scholarly journals Mantle cell lymphoma treatment options for elderly/unfit patients: A systematic review

eJHaem ◽  
2021 ◽  
Author(s):  
Tahera Alnassfan ◽  
Megan J. Cox‐Pridmore ◽  
Azzam Taktak ◽  
Kathleen J Till
Keyword(s):  
Systematic Review ◽  
Mantle Cell Lymphoma ◽  
Cell Lymphoma ◽  
Treatment Options ◽  
Lymphoma Treatment ◽  
Mantle Cell ◽  
Unfit Patients

Treatment options for mantle cell lymphoma

2015 ◽  
Vol 16 (16) ◽  
pp. 2497-2507 ◽  
Author(s):  
Piotr Smolewski ◽  
Magdalena Witkowska ◽  
Tadeusz Robak
Keyword(s):  
Mantle Cell Lymphoma ◽  
Cell Lymphoma ◽  
Treatment Options ◽  
Mantle Cell

scholarly journals A Rare Prostate Pathology: Mantle Cell Lymphoma: A Case Report and Literature Review

2021 ◽  
Author(s):  
Selman Ünal ◽  
Halil Uzundal ◽  
Turker Soydaş ◽  
Asım Özayar ◽  
Arslan Ardıçoğlu ◽  
...  
Keyword(s):  
Mantle Cell Lymphoma ◽  
Cell Lymphoma ◽  
Treatment Options ◽  
Specific Antigen ◽  
Rare Condition ◽  
Additional Treatment ◽  
Appropriate Treatment ◽  
Histopathologic Diagnosis ◽  
Mantle Cell ◽  
Secondary Lymphoma

Primary or secondary lymphoma of the prostate is a rare condition. Mantle cell lymphoma (MCL) represent 4-9% of all lymphomas. Prostate involvement with MCL is very rare, with only 11 reported cases up to now. Here we present a case with lower urinary tract symptoms and prostate-specific antigen (PSA) elevation diagnosed with MCL of the prostate. Prostate biopsy was performed in a 70-year-old patient due to increased PSA. After the pathology result was reported as prostatic MCL, imaging studies and sampling of additional pathological specimens were performed for staging. An improvement was observed in the urinary system complaints of the patient who started chemotherapy regimen. While prostatectomy was performed in some of the prostatic MCL cases reported previously, in some, no additional treatment was required after chemotherapy. Our case is the only prostatic MCL case with elevated PSA levels, but did not receive the diagnosis of prostate cancer. Physicians should keep in mind that, prostatic MCL can present with nonspecific symptoms. Staging should be performed in patients whose histopathologic diagnosis is lymphoma of the prostate so as to determine appropriate treatment options.

scholarly journals Mantle Cell Lymphoma Mimicking Rectal Carcinoma

2014 ◽  
Vol 2014 ◽  
pp. 1-4
Author(s):  
Engin Kelkitli ◽  
Hilmi Atay ◽  
Levent Yıldız ◽  
Ahmet Bektaş ◽  
Mehmet Turgut
Keyword(s):  
Mantle Cell Lymphoma ◽  
Hodgkin Lymphoma ◽  
Rectal Carcinoma ◽  
Cell Lymphoma ◽  
Treatment Options ◽  
Extranodal Involvement ◽  
Non Hodgkin Lymphoma ◽  
Rectal Involvement ◽  
Mantle Cell ◽  
Rectal Mass

Mantle cell lymphoma (MCL) is a mature B-cell non-Hodgkin lymphoma. After the (11;14) translocation was identified as its constant finding in 1992, MCL was recognized as a separate subgroup of non-Hodgkin lymphoma (NHL). In MCL, extranodal involvement may be observed in the bone marrow, the spleen, the liver, and the gastrointestinal system (GIS). Cases of MCL that present with a massive and solitary rectal mass are rare in the literature. In this case report, our aim was to present an MCL patient with a rarely observed solitary rectal involvement mimicking rectal carcinoma and to discuss treatment options for this patient.

scholarly journals Efficacy of Chemotherapeutic Regimens for Mantle Cell Lymphoma: A Systematic Review of Phase III Trials

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 6-7
Author(s):  
Ali Jaan ◽  
Muhammad Tayyeb ◽  
Farhan Khalid ◽  
Muhammad Khawar Sana ◽  
Zahoor Ahmed ◽  
...  
Keyword(s):  
Systematic Review ◽  
Clinical Trials ◽  
Mantle Cell Lymphoma ◽  
Cell Lymphoma ◽  
Interferon Alfa ◽  
Phase Iii ◽  
Cell Transplant ◽  
Mantle Cell ◽  
Combination Regimens

Background: The mainstay treatment for mantle cell lymphoma (MCL) is chemotherapy ± immunotherapy. The standard chemotherapeutic regimens have limited efficacy in MCL when used alone. In this systematic review, we have assessed the efficacy and safety of various combination regimens for the treatment of MCL evaluated in phase III clinical trials. Methods: We performed a comprehensive systematic literature search on PubMed, Embase, clinicaltrials.gov, and Web of Science databases with the date of inception to May 2020. We used MeSH (Medical Subject Headings) terms for "mantle cell lymphoma", "treatment outcome" along with their keywords, and combined their results. Our search generated a total of 3572 articles. After excluding case reports, case series, observational studies, review articles, meta-analysis, phase I/II clinical trials, and pre-clinical studies, we included five phase III randomized clinical trials (RCTs) reporting the efficacy of combination regimens for MCL treatment. Results Data from five phase III RCTs was pooled with total N=1683 (newly diagnosed (ND), n=1242, relapsed/refractory (RR), n=441). 1610 patients were evaluable. Kluin-Nelemans et al. 2020 (n=560) studied induction with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) vs R-FC (rituximab, fludarabine, and cyclophosphamide) for ND-MCL with follow-up on maintenance with rituximab (R) -vs interferon alfa. At a median follow up of 7.6 years (y), median overall survival (mOS) was 6.4 vs 3.9 y (p=0.0054) in R-CHOP vs R-FC group, respectively. The median progression-free survival (mPFS) and mOS in the R-CHOP cohort on R maintenance were significantly better when compared to those on interferon alfa maintenance (mPFS, 5.4 y vs 1.9 y, p<0.001) (mOS, 9.8 y vs 7.1 y, p=0.0026). Robak et al. (2015) (n=487) assessed bortezomib in ND-MCL by substituting it for vincristine in the standard R-CHOP therapy. A cohort of MCL ineligible for stem cell transplant (SCT) was randomly assigned to either R-CHOP or VR-CAP (bortezomib replacing vincristine). At a median follow-up of 40 months (mo), mPFS was 24.7 mo vs 14.4 mo in VR-CAP vs R-CHOP (HR 0.63, p<0.001), respectively. Similar, relative improvements were reported in complete response (CR) (53% vs 42%, p=0.007) and 4-year OS was (64% [95% CI 56-71] vs 54% [95% CI 45-62]). Jin et al. (2018) (n=121) assessed R-CHOP vs VR-CAP in ND-MCL patients ineligible for SCT. After a median follow-up of 42.4 mo, mPFS for VR-CAP was better than R-CHOP (28.6 mo vs 13.9 mo, HR=0.7, p=0.157). The overall response rate (ORR) was almost similar in VR-CAP (97%) and R-CHOP (98%). The 4-year OS was 62% vs 61% in VR-CAP vs R-CHOP, respectively. Flinn et al. (2014) (n=74) studied the efficacy of bendamustine in combination with rituximab (BR) vs R-CHOP or R-CVP (R-CHOP minus doxorubicin) as induction regimens in ND-MCL. 36 patients received BR and 38 patients received R-CHOP/R-CVP. ORR was 94% vs 85% with BR vs R-CHOP/R-CVP, respectively. Hess et al. (2009) (n=162) evaluated temsirolimus in RR-MCL. The study population was randomized to either 175/75mg temsirolimus (arm A), 175/25mg temsirolimus (arm B), and the investigator's choice of chemotherapy (arm C). The mPFS was significantly better in arm A compared to arm C (4.8 mo vs 1.9 mo, HR 0.44 [97.5% CI 0.25-0.7], p=0.0009). Arm B had slight improvement but insignificant. Similarly, mOS was 12.8 mo in arm A (HR 0.8 [95% CI 0.5-1.28], p=0.35), and 8.8 in arm B (HR 0.96 [95% CI 0.60-1.54], p=0.87), when compared to 9.5 mo in arm C. Drelying et al. (2016) (n=280), studied temsirolimus in comparison with ibrutinib, RR-MCL with mPFS of 14.6 mo (95% CI 10.4-not estimable) vs 6.2 mo (95% CI 4.2-7.9), respectively. Toxicities were typically manageable. VR-CAP was associated with a higher incidence of toxicity (100%) vs R-CHOP (94%) majority of which was hematological. Thrombocytopenia was particularly more prominent with temsirolimus. Granulocytopenia was persistent in 30-40% in the R-FC cohort after 5 y. Conclusion: The chemo-immunotherapy combination is favorable compared to chemotherapy alone for the treatment of MCL. R-CHOP induction followed by rituximab maintenance in MCL shows favorable long-term safety and efficacy profile. Bortezomib substituting for vincristine in R-CHOP improves the efficacy outcomes. Ibrutinib-based regimens are superior to temsirolimus-based regimens. Disclosures Anwer: Incyte, Seattle Genetics, Acetylon Pharmaceuticals, AbbVie Pharma, Astellas Pharma, Celegene, Millennium Pharmaceuticals.:Honoraria, Research Funding, Speakers Bureau.

Abstract 696: Development of selective CDK8 inhibitors for colorectal cancer and mantle cell lymphoma treatment.

2013 ◽  
Author(s):  
Tomasz Rzymski ◽  
Adrian Zarebski ◽  
Renata Windak ◽  
Karolina Krawczynska ◽  
Ewa Trebacz ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Mantle Cell Lymphoma ◽  
Cell Lymphoma ◽  
Lymphoma Treatment ◽  
Mantle Cell

Vitamin D3 and Lenalidomide Synergize To Induce Apoptosis In Mantle Cell Lymphoma Via Demethylation Of BIK

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 1830-1830
Author(s):  
Carole Brosseau ◽  
Christelle Dousset ◽  
Cyrille Touzeau ◽  
Sophie Maiga ◽  
Philippe Moreau ◽  
...  
Keyword(s):  
Cell Death ◽  
Mantle Cell Lymphoma ◽  
Cell Lines ◽  
Vitamin D3 ◽  
Conflicts Of Interest ◽  
Cell Lymphoma ◽  
Treatment Options ◽  
Annexin V ◽  
Dna Demethylation ◽  
Mantle Cell

Abstract Among new treatment options for mantle cell lymphoma (MCL), the targeted drug lenalidomide appears as one of the most efficient molecules. Lenalidomide has multiple modes of action targeting the tumor cell and its environment including the immune system. It is widely reported that cancer patients are deficient in vitamin D3 (1,25-dihydroxyvitamin D3, VD3) and recent studies have shown in non Hodgkin lymphomas (NHL) that VD3 levels have a prognostic value on survival (Drake, J Clin Oncol. 2010;28:4191). While the relations between VD3 and cancer incidence remain unresolved, it has been shown that VD3 displays anti-tumoral properties via its anti-proliferative, pro-differentiation, anti-inflammatory and anti-angiogenic properties. We assessed the efficacy of VD3 to potentiate cell death induced by lenalidomide in MCL cell lines and patients’ samples and explored the mechanisms of cell death in this context. Experiments were conducted on a panel of 6 MCL cell lines (JEKO-1, MINO, GRANTA-519, UPN-1, REC-1 and Z138) and 8 primary peripheral blood samples. After 6 days of treatment, MCL cells were weakly sensitive to low doses of lenalidomide (1µM and 10µM for cell lines and samples, respectively). Addition of physiological doses of VD3 (100nM) significantly and synergistically increased cell death in 67% of cell lines (Z138, JEKO-1, MINO, REC-1) and in 63% of primary samples (p<0.05). However resistance to lenalidomide alone was not reversed by VD3 since both GRANTA-519 and UPN-1 remained unsensitive. Apoptosis, characterized by Annexin V staining, appearance of a subG1 peak and caspase 9 activation, was dependent on Bax expression, since transient extinction of BAX by siRNA in JEKO-1 cells inhibited cell death (mean of inhibition 30%±5%, p=0.03). The combination of lenalidomide and VD3 dramatically increased expression of the BH3-only Bik (Bcl2-Interacting Killer) protein in sensitive (Z138, JEKO-1, MINO, REC-1) but not resistant (GRANTA-519, UPN-1) cell lines, without affecting the expression of other molecules of the Bcl2 family. By immunoprecipitation assays, we showed that induced-Bik was not bound to the anti-apoptotic molecules Bcl2, BclxL or Mcl1 in treated cells but was free to activate such pro-apoptotic molecules as Bax. Moreover, siBIK RNA significantly decreased the proportion of Annexin V+ cells observed after treatment with lenalidomide and VD3, respectively by 36%±9% (p=0.04) and 28%±4% (p=0.04) in JEKO-1 and MINO cells. This confirmed the involvement of Bik in the cell death induced by this synergistic combination. Q-RT-PCR assays disclosed that Bik accumulation was related to an increase in BIK mRNA expression. BIK expression is controlled by the transcription factor TEF and is regulated by epigenetic modifications, its expression being silenced by methylation in many cancer cells. We showed that Bik accumulation induced by lenalidomide and VD3 was not related to an increase in TEF expression. To determine whether Bik expression could be induced or increased upon demethylation in MCL, we treated cell lines for 3 days with 1µM 5-azadecytidine (5-aza). Indeed, higher expression of Bik was observed after this treatment in the four cell lines sensitive to lenalidomide. Of note, cell death induced by 5-aza correlated linearly to that induced by lenalidomide and VD3 (p<0.001, r=0.95, n=6), suggesting that BIK demethylation could be a key point in the response to this combination. To directly assess the level of BIK methylation in MCL cell lines, we then performed a DNA methylation specific PCR assay on bisulfite-treated DNA, which targets the CpG rich region located within intron 1, as previously described by Hatzimichael et al (Leuk Lymphoma. 2012;53:1709). Indeed, we showed that lenalidomide and VD3 increased the proportion of unmethylated over methylated BIKDNA CpG islands in sensitive (2 to 5-fold increase) but not in resistant cell lines. These data show that the association of lenalidomide and VD3, by increasing BIK expression through DNA demethylation, is an efficient combination to induce the apoptosis of MCL cells. They also underline the interest of measuring the level of VD3 in MCL patients especially those receiving lenalidomide, since supplementation in deprived patients might improve the effect of therapy. Disclosures: No relevant conflicts of interest to declare.

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