Recent landmark studies in follicular lymphoma

Sorigué, Marc; Sancho, Juan‐Manuel

doi:10.1016/j.blre.2019.03.006

Cited by 10 publications

(11 citation statements)

References 87 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…T-cell lymphoma is a very heterogeneous group of tumors (17,18), lacking in effective treatment strategies (19). Recent reports demonstrate that the histone deacetylase inhibitor-chidamide improves the therapeutic effect of T-cell lymphomas (2,3).…”

Section: Discussionmentioning

confidence: 99%

MiR-449a attenuates autophagy of T-cell lymphoma cells by downregulating ATG4B expression

Zhang

Qiu²,

et al. 2020

BMB Rep.

View full text Add to dashboard Cite

Increasing evidence suggests the role of miR-449a in the regulation of tumorigenesis and autophagy. Autophagy plays an important role in the malignancy of T-cell lymphoma. However, it is still unknown whether miR-449a is associated with autophagy to regulate the malignancy of T-cell lymp homa. In this study, we for the first time demonstrated that miR-449a enhanced apoptosis of T-cell lymphoma cells by decreasing the degree of autophagy. Further, miR-449a downregulated autophagy-associated 4B (ATG4B) expression, which subsequently reduced the autophagy of T-cell lymphoma cells. Mechanistically, miR-449a decreased ATG4B protein level by binding to its mRNA 3'UTR, thus reducing the mRNA stability. In addition, studies with nude mice showed that miR-449a significantly inhibited lymphoma characteristics in vivo. In conclusion, our results demonstrated that the "miR-449a/ATG4B/autophagy" pathway played a vital role in the malignancy of T-cell lymphoma, suggesting a novel therapeutic target. [BMB Reports 2020; 53(5): 254-259]

show abstract

Section: Discussionmentioning

confidence: 99%

MiR-449a attenuates autophagy of T-cell lymphoma cells by downregulating ATG4B expression

Zhang

Qiu²,

et al. 2020

BMB Rep.

View full text Add to dashboard Cite

show abstract

“…Apparently, two specific lymphomas, FL and DLBCL, account for about 65% of all NHL, and more importantly, the genomic profile of transformed FL shares similarities with that of GCB de novo DLBCL, and thus a thorough knowledge of these two entities related with PI3K/AKT pathway is essential [307][308][309]. Despite the recognized fact that overwhelming majority of FL cases have the characteristic (14;18) translocation involving the IgH/bcl-2 genes, while B-cells "arrested" in germinal centers of FL acquire dozens of additional genetic aberrations that influence key pathways controlling their physiological development including B Cell Receptor (BCR) signaling, PI3K/AKT pathway, and so on [310,311].…”

Section: Description Of the Pi3k/akt Pathway In The Hemato-immune Sysmentioning

confidence: 99%

“…Consequently, following with the world's first selective PI3Kδ inhibitor CAL-101 was approved by the FDA for the treatment of FL, CLL and SLL in 2014 [315] [NCT01282424, NCT02136511], the PI3K/AKT inhibitors have shown remarkable activity in an increasing subset of patients with NHL [316] (Tables 2, 3). Copanlisib (BAY 80-6946) and Duvelisib (IPI-145) are newly approved PI3K inhibitors that offer objective, although relatively short-lasting, responses in patients with heavily pre-treated FL and other NHL, and more such targeted agents may be approved soon [307,[317][318][319][320] (Tables 2 and 3).…”

Section: Description Of the Pi3k/akt Pathway In The Hemato-immune Sysmentioning

confidence: 99%

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

et al. 2020

View full text Add to dashboard Cite

Given that the PI3K/AKT pathway has manifested its compelling influence on multiple cellular process, we further review the roles of hyperactivation of PI3K/AKT pathway in various human cancers. We state the abnormalities of PI3K/AKT pathway in different cancers, which are closely related with tumorigenesis, proliferation, growth, apoptosis, invasion, metastasis, epithelial-mesenchymal transition, stem-like phenotype, immune microenvironment and drug resistance of cancer cells. In addition, we investigated the current clinical trials of inhibitors against PI3K/AKT pathway in cancers and found that the clinical efficacy of these inhibitors as monotherapy has so far been limited despite of the promising preclinical activity, which means combinations of targeted therapy may achieve better efficacies in cancers. In short, we hope to feature PI3K/ AKT pathway in cancers to the clinic and bring the new promising to patients for targeted therapies.

show abstract

“…However, their high activity makes them a therapeutic option for high-risk FL (particularly in patients with early progression or treatment failure for whom available strategies are unsatisfactory); in these situations PI3K inhibitors may provide a bridge to transplantation. 32 Comparatively poorer response rates have been reported for BTK inhibitors 33 and BCL2 inhibitors. 34,35 In our study, the median PFS in the 10 patients refractory to first-line rituximab-containing immunochemotherapy was 25.5 months.…”

Section: Discussionmentioning

confidence: 99%

Response‐adapted treatment with rituximab, bendamustine, mitoxantrone, and dexamethasone followed by rituximab maintenance in patients with relapsed or refractory follicular lymphoma after first‐line immunochemotherapy: Results of the RBMDGELTAMO08 phase II trial

et al. 2019

View full text Add to dashboard Cite

Background Consensus is lacking regarding the optimal salvage therapy for patients with follicular lymphoma who relapse after or are refractory to immunochemotherapy. Methods This phase II trial evaluated the efficacy and safety of response‐adapted therapy with rituximab, bendamustine, mitoxantrone, and dexamethasone (RBMD) in follicular lymphoma patients who relapsed after or were refractory to first‐line immunochemotherapy. Sixty patients received three treatment cycles, and depending on their response received an additional one (complete/unconfirmed complete response) or three (partial response) cycles. Patients who responded to induction received rituximab maintenance therapy for 2 years. Results Thirty‐three (55%) and 42 (70%) patients achieved complete/unconfirmed complete response after three cycles and on completing induction therapy (4‐6 cycles), respectively (final overall response rate, 88.3%). Median progression‐free survival was 56.4 months (median follow‐up, 28.3 months; 95% CI, 15.6‐51.2). Overall survival was not reached. Progression‐free survival did not differ between patients who received four vs six cycles (P = .6665), nor between patients who did/did not receive rituximab maintenance after first‐line therapy (P = .5790). Median progression‐free survival in the 10 refractory patients was 25.5 months (95% CI, 0.6‐N/A) and was longer in patients who had shown progression of disease after 24 months of first‐line therapy (median, 56.4 months; 95% CI, 19.8‐56.4) than in those who showed early progression (median, 42.31 months; 95% CI, 24.41–NA) (P = .4258). Thirty‐six (60%) patients had grade 3/4 neutropenia. Grade 3/4 febrile neutropenia and infection were recorded during induction (4/60 [6.7%] and 5/60 [8.3%] patients, respectively) and maintenance (2/43 [4.5%] and 4/43 [9.1%] patients, respectively). Conclusions This response‐adapted treatment with RBMD followed by rituximab maintenance is an effective and well‐tolerated salvage treatment for relapsed/refractory follicular lymphoma following first‐line immunochemotherapy. Clinical trial registration http://clinicaltrials.gov # NCT01133158.

show abstract

Recent landmark studies in follicular lymphoma

Cited by 10 publications

References 87 publications

MiR-449a attenuates autophagy of T-cell lymphoma cells by downregulating ATG4B expression

MiR-449a attenuates autophagy of T-cell lymphoma cells by downregulating ATG4B expression

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

Response‐adapted treatment with rituximab, bendamustine, mitoxantrone, and dexamethasone followed by rituximab maintenance in patients with relapsed or refractory follicular lymphoma after first‐line immunochemotherapy: Results of the RBMDGELTAMO08 phase II trial

Contact Info

Product

Resources

About