Summaries of Must-Read Clinical Literature, Guidelines, and FDA Actions
Infiltrating CD4+ T Cells Attenuate Chemotherapy Sensitivity in PC
Key clinical point: Infiltrating CD4+ T cells could promote prostate cancer chemotherapy resistance via modulation of the CCL5/STAT3 signaling pathway.
Major finding: CD4+ T cells could activate P- signal transducer and activator of transcription 3 (STAT3) signaling via secreting CCL5 and adding a STAT3 inhibitor can reverse the chemoresistance.
Study details: CD4+ T-cell infiltration in Docetaxel-treated paraffin-embedded specimens from transurethral resection of prostate, radical prostatectomy, or bone metastasis was detected by immunohistochemistry.
Citation:
Xiang P, et al. Prostate. 2019 Apr 24. doi: 10.1002/pros.23810.
Resistance to anti-neoplastic therapies occurs in response to many therapeutic modalities in prostate cancer. In this laboratory-based study, Xiang et al. identified that CD4+ T cell secretion of the cytokine CCL5 (and subsequent STAT3 activation) was associated with resistance to a standard prostate cancer treatment, docetaxel. The implications of this study are clinically relevant. First, it supports the design of clinical studies of STAT3 inhibition in heavily pretreated patients. Second, the association of CD4+ T cells with resistance to docetaxel could lead to studies that are designed to evaluate whether CD4+ T cell abundance may be predictive for treatment choice. —Mark A. Klein, MD