paclitaxel

PD-1/PD-L1 inhibitors combined with chemotherapy or as monotherapy versus chemotherapy alone or observation in triple-negative breast cancer: a systematic review and updated meta-analysis incorporating long-term survival data.

Guan Bing B, Chen Yawen Y, Zhou Rong R, Zhang Sijia S et al.

Multiple RCTs have established PD-1/PD-L1 inhibitors as standard in triple-negative breast cancer (TNBC), but prior meta-analyses lacked complete setting coverage, mature long-term survival data, and a quantification of chemotherapy-backbone impact-critical given IMpassion130 (nab-paclitaxel, positive) vs. IMpassion131 (paclitaxel, negative). This update includes final KEYNOTE-522 OS, GeparNuevo 7-year follow-up, and TORCHLIGHT Phase III data, covering neoadjuvant to metastatic disease. We searched PubMed and ClinicalTrials.gov to May 2026 plus conference proceedings; an Embase search found no additional trials. Included RCTs compared ICI + chemotherapy vs. chemotherapy alone in TNBC, stratified by setting. The primary endpoints are OS (metastatic) and EFS/iDFS (early-stage). Pooled HRs used random-effects meta-analysis with HKSJ adjustment. A total of 10 RCTs (5,953 patients) met the inclusion. In the metastatic setting (five RCTs, n = 3,526), ICI improved OS (HR 0.85, 95% CI 0.74-0.96; HKSJ-adjusted 0.70-1.03; I² = 27%) and PFS (HR 0.82, 0.73-0.92; I² = 35%); OS benefit was greater in PD-L1+ patients (HR 0.79, 0.65-0.95; I² = 51%). Numerically greater OS with anti-PD-1 vs. anti-PD-L1 was not robust in the sensitivity analysis. In the early-stage setting (five RCTs, n = 2,427), ICIs improved EFS/iDFS (HR 0.75, 0.63-0.90; I² = 0.2%) and OS (HR 0.64, 0.53-0.78; I² = 0%) and increased pCR (OR 1.65, 1.39-1.98; I² = 1%). HKSJ adjustment widened the Cis, but the effect patterns remained consistent. This update confirms a consistent survival benefit of ICI + chemotherapy in both early and metastatic TNBC, which was most pronounced in PD-L1+ populations. Long-term data show durability, especially in neoadjuvant/adjuvant settings. The divergent outcomes with nab-paclitaxel vs. paclitaxel underscore the critical role of the chemotherapy backbone. These findings support current guidelines and highlight the need for refined biomarkers to extend benefit to PD-L1-negative patients. https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD420261356428, identifier CRD420261356428.

SLC7A11 suppresses paclitaxel resistance and improves survival via the KLF2 regulatory axis associated with autophagy in ovarian cancer.

Chen Xiaoying X, Ke Yao Y, Xie Shanzhou S, Guo Yulin Y et al.

SLC7A11 is well-established as a key mediator of ferroptosis. However, its functional role in regulating autophagy, particularly in the context of ovarian cancer (OC) chemoresistance, remains poorly characterized. Our preliminary results suggested that low SLC7A11 expression is associated with paclitaxel resistance in OC, likely through inhibition of autophagy. Despite this initial observation, systematic functional investigations into the role of SLC7A11 in autophagy regulation and OC chemoresistance are lacking, and the underlying molecular mechanisms remain unclear. Therefore, this study aims to elucidate how SLC7A11 mediates chemoresistance in OC through the regulation of autophagy. The effects of SLC7A11 modulation were assessed in paclitaxel-resistant and parental OC cells using functional assays. Autophagy was evaluated via transmission electron microscopy, immunofluorescence, and Western blotting. Autophagy was inhibited using 3-methyladenine or LC3B knockdown. A subcutaneous xenograft model was used for in vivo validation. Clinical relevance was analyzed using patient tissues. Proteomics, bioinformatics, molecular, and CCK-8 assays were integrated to investigate the SLC7A11/KLF2-autophagy axis. SLC7A11 knockdown enhanced the viability of paclitaxel-resistant OC cells (HeyA8-R) following paclitaxel treatment. In contrast, SLC7A11 overexpression sensitized both HeyA8-R cells and their parental HeyA8 cells to paclitaxel, as evidenced by reduced viability, increased intracellular paclitaxel accumulation, and elevated DNA damage. Moreover, SLC7A11 overexpression augmented autophagy-associated activity, and inhibition of autophagy partially attenuated SLC7A11-mediated sensitization to paclitaxel. In vivo studies showed that SLC7A11 suppressed tumor growth and overcame paclitaxel resistance in OC, accompanied by upregulated autophagy-related markers (LC3B, LC3B-II/I, and LAMP1). Mechanistically, SLC7A11 negatively regulated KLF2, a key oncogenic autophagy regulator, and the SLC7A11/KLF2 regulatory axis was associated with LC3B expression and autophagy-associated activity, which may contribute to paclitaxel sensitivity in OC. Clinically, low SLC7A11 expression correlated with chemoresistance and shorter survival in OC. Our findings underscore the significance of the SLC7A11/KLF2-autophagy regulatory axis in OC paclitaxel resistance. They also suggest that SLC7A11 may serve as a prognostic biomarker and therapeutic target for overcoming OC chemoresistance.

Corrigendum to "Synergistic enhancement of cytotoxicity against cancer cells by incorporation of rectorite into the paclitaxel immobilized cellulose acetate nanofibers" [Int. J. Biol. Macromol. 152 (2020) 672-680].

Liu Yin Y, Wang Qin Q, Lu Yuan Y, Deng Hongbing H et al.

Salvage gastrectomy for perforated gastric intramural metastasis after definitive chemoradiotherapy for distal esophageal squamous cell carcinoma: a case report.

Leelapatanadit Jirat J, Sangthong Sawanya S, Waratchanont Rawat R, Asanprakit Wichitra W et al.

Gastric intramural metastasis from esophageal squamous cell carcinoma (ESCC) is rare, and chemotherapy-associated perforation is exceptionally uncommon. We report a case of a 67-year-old man with distal ESCC and a separate cardia squamous cell carcinoma (SCC). He declined esophagectomy and received definitive chemoradiotherapy (dCRT) with paclitaxel, carboplatin, and 50.4 Gy radiotherapy. During the second chemotherapy cycle, the cardia tumor perforated and was treated by emergency omental patch repair. Chemoradiotherapy was subsequently completed. Three months after completion of dCRT, the esophageal lesion showed a clinical complete response, whereas residual cardia disease persisted. Extended total gastrectomy with splenectomy achieved R0 resection; pathology showed a 6-cm pT3 moderately differentiated SCC with partial treatment response and 0/12 positive nodes. Postoperative nivolumab was administered. This case illustrates a staged salvage strategy for persistent gastric intramural disease after definitive chemoradiotherapy.