Neoadjuvant chemo-immunotherapy modifies CD4+CD25+ regulatory T cells (Treg) in non-small cell lung cancer (NSCLC) patients

Pircher, Andreas; Gamerith, Gabriele; Amann, Arno; Reinold, Susanne; Popper, Helmut; Gächter, Anneliese; Pall, Georg; Wöll, Ewald; Jamnig, Herbert; Gastl, Günther; Wolf, Anna Maria; Hilbe, Wolfgang; Wolf, Dominik

doi:10.1016/j.lungcan.2014.04.001

Cited by 42 publications

(27 citation statements)

References 25 publications

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“…This is consistent with a previous report, which suggested that aborted TGF-β programming in T cells confers protection against B16 melanoma and EL4 thymoma cells (36). Indeed, lower numbers of Tregs in cancer patients have been observed to correlate with better responses to chemotherapy (37), and multiple experiments suggest that therapeutically targeting Tregs promotes antitumor immunity and tumor rejection in mouse models of cancer (38). Moreover, analyses of moesin levels in tumors also correlate with poor prognosis of many cancers (39)(40)(41).…”

Section: Methodssupporting

confidence: 93%

Membrane-organizing protein moesin controls Treg differentiation and antitumor immunity via TGF-β signaling

Ansa-Addo¹,

Zhang²,

Yang³

et al. 2017

Journal of Clinical Investigation

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Section: Methodssupporting

confidence: 93%

Membrane-organizing protein moesin controls Treg differentiation and antitumor immunity via TGF-β signaling

Ansa-Addo¹,

Zhang²,

Yang³

et al. 2017

Journal of Clinical Investigation

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“…Lenalidomide has been demonstrated to inhibit proliferation and function of peripheral blood-derived Tregs in vitro (27). Tregs, in turn, have been demonstrated to inhibit natural killer (NK) cell functions, including NK cell-mediated ADCC using another mAb in vitro (28). It is conceivable that lenalidomide-induced reduction of Tregs number and function enhances rituximab-induced ADCC by NK cells, and that this mechanism reverses rituximab resistance in some patients.…”

Section: Discussionmentioning

confidence: 99%

Combination of Lenalidomide and Rituximab Overcomes Rituximab Resistance in Patients with Indolent B-cell and Mantle Cell Lymphomas

Chong

Ahmadi

Aqui

et al. 2015

Clinical Cancer Research

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Purpose: Lenalidomide, an immunomodulatory agent that enhances antibody-dependent cell-mediated cytotoxicity, has the potential to synergize with rituximab, an anti-CD20 mAb. We hypothesized that the addition of lenalidomide to rituximab would improve clinical outcomes in patients with B-cell lymphomas who were previously rituximab resistant, defined as no response to or progression of lymphoma within 6 months of rituximab-based therapy.Experimental Design: We conducted a single-center, phase II trial in patients with indolent B-cell or mantle cell lymphomas who were previously rituximab resistant. Patients received 10 mg lenalidomide daily for 8 weeks, and then received four weekly doses of 375 mg/m 2 rituximab; lenalidomide continued during and after rituximab. Response to therapy was assessed after 8 weeks of lenalidomide and 12 weeks after first dose of rituximab. The primary endpoint was overall response rate (ORR) after lenalidomide and rituximab.Results: Fifty patients were enrolled and 43 patients completed both response assessments. ORR after 8 weeks of lenalidomide was 30.2%; 12 weeks after the addition of rituximab to lenalidomide, ORR increased to 62.8% (N ¼ 43). For all patients (N ¼ 50), median progression-free survival (PFS) is 22.2 months (median follow-up, 39.2 months). PFS after lenalidomide-rituximab was significantly longer than the PFS for the antecedent regimen used to define rituximab resistance (22.2 vs. 9.13 months, P ¼ 0.0004).Conclusions: This trial is the first to show that the combination of lenalidomide and rituximab overcomes prior rituximab resistance in patients with indolent B-cell and mantle cell lymphomas.

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“…The effect of the E:R ratio is nonlinear, with small values corresponding to virtually no cell kill regardless of how small they are. In view of experimental studies [42,43] which clearly show different time courses of nadir and recovery for Tregs and effector (or CD4) cells, there is evidence that a window with a more favorable E:R ratio exists regardless of whether the rodent estimates for the T-cell population kinetics are close to human values. Additionally, comparison of the Pircher et al [43] data with Lutsiak et al [24] suggests little difference in these time scales between rodent and human.…”

Section: Discussionmentioning

confidence: 99%

A model for effects of adaptive immunity on tumor response to chemotherapy and chemoimmunotherapy

Robertson-Tessi

El-Kareh

Goriely

2015

Journal of Theoretical Biology

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Neoadjuvant chemo-immunotherapy modifies CD4+CD25+ regulatory T cells (Treg) in non-small cell lung cancer (NSCLC) patients

Cited by 42 publications

References 25 publications

Membrane-organizing protein moesin controls Treg differentiation and antitumor immunity via TGF-β signaling

Membrane-organizing protein moesin controls Treg differentiation and antitumor immunity via TGF-β signaling

Combination of Lenalidomide and Rituximab Overcomes Rituximab Resistance in Patients with Indolent B-cell and Mantle Cell Lymphomas

A model for effects of adaptive immunity on tumor response to chemotherapy and chemoimmunotherapy

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