit diffuse large b cell lymphoma





Valid till 2017/5/25



Double hit lymphoma studies hot topic in Blood, at ASH Annual Meeting. Double hit lymphoma Currently found primarily in diffuse large B-cell lymphoma. Abstract. Identification of large B-cell lymphomas that are “extra-aggressive” and may require therapy other than that used for diffuse large B. Abstract: Although diffuse large B-cell lymphoma (DLBCL) is curable with standard chemoimmunotherapy, over 30% of patients with advanced stage disease experience.
Diagnosis of DLBCL is made by removing a portion of the tumor through a biopsyand then examining this tissue using a microscope. UpToDate synthesizes the most recent medical information into evidence-based practical recommendations that healthcare professionals trust to make the right point-of-care decisions. Diffuse large B-cell lymphoma Double-Hit 6 Dec Gisselbrecht et al, JCO ; 2: Several intensive treatment regimens are available.
Double hit lymphoma studies hot topic in Blood, at ASH Annual Meeting. Double hit lymphoma Currently found primarily in diffuse large B-cell lymphoma. Abstract. Identification of large B-cell lymphomas that are “extra-aggressive” and may require therapy other than that used for diffuse large B. Abstract: Although diffuse large B-cell lymphoma (DLBCL) is curable with standard chemoimmunotherapy, over 30% of patients with advanced stage disease experience.

double hit diffuse large b cell lymphoma

double hit diffuse large b cell lymphoma

double hit diffuse large b cell lymphoma

double hit diffuse large b cell lymphoma

double hit diffuse large b cell lymphoma

double hit diffuse large b cell lymphoma

double hit diffuse large b cell lymphoma

double hit diffuse large b cell lymphoma

Logiciel montage diffuse large cell lymphoma hit b double for

The names of different drug combinations often are derived from the first letter of each of the drugs used e. As a result of the BCL6 – mediated repression of TP53 , 73 somatic hypermutation and class switch recombination are facilitated. The revision of the World Health Organization classification of lymphoid neoplasms. Concurrent activation of a novel putative transforming gene, myeov, and cyclin D1 in a subset of multiple myeloma cell lines with t 11;14 q13;q Double hit lymphoma refers to those whose DLBC has two adverse genetic mutations.

The tumour microenvironment is quickly becoming a topic of interest as it has been for years with follicular lymphoma. What this refers to is how the normal immune cells surrounding the tumour affect how the lymphoma behaves and ifs effect on the prognosis.

It is not just the cancer cells themselves that determine the prognosis. See our DLBC microenvironment page for more details. Many patients will be cured using this chemotherapy regimen.

A “cure” is generally defined as 5 year disease free survival. The aggressive nature of DLBC means that if it has not relapsed within 5 years it is statistically highly unlikely that it ever will.

In fact the vast majority of relapses occur within the first 2 years following treatment. While a relapse after 5 years is unlikely it does occur in a small subset of patients. Studies seemed to show that by intensifying the regimen to 14 days there were better results.

It examines how he approaches the treatment of elderly patients with DLBC. Note that the treatment approach for younger patients may often be more aggressive due to their better health status.

Perhaps the next question to ask is if these results for elderly patients over 60 also apply to younger patients. In the study above Dr. Pfreundshuh notes that he does not consider 60 to be elderly but rather around 75, and perhaps even older than that if the person is in otherwise good health.

A persons performance status is what determines their age rather than the number of years they have lived. Work is being done to change that and a lot of progress has been made.

Several clinical studies have been done where adding various other agents to the chemotherapy regimen have improved the survival of ABC patients to nearly the same as the GBC patients.

Lenalidomide is one example Read the review article below. The DA means Dose Adjusted. The dose adjustment allows the doctors to tailor the drug doses to the patient to achieve optimum efficacy while keeping the toxicity in check.

Where this particular protocol is showing the most promise is for those patients with higher risk factors and poorer prognosis DLBC. Below is one recent study regarding this protocol. There are many ongoing studies using different drugs to replace Doxorubicin.

Pixantrone is getting a lot of attention. Some of the other anthracyclines are showing promise, by having equal efficacy, but lower cardiac toxicity. A small study about Amrubicin, showed excellent results and no cardiac toxicity.

Of greater concern is the risk of having a relapse with central nervous system involvement. There is currently no consensus on what is the best treatment for patients who present with very high risk disease.

One option is chemotherapy followed immediately by an SCT. Bendamustine has been gaining widespread use in follicular lymphoma. There has been less study of using Bendamustine for DLBC, but in one study for the very elderly patients with a median of 85 years of age, Bendamustine and Rituxan achieved impressive results.

Maintenance Rituxan was originally popular for indolent lymphomas. It consistently showed an improvement in progression free survival. But over time studies failed to show that it offered any survival benefit so there is much controversy about it.

Read here for more. Early studies showed no improvement so it never became popular. But later study results started to show some interesting things. Primarily that men clear Rituxan from their system faster than woman which partially explains why men with DLBC have inferior outcomes to women.

Again, murine studies suggest that the interaction between alisertib plus with standard treatments like vincristine and rituximab is synergistic and synthetic lethal in Myc and Bcl-2 co-expressing DLBCL An alternative function of myc is apoptosis, and preclinical studies have demonstrated that bortezomib may increases MYC protein levels and that endogenous MYC is necessary for the induction of apoptosis in the setting of bortezomib.

This kind of MYC-induced cell death is mediated by enhanced expression of the pro-apoptotic BCL2 family members, suggesting combinations of bortezomib with chemotherapy or bcl-2 inhibitors could have activity in double hit DLBCL Bromodomains are conserved protein regions that recognize specific histone modifications.

Bromodomain inhibition reduces tumor growth in lymphomas, and it is felt this may be largely through the disruption of transcriptional networks driven by oncogenic MYC The small molecule JQ1 suppresses c-MYC expression through inhibition of the bromodomain and extra-terminal family of bromodomain proteins.

Similar results have been demonstrated in primary effusion lymphomas, suggesting that bromodomain inhibitor activity may not be limited to translocations involving MYC and they may have activity where c-Myc protein is deregulated at the post-translational level, such as FISH negative, IHC positive double hit DLBCL The mechanisms leading to poor outcome in double hit DLBCL are unclear, but involve more than myc dysregulation, since Burkitt lymphoma, also involving myc, has a superior prognosis.

The synergistic action of myc and bcl-2, and other molecular features such as genetic complexity both contribute to poor outcome in patients with double hit DLBCL 45 , The existing literature is not adequate to answer the question of optimal therapy for double hit biology DLBCL.

It is clear that R-CHOP needs to be replaced for this group of patients; however, there are no prospective trials suggesting alternatives. Age and frailty of this population of patients will limit the role of dose-escalated or intensified therapy.

It is likely that rational combinations of novel targeted agents with standard chemoimmunotherapy platforms will ultimately provide the highest impact for double hit, and other molecularly defined subsets of DLBCL Double hit diffuse large B-cell lymphomas: Use of immunohistochemistry to define myc positive disease All of the aforementioned series utilized FISH to determine the presence of a myc rearrangement.

Treatment approaches to double hit DLBCL Although the prognosis of double hit lymphoma, defined either by FISH or immunohistochemistry, is clearly poor with R-CHOP, there is very limited data evaluating alternative therapy, and no published prospective data focused on this patient population.

Novel approaches and future directions Novel agents with particular promise in these patients with double hit DLBCL may include small molecule inhibitors of bcl The author declares no conflict of interest.

Introduction of combined CHOP plus rituximab therapy dramatically improved outcome of diffuse large B-cell lymphoma in British Columbia. J Clin Oncol ; N Engl J Med ; Molecular diagnosis of the hematologic cancers.

Stromal gene signatures in large-B-cell lymphomas. Molecular profiling of diffuse large B-cell lymphoma identifies robust subtypes including one characterized by host inflammatory response.

Burkitt lymphoma in adults. Double-hit diffuse large B-cell lymphoma. Rearrangement of MYC is associated with poor prognosis in patients with diffuse large B-cell lymphoma treated in the era of rituximab.

Aberrations of the MYC gene in unselected cases of diffuse large B-cell lymphoma are rare and unpredictable by morphological or immunohistochemical assessment. J Clin Pathol ; Eur J Haematol ; MYC-associated and double-hit lymphomas: Immunohistochemical detection of MYC-driven diffuse large B-cell lymphomas.

Immunohistochemical double-hit score is a strong predictor of outcome in patients with diffuse large B-cell lymphoma treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone.

Concurrent expression of MYC and BCL2 in diffuse large B-cell lymphoma treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone.

Outcomes of patients with Burkitt lymphoma older than age 40 treated with intensive chemotherapeutic regimens. In a recent analysis from British Columbia, the incidence of myc and bcl-2 genetic alterations and their clinical significance were largely dependent on cell-of-origin subtypes.

In the setting of myc translocation, bcl-2 translocation association with poor outcome was limited to GCB lymphoma. There are similar limitations to using the Ki proliferation index or MYC expression on immunohistochemistry to determine which cases should be referred for FISH evaluation of translocations.

A recently published analysis of cases of aggressive lymphoma included 7. For example, in a study from the University of Pennsylvania, double-hit status could not be inferred by any baseline disease – or patient-related characteristics.

If resources preclude this broad approach, the majority of double-hit cases are of the GCB subtype Figure 2 and express MYC on immunohistochemistry, so limiting testing to this group is an acceptable, but inferior alternative.

In addition to de novo disease, double-hit lymphoma occurs in the setting of transformation of underlying indolent lymphoma, particularly follicular lymphoma, when this t 14;18 lymphoma acquires a myc translocation.

Exceptions include patients who present with early-stage disease, where CSF involvement is much less common, or frail elderly patients, where treatment with curative intent is contraindicated. When performed, CSF should always be analyzed with flow cytometry, given its substantially increased sensitivity as compared with routine cytological analysis.

As previously noted, the outcome of patients with double-hit lymphoma treated with conventional RCHOP chemotherapy is poor. Unfortunately, there are no published prospective trials in the setting of double-hit lymphoma.

These patients represent the greatest unmet clinical need in DLBCL according to a recent clinical trials planning meeting from the National Cancer Institute National Clinical Trials Network, and prospective randomized trials are currently being developed for double-hit lymphoma, as well as for the larger group of double-expressor lymphoma.

Intensive induction was associated with improved progression-free survival and improved overall survival on multivariable analysis. A small subset of patients with low LDH and early-stage disease had excellent outcomes.

Patients with bone marrow involvement and poor performance status had the worst prognosis. Double-hit lymphoma is associated with advanced age in many of these retrospective experiences.

Further support of the R-EPOCH regimen is provided by results from a German randomized trial in younger patients with high-risk aggressive B-cell lymphoma demonstrating high event-free survival with the R-CHOEP regimen cyclophosphamide, doxorubicin, vincristine, etoposide, prednisone every 14 days, which, similar to R-EPOCH, intensifies the treatment interval and incorporates etoposide into the regimen.

Despite the limitations of these data, I currently approach most patients with double-hit lymphoma by using the dose-adjusted R-EPOCH regimen. The National Clinical Trials network is planning to conduct a randomized trial for patients with double-expressor lymphoma, including double-hit lymphoma.

As previously noted, it is not uncommon for patients with follicular lymphoma who experience histologic transformation to acquire a myc translocation, resulting in a double-hit lymphoma.

There are no trials to guide the management of these patients, who again are often elderly and not infrequently extensively pretreated with various chemotherapy regimens for follicular lymphoma.

For the majority of other patients who have had prior anthracycline, I consider a salvage lymphoma regimen followed by ASCT. The standard curative approach to the treatment of relapsed aggressive lymphoma in patients who are fit is to administer non—cross-resistant salvage chemotherapy followed by consolidation with high-dose therapy and ASCT.

Novel agents with particular promise in patients with double-hit DLBCL may include small molecule inhibitors of BCL-2, such as venetoclax, which has demonstrated in vivo efficacy against aggressive myc – driven mouse lymphomas 63 and has been studied in patients with relapsed lymphoma with limited activity in aggressive histologies.

Bromodomain inhibition reduces tumor growth in lymphomas, in part through the disruption of myc – driven transcriptional networks. JQ1 treatment significantly suppressed growth of DLBCL cells engrafted in mice, including myc-rearranged DLBCL, 66 and several bromodomain inhibitors are currently under study in myc-associated lymphomas.

Synergy has been demonstrated when venetoclax is combined with JQ1 in vitro. At present, I consider a trial of chimeric antigen receptor T cells a preferred option for fit patients with refractory double-hit lymphoma.

For the patient presented in the first case, given the triple-hit status and retrospective studies suggesting a benefit to aggressive induction approaches, I would advise that the patient be switched to dose-adjusted R-EPOCH for subsequent cycles.

He should receive a total of 6 cycles of induction therapy, with appropriate dose escalations as mandated in the original publications on R-EPOCH. Given the high-risk nature of the bone destruction, I would immediately consult with an orthopedic surgical oncologist to ensure there is stability and no rod placement is indicated.

For the patient in the second case, he was started on appropriate induction therapy for double-hit lymphoma with dose-adjusted R-EPOCH. At baseline, his CNS risk score was high given the renal involvement and high-risk International Prognostic Index score.

As previously noted, this is a common site leading to treatment failure in double-hit lymphoma, and unfortunately his expected outcome is poor. I would place an Ommaya reservoir to facilitate frequent intrathecal therapy with methotrexate, with the goal of achieving a negative CSF as quickly as possible.

There is inadequate data to guide the management of this uncommon, high-risk scenario. A recently published phase 2 study demonstrated the efficacy of high-dose methotrexate and cytarabine, followed by intensification, high-dose therapy, and ASCT for secondary CNS lymphoma.

Double-hit status was not reported. These results are similar to another phase 2 trial incorporating thiotepa into ASCT after aggressive salvage therapy. We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail.

We do not retain these email addresses. Skip to main content. Abstract The revision of the World Health Organization WHO classification for lymphoma has included a new category of lymphoma, separate from diffuse large B-cell lymphoma, termed high-grade B-cell lymphoma with translocations involving myc and bcl-2 or bcl Case presentation 1 A year-old man presents with a 2-month history of left hip pain.

Case presentation 2 A year-old man presented with progressive fatigue and right shoulder pain. View inline View popup. Terminology of myc-associated disease. Which lymphomas should be evaluated for double-hit status?

How do I evaluate patients with double-hit lymphoma? How do I treat patients with de novo double-hit lymphoma? How do I treat patients with double-hit lymphoma occurring in the setting of transformed follicular lymphoma?

Relapsed double-hit lymphoma and novel agents The standard curative approach to the treatment of relapsed aggressive lymphoma in patients who are fit is to administer non—cross-resistant salvage chemotherapy followed by consolidation with high-dose therapy and ASCT.

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All myc rearranged cases had increased myc protein expression using this immunohistochemical assay; there were four additional cases that were negative on FISH but had increased protein expression.

These cases had confirmed increased myc transcriptional activity by gene set enrichment analysis, suggesting alternative mechanisms for myc deregulation in these cases. Importantly, these cases had similar poor outcome, inferior to patients without this abnormality, as those cased detected by FISH.

The group from Denmark evaluated cases of DLBCL uniformly treated with R-CHOP therapy, and performed routine staining for myc, bcl-2 as well as markers allowing for cell of origin classification In addition, FISH was performed for detection of myc rearrangement and for t 14 ; Poor outcome was only observed in the double hit cases.

These cases had similar inferior overall survival on multivariate analysis, controlled for clinical and molecular prognostic factors, specifically germinal center genotype vs.

These results were confirmed in a validation set. Johnson and colleagues from British Columbia used a similar platform to evaluate prospective cases of DLBCL with immunohistochemical stains for bcl-2 and myc Increased myc was only predictive of outcome if increased bcl-2 was also present, and these results were also validated in an independent cohort after adjusting for clinical and molecular high risk features.

Concurrent overexpression of myc and bcl-2 is present in both germinal center and activated B-cell DLBCL suggesting heterogeneous molecular pathways may be responsible for myc deregulation, but the impact of these pathways results in a universally poor outcome with conventional therapy.

Although the prognosis of double hit lymphoma, defined either by FISH or immunohistochemistry, is clearly poor with R-CHOP, there is very limited data evaluating alternative therapy, and no published prospective data focused on this patient population.

It is clear from the aforementioned studies that R-CHOP is not sufficient induction therapy for this group of patients, as the majority of patients will experience disease progression after standard treatment.

As myc positivity is present in Burkitt lymphoma, and Burkitt lymphoma has superior outcomes with more aggressive chemotherapy regimens 8 , 26 , several have advocated for a more aggressive approach to patients with double hit DLBCL.

Whether or not this will impact patients in a favorable way is not yet clear from limited published series. We have subsequently identified a subset of these patients with double hit histology.

Patients who were able to receive ASCT appeared to have superior outcome, but early progression and refractory disease limited the efficacy of this approach. In the Vancouver and Denmark series, the median age of patients with double hit DLBCL by IHC exceeded 65 years, making dose escalation a challenge for the majority of patients with this high risk feature.

Dunleavy, personal communication, but the frequency of patients with double hit disease is very low, and follow-up to date is short. Recently, a large group of investigators pooled data for a multicenter retrospective analysis addressing the impact of induction regimen on stem cell transplantation on outcomes in double hit DLBCL Intensive induction was associated with improved progression-free survival, and ASCT was not associated with improved overall survival.

When the authors tried to adjust for clinical risk factors, intensive induction appeared to be associated with improved overall survival. Novel agents with particular promise in these patients with double hit DLBCL may include small molecule inhibitors of bcl Using cell lines with t ABT, a more specific and safer bcl-2 inhibitor is currently in clinical trials This agent has been shown to have in vivo efficacy against aggressive Myc-driven mouse lymphomas Combinations of standard chemoimmunotherapy and ABT are currently in clinical trials, and it may be of particular interest to study patients with double hit DLBCL.

Another approach of interest results from the fact that myc induces aurora A kinase, and blocking aurora A kinase activity in a murine model system triggers apoptosis of myc-driven DLBCL Alisertib, a specific inhibitor of aurora A kinase, is currently under clinical development in DLBCL, and preliminary results suggest significant anti-tumor activity Again, murine studies suggest that the interaction between alisertib plus with standard treatments like vincristine and rituximab is synergistic and synthetic lethal in Myc and Bcl-2 co-expressing DLBCL An alternative function of myc is apoptosis, and preclinical studies have demonstrated that bortezomib may increases MYC protein levels and that endogenous MYC is necessary for the induction of apoptosis in the setting of bortezomib.

This kind of MYC-induced cell death is mediated by enhanced expression of the pro-apoptotic BCL2 family members, suggesting combinations of bortezomib with chemotherapy or bcl-2 inhibitors could have activity in double hit DLBCL Bromodomains are conserved protein regions that recognize specific histone modifications.

Bromodomain inhibition reduces tumor growth in lymphomas, and it is felt this may be largely through the disruption of transcriptional networks driven by oncogenic MYC The small molecule JQ1 suppresses c-MYC expression through inhibition of the bromodomain and extra-terminal family of bromodomain proteins.

Similar results have been demonstrated in primary effusion lymphomas, suggesting that bromodomain inhibitor activity may not be limited to translocations involving MYC and they may have activity where c-Myc protein is deregulated at the post-translational level, such as FISH negative, IHC positive double hit DLBCL The mechanisms leading to poor outcome in double hit DLBCL are unclear, but involve more than myc dysregulation, since Burkitt lymphoma, also involving myc, has a superior prognosis.

The synergistic action of myc and bcl-2, and other molecular features such as genetic complexity both contribute to poor outcome in patients with double hit DLBCL 45 , The existing literature is not adequate to answer the question of optimal therapy for double hit biology DLBCL.

It is clear that R-CHOP needs to be replaced for this group of patients; however, there are no prospective trials suggesting alternatives. Age and frailty of this population of patients will limit the role of dose-escalated or intensified therapy.

It is likely that rational combinations of novel targeted agents with standard chemoimmunotherapy platforms will ultimately provide the highest impact for double hit, and other molecularly defined subsets of DLBCL Double hit diffuse large B-cell lymphomas: Use of immunohistochemistry to define myc positive disease All of the aforementioned series utilized FISH to determine the presence of a myc rearrangement.

Treatment approaches to double hit DLBCL Although the prognosis of double hit lymphoma, defined either by FISH or immunohistochemistry, is clearly poor with R-CHOP, there is very limited data evaluating alternative therapy, and no published prospective data focused on this patient population.

Novel approaches and future directions Novel agents with particular promise in these patients with double hit DLBCL may include small molecule inhibitors of bcl The author declares no conflict of interest.

Introduction of combined CHOP plus rituximab therapy dramatically improved outcome of diffuse large B-cell lymphoma in British Columbia. J Clin Oncol ; N Engl J Med ; Molecular diagnosis of the hematologic cancers.

Stromal gene signatures in large-B-cell lymphomas. Primary mediastinal large B-cell lymphoma: Can occur at any time from early adulthood, but is most common between years of age. It is twice as common in women as in men.

Develops in the mediastinum in the chest and can cause problems due to the pressure of the mass on the lungs or gut, or on the superior vena cava the second largest vein in the body which returns blood from the upper half of the body to the heart.

Symptoms include breathlessness, persistent cough, difficulty swallowing dysphagia, swelling of the neck and face, dizziness and headaches. Treatment involves the use of R-CHOP often followed by radiotherapy or high-dose chemotherapy regimens.

Stem cell transplants may be offered if this type of lymphoma relapses. This type of DLBCL has all three types of cells present – T-cells, histiocytes and large B-cells, when viewing a biopsy specimen under the microscope.

Symptoms include swollen lymph nodes, fever and swelling of the liver or spleen. People with this type of DLBCL will feel generally unwell and have abdominal swelling and discomfort.

If it relapses, the other high-dose chemotherapy regimens mentioned below may be used. Stem cell transplantation may also be an option for some people. Intravascular large B-cell lymphoma: Occurs in adults with the average age at diagnosis being 65 years.

Malignant lymphocytes are found within small blood vessels meaning it could affect just about any part of the body, although it is rare to find it in the bone marrow or lymph nodes.

These symptoms are a result of the impact of the lymphoma on the nervous system. Some people may also develop patches of inflamed skin across their body or experience fevers, night sweats and unexplained weight loss.

How does Diffuse Large B-cell lymphoma affect the body?

Should these patients with CNS involvement obtain a remission, I consider consolidation with high-dose therapy and autologous hematopoietic cell transplantation AHCT.

Finally, for the small subset of patients with limited-stage DLBCL who present with double-hit lymphoma, but normal LDH, and no other clinical risk factors, I generally use a combined modality regimen of R-CHOP followed by radiation therapy consolidation, given the favorable prognosis and limited data supporting this approach.

Double-hit lymphoma can occur in the setting of transformation of underlying indolent lymphoma, particularly follicular lymphoma, when this t 14;18 lymphoma acquires an MYC translocation.

These patients are often older and extensively pretreated with various chemotherapy regimens. For most other patients who have had prior anthracycline, I consider a salvage lymphoma regimen followed by AHCT.

The standard curative approach to the treatment of relapsed aggressive lymphoma in fit patients is to administer non—cross-resistant salvage chemotherapy followed by consolidation with high-dose therapy and AHCT, but outcomes in patients with MYC – rearranged disease are poor.

Based on results from retrospective analyses, if a patient with double-hit lymphoma was treated with intensive induction and still experienced progressive disease, I would refer him or her to a clinical trial involving novel agents rather than trying conventional salvage therapy.

Novel agents with promise in patients with double-hit DLBCL include small molecule inhibitors of BCL2 , such as venetoclax, which has been studied in patients with relapsed lymphoma with limited activity in aggressive histologies.

Several bromodomain inhibitors are also under investigation in MYC-associated lymphomas. At present, I consider a trial of CAR T cells a preferred option for fit patients with refractory double-hit lymphoma.

Log into your account. November, Volume 3, Issue October, Volume 3, Issue Focus on Immunotherapy October, Volume 3, Issue September, Volume 3, Issue FISH testing for double-hit status should be performed in newly diagnosed aggressive large B-cell lymphoma, but can be restricted to GCB subtype lymphomas and those that express MYC on immunohistochemistry.

Because patients with MYC – rearranged lymphoma have an increased risk of CNS involvement, baseline lumbar puncture and CSF sampling is recommended in most patients with double-hit lymphoma.

Treating Double-Hit Lymphoma Patients with double-hit lymphomas have a poor prognosis when treated with standard chemoimmunotherapy. Transformed Double-Hit Lymphoma Double-hit lymphoma can occur in the setting of transformation of underlying indolent lymphoma, particularly follicular lymphoma, when this t 14;18 lymphoma acquires an MYC translocation.

Relapsed Double-Hit Lymphoma The standard curative approach to the treatment of relapsed aggressive lymphoma in fit patients is to administer non—cross-resistant salvage chemotherapy followed by consolidation with high-dose therapy and AHCT, but outcomes in patients with MYC – rearranged disease are poor.

Future Directions Novel agents with promise in patients with double-hit DLBCL include small molecule inhibitors of BCL2 , such as venetoclax, which has been studied in patients with relapsed lymphoma with limited activity in aggressive histologies.

Evolution of B-cell malignancy: C-MYC translocation in t 14;18 positive follicular lymphoma at presentation: An adverse prognostic indicator? B cell lymphoma, unclassifiable, with features intermediate between diffuse large B cell lymphoma and Burkitt lymphoma.

Salaverria I, Siebert R. Molecular distinctions between pediatric and adult mature B-cell non-Hodgkin lymphomas identified through genomic profiling. Lin P, Medeiros LJ. High-grade B cell lymphoma, unclassifiable, with blastoid features: Adult B-cell lymphomas with burkitt-like morphology are phenotypically and genotypically heterogeneous with aggressive clinical behavior.

MYC rearrangements are useful for predicting outcomes following rituximab and chemotherapy: B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma and burkitt lymphoma: Prognostic value of MYC rearrangement in cases of B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma and Burkitt lymphoma.

Does the proliferation fraction help identify mature B cell lymphomas with double – and triple-hit translocations? Burkitt lymphoma and atypical Burkitt or Burkitt-like lymphoma: Curr Hematol Malig Rep.

Inactivating mutations of acetyltransferase genes in B-cell lymphoma. Analysis of the coding genome of diffuse large B-cell lymphoma. Frequent mutation of histone-modifying genes in non-Hodgkin lymphoma.

Concurrent expression of MYC and BCL2 in diffuse large B-cell lymphoma treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone. Proposed that the poor prognosis of ABC type was related to MYC expression rather than stage of cell differentiation or cell of origin per se.

Rapid generation of human B-cell lymphomas via combined expression of Myc and Bcl2 and their use as a preclinical model for biological therapies. Simple karyotype and bcl-6 expression predict a diagnosis of Burkitt lymphoma and better survival in IG-MYC rearranged high-grade B-cell lymphomas.

Paramount prognostic factors that guide therapeutic strategies in diffuse large B-cell lymphoma. Cite article How to cite?

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The Table of Neoplasms should be used to identify the correct topography code. This may include people who have previously been treated for other forms of cancer including a low-grade lymphoma, or people who have an autoimmune disorder. An adverse prognostic indicator? As reported by the LNH A molecular cytogenetic test, using fluorescent in situ hybridization FISH, revealed significant concurrent chromosomal translocations: Click here for more information.

Expert Perspective on ASH I hope we can help. Inhibition of bromodomain proteins for the treatment of human diffuse large B-cell lymphoma. Another approach of interest results from the fact that myc induces aurora A kinase, and blocking aurora A kinase activity in a murine model system triggers apoptosis of myc-driven DLBCL

Concurrent expression of MYC and BCL2 in diffuse large B-cell lymphoma treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone. Organs or structures that are part of the lymphatic system, such as the lymph nodes, spleen, and thymus gland. Occurs in patients who are greater than 50 years old and have no known immunodeficiency or history of lymphoma.

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Double-hit status was not reported. Outcomes of patients with Burkitt lymphoma older than age 40 treated with intensive chemotherapeutic regimens. Follicular lymphoma, grade 2. See…

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