PAX3::FOXO1 fusion should replace FOXO1 fusion as an adverse prognostic factor in risk stratification of patients with rhabdomyosarcoma. The prognostic relevance of PAX7::FOXO1-positive and FN alveolar rhabdomyosarcoma (aRMS), along with the clinical factors described in this report, allows further refinement of risk assessment of patients with localized and metastatic (aRMS).

Immunotherapy is ineffective in mCRC; however, the efficacy could be significantly enhanced by modifying the tumor immune microenvironment. Comparison of immune cell populations and cell signaling in colorectal liver, lung, and peritoneal (PM) metastases using immune cell deconvolution tools and transcriptomic data, revealed enrichment of CAFs and CAF-related secreting factors in the CMS4 PM microenvironment, that could facilitate intraperitoneal spread, immune suppression, and chemotherapy resistance. Targeting CAF-associated pathways, M2 macrophages, and TNF-⍺ signaling could be novel therapeutic strategies for CMS4 PM-CRC, as they might alter the tumor immune interplay and improve immunotherapy response.

Lower prostate-specific antigen (PSA) values were found among statin users, compared to statin non-users. A significant prostate cancer (PCa) risk reduction in statin users was not observed. Statin users had a significantly higher overall mortality risk than statin non-users.

We analyzed nationwide Belgian data to assess changes in cancer mortality during the early stages of the COVID-19 pandemic (March–December 2020) compared to the same period in 2019, focusing on potential shifts in social disparities. Our findings showed decreases in reported cancer deaths, particularly among individuals aged 75 and older, without significant alterations in existing socioeconomic patterns. These reductions may reflect the prioritization of COVID-19 in cause-of-death coding and its role as a competing risk, highlighting the need for continued policy and healthcare efforts to address persistent educational inequalities.

Existing evidence on depression and cancer risk is conflicting, likely reflecting differences in methodology, as well as study limitations, such as small study population and short follow-up periods. Moreover, there has been almost no investigation of how any mental health disparity in cancer risk has changed over time or differs by population sub-group. We therefore addressed these gaps in a cohort study using Scottish linked administrative healthcare data to compare cancer incidence (all cancers and common cancer subtypes) in those with versus without a hospital admission record for depression, over a 29-year study period.

This review comprehensively covers the TRAIL fusion proteins that have been reported in recent years. It also summarizes six commonly employed strategies used in the construction of TRAIL fusion proteins.

Summary of the dynamics of immune cell types in peripheral blood showing a decrease in the number of eosinophils in the early premetastatic phase, an increase in Tregs in the late premetastatic phase, and an increase in PMN-MDSCs and interstitial macrophages and a decrease in B cells and CD8 T cells in the micrometastatic phase.

Circulating CD3⁺CD8⁺ cell levels were lower in breast cancer patients, elevated posttreatment, and subsequently declining upon recurrence. Elevated plasma chemokine (C–C motif) ligand 2 (CCL2) levels distinguished patients with breast cancer from healthy controls. In summary, circulating CD3⁺CD8⁺ CTL and plasma CCL2 levels emerged as promising dual-purpose biomarkers and therapeutic targets in breast cancer management.

We report differential molecular mechanisms including pathways, key modules, and hub genes, induced by combination of oxaliplatin (L-OHP) and PRIMA-1^met (APR-246, eprenetapopt) in p53-wild type vs. p53-mutant colorectal cancer. Our in vivo studies show that the additional of PRIMA-1^met offers a threefold advantage: enhanced therapeutic effects, reduced L-OHP resistance, and prevention of L-OHP-related side effects.

Pancreatic ductal adenocarcinoma (PDAC) remains one of the world's deadliest cancers, and there is significant imperative to develop novel prognostic biomarkers to guide our limited therapeutic options. FXYD3 is a transmembrane protein overexpressed in numerous cancers including pancreatic cancer and, like other seven members of the FXYD family, is known to modulate Na/K-ATPase activity. However, despite knowledge of its upregulation, the role of FXYD3 in pancreatic cancer survival has not yet been assessed on a larger scale. Herein, we present a study establishing the rate of immunohistochemically-evaluated FXYD3 expression in chemotherapy-naïve resected PDAC tumours. Furthermore, we demonstrate that FXYD3 expression does not correlate with survival in these patients.

Mismatch repair–deficient colorectal cancer patients are generally older, with often significant comorbidities, and only a limited portion of patients with metastatic tumors underwent oncological treatments. Many of the metastatic tumors present features that may impair response to PD-1 blockade therapy. High proportions of necrosis and stroma were common in metastatic tumors and were associated with worse survival; however, high Crohn's-like reaction density, T-cell proximity score, and CD68+/PD-L1+ cell number in the tumor center and invasive margin were independent prognostic immune factors for improved survival.

The incidence rate of arterial thromboembolism (ATE) was 4.1% over a 2-year follow-up in advanced lung cancer patients. Venous thromboembolism (VTE) was further identified as an independent risk factor for ATE, while intervention with direct oral anticoagulants was seen as less effective for the prevention of ATE in advanced lung cancer patients with VTE.

This study investigates the effect of epigenetic regulator GSK-J4 in the downregulation of CREB and CREBBP in acute lymphoblastic leukemia (ALL) cell lines and relapsed patient samples, leading to apoptosis induction and cell cycle arrest. We propose H3K27 demethylase inhibition as a potential treatment strategy for patients with treatment-resistant ALL, using CREBBP as a biomarker for drug response and combining GSK-J4 with venetoclax and navitoclax as synergistic partners.