Correlation of tumoricidal activity of lenalidomide against hematologic tumor cells with cyclin D1/D2 expression and effect on tumor-suppressor gene upregulation.

Zhang, L.; Kosek, Jolanta; Schafer, PH; Bartlett, J. Blake

doi:10.1200/jco.2010.28.15_suppl.8090

Cited by 2 publications

(3 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The study was divided into three stages: an induction phase (cycles 1-3), a consolidation phase (cycles [4][5][6][7][8][9][10][11][12], and a follow-up phase. During each 28-day cycle, lenalidomide was given orally in a single daily administration at a dose of 25 mg on days 1-21, while dexamethasone was administered orally in a single dose of 40 mg on days 1, 8, 15, and 22.…”

Section: Treatmentmentioning

confidence: 99%

“…This agent has pleiotropic anti-tumoral activity and, in lymphoma, acts principally by decreasing proliferation of tumor cells by means of a direct effect on specific pathways, such as p21 and SPARC. 4,5 Moreover, in recent studies, lenalidomide demonstrated strong immune-modulating activity by enhancing the activity of natural killer (NK) cells and promoting the formation of immune synapses between MCL cells and NK cells. 6 Previous studies have demonstrated that lenalidomide has clinical activity across a broad range of lymphoma histologies in the relapsed/refractory setting, [7][8][9] particularly in MCL, in which overall response rates of 42% to 53% and complete response rates of 20% were observed in two small subgroups of patients enrolled in studies investigating aggressive non-Hodgkin's lymphomas.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Salvage treatment with lenalidomide and dexamethasone in relapsed/refractory mantle cell lymphoma: clinical results and effects on microenvironment and neo-angiogenic biomarkers

Zaja¹,

Luca

Vitolo

et al. 2011

Haematologica

View full text Add to dashboard Cite

BackgroundPreclinical studies have highlighted the activity of lenalidomide in mantle cell lymphoma and its anti-proliferative synergy with dexamethasone. Design and MethodsIn this prospective, multicenter, phase II study, patients with relapsed/refractory mantle cell lymphoma who were not eligible for, or had relapsed after, intensive treatments received lenalidomide 25 mg/day (days 1-21 of each 28-day cycle) and dexamethasone (40 mg/day on days 1, 8, 15, and 22) for up to 12 months. ResultsThe primary end-points, overall and complete response rates, were achieved by 17 of 33 (52%; 95% confidence interval [CI], 35-68%) and 8 of 33 patients (24%; 95% CI, 13-41%), respectively, by the end of treatment. Fifteen patients (45%) discontinued treatment prematurely, 13 due to lack of response. The median progression-free and overall survival were 12 months (95% CI, 5-19 months) and 20 months (95% CI, 12 months to not estimable), respectively. Treatment resulted in a significant increase in microvessel density (P=0.033) and non-significant increases in macrophage and natural killer cell counts, while serum levels of neoangiogenic factors did not change significantly. Grade 3/4 adverse events were neutropenia (53%), leukopenia (25%), thrombocytopenia (22%), infections (12%), and febrile neutropenia (12%). ConclusionsThese results confirm a favorable safety and activity profile of lenalidomide in relapsed/refractory mantle cell lymphoma. The contribution of dexamethasone in achieving these results is unclear because of its possible detrimental effect on the immune activation generated by lenalidomide and a higher risk of developing infectious complications. (clinicaltrials.gov identifier: NCT00786851).

show abstract

Section: Treatmentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Salvage treatment with lenalidomide and dexamethasone in relapsed/refractory mantle cell lymphoma: clinical results and effects on microenvironment and neo-angiogenic biomarkers

Zaja¹,

Luca

Vitolo

et al. 2011

Haematologica

View full text Add to dashboard Cite

show abstract

“…The metabolic pathway involving PI3K/AKT is dysregulated in many cases: the activation of AKT supports cell proliferation and may represent a therapeutic target for inhibitors of mTOR, a regulator of AKT [ 37 , 38 ]. Furthermore, overexpression of p21 and SPARC has been documented in MCL: lenalidomide directly represses the expression of these oncogenes, and this could explain its documented efficacy even in patients with advanced and refractory disease [ 39 , 40 ].…”

Section: Aggressive B-cell Lymphomasmentioning

confidence: 99%

Navigating Lymphomas through BCR Signaling and Double-Hit Insights: Overview

Argentiero,

Andriano,

Marziliano

et al. 2024

Hematology Reports

View full text Add to dashboard Cite

Non-Hodgkin’s lymphomas (NHLs) are a heterogeneous group of lymphoproliferative disorders originating from B, T, or NK lymphocytes. They represent approximately 4–5% of new cancer cases and are classified according to the revised WHO system based on cell lineage, morphology, immunophenotype, and genetics. Diagnosis requires adequate biopsy material, though integrated approaches are used for leukemic presentations. Molecular profiling is improving classification and identifying prognostic markers. Indolent NHLs, such as follicular lymphoma and marginal zone lymphoma, typically pursue a non-aggressive clinical course with long survival. Aggressive diffuse large B-cell lymphoma (DLBCL) is the most common subtype. Recent studies have elucidated pathogenic mechanisms like MYC translocations and BCR pathway mutations. “Double hit” lymphomas with MYC and BCL2/BCL6 alterations confer a poor prognosis. Treatment approaches are evolving, with chemoimmunotherapy remaining standard for many indolent cases while intensified regimens and targeted agents show promise for refractory or high-risk aggressive disease. Continued elucidation of the genetic and microenvironmental underpinnings of lymphomagenesis is critical for developing personalized therapeutic strategies.

show abstract

Correlation of tumoricidal activity of lenalidomide against hematologic tumor cells with cyclin D1/D2 expression and effect on tumor-suppressor gene upregulation.

Cited by 2 publications

References 0 publications

Salvage treatment with lenalidomide and dexamethasone in relapsed/refractory mantle cell lymphoma: clinical results and effects on microenvironment and neo-angiogenic biomarkers

Salvage treatment with lenalidomide and dexamethasone in relapsed/refractory mantle cell lymphoma: clinical results and effects on microenvironment and neo-angiogenic biomarkers

Navigating Lymphomas through BCR Signaling and Double-Hit Insights: Overview

Contact Info

Product

Resources

About