Hematopoietic stem cell transplantation (HSCT) is a critical treatment for non-Hodgkin lymphoma (NHL) but involves significant post-transplant risks. Frailty, measured by the Modified Frailty Index-11 (mFI-11), may influence outcomes.

We analyzed NHL patients undergoing autologous or allogeneic HSCT from the Nationwide Inpatient Sample (2016-2020). Frailty was defined by mFI-11, and outcomes included in-hospital mortality, unfavorable discharge, prolonged length of stay (LOS), complications, and costs. Multivariable regression models with stratification by age and Charlson Comorbidity Index were applied.

Of 2807 patients (ages 18-85), frail patients were older and had more comorbidities. In autologous HSCT, frailty was linked to higher mortality (2.02% vs. 0.27%, p < 0.001), increased unfavorable discharges (19.75% vs. 10.80%, p < 0.0001), and prolonged LOS (15.92% vs. 7.75%, p < 0.0001). Similar trends were observed in the allogeneic cohort.

Frailty predicts worse post-transplant outcomes in NHL patients undergoing HSCT, emphasizing the need for pre-transplant frailty screening.

Neoadjuvant therapy has become a cornerstone in the management of locally advanced rectal cancer (LARC). In this single-arm, open-label phase II study, we evaluated the efficacy and safety of total neoadjuvant chemotherapy (TNT) using a CapOX regimen combined with a programmed cell death protein 1 (PD‑1) antibody (sintilimab) and interleukin‑2 (IL‑2) in patients with microsatellite stable (MSS)/defining proficient mismatch repair (pMMR) LARC. A total of 33 patients, aged 18-75 years, with rectal tumors located within 12 cm from the anal verge and staged as cT3/4N_anyM0 or cT_anyN⁺M0, were enrolled. Patients received a regimen consisting of oxaliplatin, sintilimab, capecitabine, and IL‑2 administered in a three‑week cycle, with response evaluations performed after every two cycles. Following six cycles of treatment, 33 patients underwent radical surgery, achieving a 100% R0 resection rate. The pathological complete response (pCR) rate was 42.4% (95% CI: 25.68-59.16%) while the remaining 19 patients (57.6%, 95% CI: 41.07-74.09%) were assessed as having a partial response. The tumor regression grades (TRG) were, TRG1: 3 cases (9.1%, 95% CI: 1.90-25.97%), TRG2: 14 cases (42.4%, 95% CI: 26.27-60.38%), and TRG3: 2 cases (6.1%, 95% CI: 0.73-20.37%), respectively. Surgical safety reported as no cases of grade B/C anastomotic leakage or bowel obstruction. Adverse events (AEs) were manageable, with a 21.2% incidence of grade 3 events and no grade IV/V events or treatment‑related deaths. With a median follow‑up of 25.5 weeks, no recurrences were observed. Analysis of blood and tissue samples from patients with different treatment outcomes revealed significant activation of CD8⁺ T cells, NK cells, and M1 macrophage subsets in the tumor microenvironment of patients achieving pCR. These compelling data demonstrate promising efficacy with a favorable safety profile in MSS/pMMR LARC. These findings warrant studies to validate this regimen as a novel treatment paradigm for rectal cancer. ClinicalTrials.gov registration: NCT06108596.

Pancreatic ductal adenocarcinoma (PDAC) is the sixth leading cause of global cancer death. The process of epithelial-to-mesenchymal transition (EMT) is a key driver of early progression and metastasis in PDAC.

Our study aimed to explore the correlation between the expression of EMT markers and survival outcomes.

We conducted a retrospective longitudinal study on patients diagnosed with resectable PDAC between January 2005 and June 2019, with a 5-year follow-up for survival analysis. Immunohistochemical staining was performed to assess E-cadherin and vimentin expression. EMT was defined as the presence of high Vimentin (mesenchymal) expression combined with low E-cadherin (epithelial) expression. The study cohort included 135 patients with resectable PDAC, with 86 males (63.7%) and a mean age of 63.5 years (SD 10.1); most tumors were grade 2 (84, 64.6%). Cox regression analysis revealed that Vimentin expression (p = 0.005), positive margin (p = 0.008), and absence of metformin intake (p = 0.023) were independent predictors of poor OS. High Vimentin was associated with lower median OS (17.0 ± 4.4 vs. 25.8 ± 2.3 months, p = 0.037) and DFS (8.6 ± 1.2 vs. 13.0 ± 2.3 months, p = 0.014), compared to low Vimentin, and it was correlated with higher tumor grade (p = 0.028) and metastasis rate (p = 0.032). The poorest outcomes were observed when high Vimentin was coupled with low E-cadherin (median OS of 12.6 ± 4.7 vs. 24.5 ± 2.1 months, p = 0.038; median DFS of 9.5 ± 0.5 vs. 10.8 ± 2.1 months, p = 0.029), compared to the rest of the population.

Our findings showed that Vimentin overexpression and the EMT phenomenon are strongly associated with poor OS and DFS in resectable PDAC, underscoring their potential as prognostic biomarkers and therapeutic targets.

Cancer therapy-related cardiac dysfunction (CTRCD) is among the most important adverse effects of treatment of childhood cancer. In the EARLY study (Early detection of acute and early-onset cARdiovascuLar toxicity in children with cancer using a multiparametric approach), cardiac function in children treated for cancer was monitored during and shortly after treatment, using advanced echocardiography, electrocardiography, and cardiac magnetic resonance (CMR) techniques.

In this prospective pilot study, 100 children newly diagnosed with childhood cancer receiving anthracyclines as part of their cancer treatment were included. A subgroup of 30 children was included in the CMR sub-study. Echocardiography, electrocardiography, and CMR were performed before (T0), three and a half months after (T1), and one year after (T2) start of anthracycline treatment. In this article, we focus on the methodological aspects of the EARLY study, including patient enrollment and characteristics of the study cohort, as well as the feasibility of advanced echocardiography.

The last patient was included in August 2022. Follow-up for the last patient was finalized in August 2023. Follow-up was completed by 92% of the total study population and 97% of the CMR sub-study.

Protocol adherence was high (92%-97%) and a full collection of data on each included individual was achieved. Advanced echocardiography, i.e., 4D ejection fraction and global longitudinal strain, was feasible in 76% and 69% of measurements, respectively. Cardiac outcomes during and shortly after treatment, as well as associations with known risk factors for CTRCD, such as anthracycline dose, dose of radiotherapy involving the heart, childhood cancer disease profile, age at diagnosis and sex will be reported in a future publication. The feasibility of the study allows for future insight into the correlation between early-onset CTRCD and heart failure during long-term follow-up of childhood cancer patients.

ClinicalTrials.gov identifier: NL-OMON22737.

Recent studies have demonstrated the significance of gut microbiota in the colorectal cancer (CRC) pathogenesis. But their role in carcinogenesis remains to be established. Thus, we established a clinical cohort and the faecal samples from CRC and healthy control were collected. Our metagenomic analysis found that the presence of Parvimonas micra exhibited the most significant relationship with the occurrence of CRC. Increased colonisation of P. micra in CRC was validated with analysis of 1379 faecal metagenomes from eight public cohorts. Untargeted metabolomics subsequently identified an accumulation of phenyllactic acid (PLA) in faecal samples from CRC patients. Higher concentration of PLA was detected in the supernatant from our isolated P. micra. Whole-genome sequencing confirmed that a series of genes associated with PLA biosynthesis such as pdhD were observed in the P. micra genome. Importantly, both P. micra and PLA-induced carcinogenesis in Apc^Min/+ and azoxymethane/dextran sulphate sodium salt mice model. The roles of P. micra and PLA in CRC development were associated with DNA damage. Engineered Escherichia coli BL21 that encoded the heterologous pdhD from P. micra could also induce DNA damage. Mechanically, PLA-induced DNA damage and CRC carcinogenesis were significantly alleviated in Ahr^-/- mice. Aryl hydrocarbon receptor (AHR) inhibitor exhibited a therapeutic potential to reduce mice carcinogenesis. These findings established the role of P. micra and its metabolite, therefore providing diagnostic and therapeutic targets for treating CRC.

To evaluate the association between low-dose ionizing radiation from dental imaging (conventional radiography and cone-beam/medical CT) and cancer risk using contemporary epidemiological evidence.

This systematic review and meta-analysis followed PRISMA 2020 guidelines. PubMed, Scopus, and Web of Science were searched up to March 2026 for observational cohort and case-control studies assessing cancer risk after dental radiographic exposure. Risk of bias was assessed using Joanna Briggs Institute tools, causal inference with COSMOS-E guidance, and certainty of evidence with the GRADE framework. Random-effects models pooled adjusted Odds Ratios (ORs) and adjusted Hazard Ratios (HRs) with 95% confidence intervals (CIs).

Among 1,883 records, 24 studies met inclusion criteria, and 19 were included in meta-analysis (415,887 participants). In the 16 case-control studies, thyroid cancer was significantly associated with dental imaging (OR = 2.21; 95% CI: 1.63-2.99), while central nervous system (CNS) tumors showed a non-significant elevation (OR = 1.31; 95% CI: 0.89-1.91). In the three cohort studies, thyroid cancer showed a small but significant association with conventional radiography (HR = 1.13; 95% CI: 1.01-1.26), and CNS tumors risk was moderately associated with CT scan exposure (HR = 1.54; 95% CI: 1.03-2.29). Certainty of evidence was rated low for thyroid cancer, and very low for central nervous system cancers, lymphoid cancer, oral cancer and salivary gland cancer due to risk of bias, inconsistency, and imprecision.

Current evidence is insufficient to confirm an association between low-dose dental radiographic exposure and cancer. A small increased risk was observed, but certainty remains very low, highlighting the need for well-designed prospective research.

Lactylation and liquid-liquid phase separation related genes have been reported to be associated with tumor prognosis and immunity, but their specific influence on the prognosis and immune characteristics of diffuse large B-cell lymphoma (DLBCL) remains unclear.

GSE56315 (33 control samples and 55 DLBCL patient samples) has been used to screen for lactylation and liquid‒liquid phase separation related differentially expressed genes (LLRDEGs). Based on the optimal cutoff, LLRDEGs associated with DLBCL prognosis (overall survival) was further screened through LASSO and univariate Cox regression. Then, based on the GSE10846 dataset (414 DLBCL samples), a prognostic model was constructed based on the LLRDEGs. The Kaplan-Meier curve is used to evaluate the prognostic value (median risk score). And validate the prognostic model on an independent external validation dataset (GSE181063 (1310 DLBCL samples)). Finally, further analysis was conducted on consensus clustering, biological pathways, the immune microenvironment and drug sensitivity.

4 LLRDEGs were ultimately identified as genes associated with the DLBCL' prognosis. A prognostic model was constructed based on the 4 LLRDEGs. An independent external validation dataset confirmed the prognostic model's prognostic value. 4 LLRDEGs were significantly correlated with various immune cells.

This study screened four LLRDEGs significantly associated with prognosis and constructed a prognostic risk stratification model. The Kaplan-Meier curve confirms the prognostic value of the prognostic risk stratification model. This prognostic model is related to the clinical characteristics and immune microenvironment of DLBCL patients.

This study elucidates the role of LLRDEGs in the prognosis and immune features of DLBCL, providing insights into potential therapeutic targets.

Atypical fibroxanthoma (AFX) and pleomorphic dermal sarcoma (PDS) are rare cutaneous mesenchymal tumours sharing clinical and histopathological features. Compared to AFX, PDS has an increased risk of local recurrence and metastasis. A precise diagnosis is critical to ensure proper clinical management and follow-up. AFX and PDS show a similar genetic background, but also a heterogeneous pattern of different molecular abnormalities still poorly investigated due to the rarity of these tumours. Multiple data from different institutions and geographical areas, facilitate the identification of molecular alteration/s of valuable diagnostic and/or sub-classification power. We investigated the DNA profile of 32 AFX and PDS samples using a custom targeted Next-Generation Sequencing panel including 228 cancer genes. We confirm a common pattern of gene mutations affecting TP53, CDKN2A and NOTCH1. Differences appeared in less frequently detected genes (e.g. TSC2) and in NF2 harbouring novel genetic alterations. Integrating our results with published datasets of AFX and PDS mutation profiles we observed a divergent distribution of alterations in genes signalling through angiogenic pathway (KDR, PDGFRB), DNA damage response (ATR), cellular migration/metastasis (DDR2, CDH1). These differences do not reach statistical significance, and histopathological evaluation remains the diagnostic gold standard, however, they offer valuable insights into the pathogenesis of these tumours.

Serrated lesions of the appendix are rare, often incidental findings in routine appendectomy specimens. Their true frequency, histopathologic spectrum, and anatomic distribution remain incompletely characterized, partly due to variability in sampling practices.

We retrospectively reviewed 2,137 appendectomy specimens (2015-2025) from a single tertiary pathology center. Cases with histologically confirmed serrated lesions were reexamined, classified as hyperplastic polyp (HP) or sessile serrated lesion/polyp (SSL/P), and assessed for clinicopathologic parameters including lesion size, location, and associated pathologies. Nonparametric tests were used, with statistical significance defined as p < .05.

Serrated lesions were identified in 34 cases (1.6%), comprising 17 HPs (0.8%) and 19 SSL/Ps (0.9%). SSL/Ps were significantly larger than HPs (median 10.0 vs. 2.7 mm, p < .001) and were more frequently located in the distal appendix (68.4% vs. 33.3%, p = .045, one-tailed Fisher's exact test). No dysplasia or traditional serrated adenoma was detected. Acute appendicitis was present in 88% of cases, and associated neoplasms in 9%.

Appendiceal serrated lesions are uncommon and often incidental. In this large appendectomy series, SSL/Ps differed from HPs by larger size and distal predilection. These findings primarily support diagnostic awareness and optimized sampling/ grossing practices-particularly careful evaluation of the distal appendix-rather than clinical risk stratification. Further studies incorporating systematic clinical correlation and molecular/immunohistochemistry analyses are warranted.

This UK-based retrospective analysis describes real-world treatment patterns and outcomes in 175 patients with accelerated (AP, n = 69) or blast-phase (BP, n = 106) 'Philadelphia-negative' myeloproliferative neoplasms (MPN-AP/BP) diagnosed between 2013 and 2025. Median age at transformation was 71 years. With a median follow-up of 45.2 months, median overall survival (OS) was 14.9 months, significantly worse for MPN-BP (6.7 months) versus MPN-AP (25.3 months). Treatment selection was heterogeneous across centres. Intensive chemotherapy (IC) improved outcomes only when followed by allogeneic haematopoietic stem cell transplant (allo-HSCT) (median OS 24.7 months). Ruxolitinib-based regimens, particularly combined with azacitidine, showed acceptable activity in AP (median OS 27.2 months). Venetoclax-based regimens achieved a median OS of 14.9 months across the cohort. Multivariable analysis identified IC and venetoclax-based therapy as independently associated with better outcomes, reflecting patient selection, while TP53 mutations predicted inferior survival. IC carried high rates of febrile neutropenia and sepsis; venetoclax was associated with prolonged cytopenias. This study confirms the poor prognosis of MPN-AP/BP, the absence of a unified UK consensus approach and the need for improved therapies and prospective studies to determine optimal treatment approaches for this challenging cohort.