Idelalisib: a rare cause of enterocolitis

Balagoni, Harika; Chaudhari, Dhara; Reddy, Chakradhar; Young, Mark

doi:10.20524/aog.2016.0022

Cited by 12 publications

(6 citation statements)

References 7 publications

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“…37 One caveat to this culture strategy is the potential to expand autoreactive cells, as autoimmune pathology has been observed in CLL patients taking idelalisib. [15][16][17] Whether addition of idelalisib to T-cell expansion cultures preferentially expands autoreactive cells will need to be determined prior to employment of this culture strategy in a clinical setting.…”

Section: Discussionmentioning

confidence: 99%

“…The rationale for using these agents was previous data from our laboratory showing enhancement of CD8 T-cell dependent anticancer immunity in peptide antagonist to vasoactive intestinal peptide (VIPhyb)-treated mice 13,14 and reports of autoimmunity after stopping PI3K d inhibitor (idelalisib) in lymphoma and chronic lymphocytic leukemia (CLL) patients. [15][16][17] To test this hypothesis, we studied blood samples from healthy volunteers, DLBCL patients prior to treatment, and samples from DLBCL patients who had received multiple courses of cytotoxic treatment. Of note, lymphoma patients who had received prior treatment had a significantly higher proportion of CD27 2 CD28…”

Section: Introductionmentioning

confidence: 99%

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Improving T-cell expansion and function for adoptive T-cell therapy using ex vivo treatment with PI3Kδ inhibitors and VIP antagonists

et al. 2018

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Improving T-cell expansion and function for adoptive T-cell therapy using ex vivo treatment with PI3Kδ inhibitors and VIP antagonists

et al. 2018

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“…Taken together, optimization of CAR constructs and a greater understanding of favorable CART T-cell phenotypes on intrinsic function are areas for further research. Unfortunately, standard methods for CART manufacturing at this time do not automatically enrich the product for favorable T-cell phenotypes and inadvertently may also promote antigendriven terminal differentiation (41,(176)(177)(178).…”

Section: Naïve and CM T-cell Phenotypementioning

confidence: 99%

Strategies to Overcome Failures in T-Cell Immunotherapies by Targeting PI3K-δ and –γ

et al. 2021

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PI3K-δ and PI3K-γ are critical regulators of T-cell differentiation, senescence, and metabolism. PI3K-δ and PI3K-γ signaling can contribute to T-cell inhibition via intrinsic mechanisms and regulation of suppressor cell populations, including regulatory T-cells and myeloid derived suppressor cells in the tumor. We examine an exciting new role for using selective inhibitors of the PI3K δ- and γ-isoforms as modulators of T-cell phenotype and function in immunotherapy. Herein we review the current literature on the implications of PI3K-δ and -γ inhibition in T-cell biology, discuss existing challenges in adoptive T-cell therapies and checkpoint blockade inhibitors, and highlight ongoing efforts and future directions to incorporate PI3K-δ and PI3K-γ as synergistic T-cell modulators in immunotherapy.

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“…Although a definitive underlying mechanism for idelalisib-associated diarrhea is unknown, PI3K δ inhibition has been associated with immune dysregulation resulting in inhibition of regulatory T cells and increased damage via CD8 + cytotoxic T cells. 35 , 79 – 81 …”

Section: Idelalisibmentioning

confidence: 99%

Incidence and management of toxicity associated with ibrutinib and idelalisib: a practical approach

et al. 2017

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The use of novel B-cell receptor signaling inhibitors results in high response rates and long progression-free survival in patients with indolent B-cell malignancies, such as chronic lymphocytic leukemia, follicular lymphoma, mantle cell lymphoma and Waldenström macroglobulinemia. Ibrutinib, the first-in-class inhibitor of Bruton tyrosine kinase, and idelalisib, the first-in-class inhibitor of phosphatidylinositol 3-kinase δ, have recently been approved for the treatment of several indolent B-cell malignancies. These drugs are especially being used for previously unmet needs, i.e., for patients with relapsed or refractory disease, high-risk cytogenetic or molecular abnormalities, or with comorbidities. Treatment with ibrutinib and idelalisib is generally well tolerated, even by elderly patients. However, the use of these drugs may come with toxicities that are distinct from the side effects of immunochemotherapy. In this review we discuss the most commonly reported and/or most clinically relevant adverse events associated with these B-cell receptor inhibitors, with special emphasis on recommendations for their management.

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Idelalisib: a rare cause of enterocolitis

Cited by 12 publications

References 7 publications

Improving T-cell expansion and function for adoptive T-cell therapy using ex vivo treatment with PI3Kδ inhibitors and VIP antagonists

Improving T-cell expansion and function for adoptive T-cell therapy using ex vivo treatment with PI3Kδ inhibitors and VIP antagonists

Strategies to Overcome Failures in T-Cell Immunotherapies by Targeting PI3K-δ and –γ

Incidence and management of toxicity associated with ibrutinib and idelalisib: a practical approach

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