Our findings provide further insights into the pathogenesis of CIPN. Integrating biomarkers and proteomics paves the way for precision medicine to manage chemotherapy-induced toxicities.

Preoperative CA153 and CA199 levels were found to be independent factors influencing ovarian tumour organoid generation. The drug responses of most PDOs to paclitaxel and carboplatin were consistent with the clinical treatment outcomes.

Such therapeutic effects were more pronounced in combination than monotherapy. In conclusion, our study found that combining SIT and MAN had a remarkably beneficial impact on PTX-induced testicular toxicity by mediating the Sestrin2/Keap1/Nrf2 signaling pathway.

Standard chemotherapy regimens for patients with breast cancer are based on epirubicin-cyclophosphamide (EC) and paclitaxel (TAX) administrations. In only 4 days, the first TAX administration induced severe skeletal muscle mitochondrial remodelling in patients with breast cancer, characterized by impaired mitochondrial dynamics that resulted in swollen and damaged organelles. These findings demonstrate that mitochondrial toxicity, classically documented at the end of treatment, occurs acutely and after only one chemotherapy administration.

While next-generation androgen receptor signaling inhibitors (ARSIs), such as enzalutamide and abiraterone, have revolutionized CRPC treatment, resistance to these therapies remains a significant challenge, rendering the disease incurable. Compelling evidence further suggests that combining PLK1 inhibition with paclitaxel could serve as an effective therapeutic strategy to overcome resistance in CRPC by targeting microtubule dynamics. This review examines the mechanistic role and broader implications of PLK1 in CRPC treatment, offering valuable insights into potential combination therapies to improve efficacy and patient outcomes.

Our findings not only unveiled a novel mechanistic basis for the repurposing of DSF but also highlighted AIF-mediated necroptosis as a promising therapeutic strategy to overcome chemoresistance in ovarian cancer.

Using a paclitaxel (PTX)-resistant Lewis lung carcinoma cell line, we demonstrated that ERK-dependent Pgp1 functions as a shared upstream regulator of both chemoresistance and metastatic competence...Importantly, meta-analysis of clinical datasets further linked co-elevated FN and Pgp1 expression with poor prognosis and relapse in early-stage cancer patients, underscoring the translational relevance of targeting this shared pathway. These findings identify Mul A as a promising non-cytotoxic therapeutic candidate and elucidate the shared upstream molecular mechanism linking distinct downstream chemoresistance and metastasis.

The high HICDI group exhibited a propensity for "cold" tumors marked by immune suppression and exclusion; however, drugs such as paclitaxel may present viable therapeutic options for these patients. We verified the model gene kinesin family member 2C through in vitro experiments, demonstrating its role as a potential oncogene affecting HCC progression and as a promising therapeutic target. Overall, HICDI possesses the potential for extensive applications in informing personalized treatment decisions and improving outcomes for patients with HCC.

A 52-year-old woman with de novo metastatic, grade 1, luminal A ILC (ER+/PR+, HER2 0; Ki-67 5%) diagnosed in 2022 achieved durable disease control with systemic therapy and maintenance ribociclib plus ovarian suppression...Despite no clear radiologic progression on CT, symptomatic gastric involvement and weight loss prompted initiation of second-line weekly paclitaxel. Signet ring morphology in gastric biopsies is not pathognomonic for primary gastric carcinoma. In patients with current or prior ILC, an IHC panel incorporating breast-lineage markers (e.g., GATA3, TRPS1) and GI markers (e.g., CDX2, CK20), alongside E-cadherin status, is pivotal to avoid misdiagnosis, inappropriate surgery, and delay of systemic therapy.

LMSCC16 also harbored two TP53 mutations and showed increased resistance to Cisplatin and Paclitaxel compared to established TSCC cell lines. In contrast, LMSCC16 showed significant modulation of OCT4, increased CCND1 and CCNB1 expression, and reduced CDH1 levels following treatment. We established two novel TSCC cell lines that represent clinically relevant models to explore TSCC carcinogenesis and therapeutic responses, particularly in non-smoking populations.

Among the tested compounds, compound 7 exhibited notable antiproliferative activity, showing a faster reduction in cell index compared to the reference drug paclitaxel during the initial 24 h of treatment, along with a dose-dependent decrease in cell index...Molecular docking studies further indicated favorable binding interactions of compound 7 with several cancer-related targets, including EGFR, VEGFR-2, and AKT1. Overall, the obtained results suggest that this family of compounds, particularly compound 7, may represent an interesting scaffold for further investigation in the development of anticancer agents.

Our findings provide preclinical evidence that CBD exerts potent anti-tumor activity in NSCLC by coordinating inhibition of oncogenic signaling and activation of programmed cell death pathways. To our knowledge, this study provides evidence that CBD concurrently inhibits STAT3 and NF-κB signaling, affecting both constitutive and inducible activation in NSCLC, and enhances paclitaxel efficacy in vivo, thereby establishing a novel mechanistic and translational basis for its therapeutic potential. These results support the therapeutic effect of CBD as a potential adjuvant in lung cancer treatment.