Cancer patients experience severe financial toxicity, with the mechanisms influencing the relationship between socioeconomic status and financial toxicity in lung cancer patients remaining poorly defined. This study aims to investigate how social support and self-efficacy mediate the association between socioeconomic status and financial toxicity among lung cancer patients in China.

A survey of 755 lung cancer patients was conducted at a tertiary oncology hospital in Shandong Province, China, from October to December 2023, utilizing random sampling. Data collection included demographic and socioeconomic details, along with assessments of social support, self-efficacy, and financial toxicity. Regression and Bootstrap analyses were used to explore the sequential mediating effects of socioeconomic status, self-efficacy, social support, and financial toxicity.

(1) Significant correlations emerged among socioeconomic status, social support, self-efficacy, and financial toxicity (p < 0.05). (2) Socioeconomic status was significantly associated with financial toxicity (p < 0.05). (3) Self-efficacy mediated the relationship between socioeconomic status and financial toxicity (β = 0.203, p < 0.05), whereas social support did not exhibit a mediating effect in this relationship (β = 0.039, p = 0.194). (4) Social support and self-efficacy had a chain-mediated role in the relationship between socioeconomic status and financial toxicity in patients with multimorbidity (β = 0.072, p < 0.05).

This study identifies social support and self-efficacy as chained mediators that link socioeconomic status with financial toxicity among lung cancer patients. It is recommended that targeted interventions be implemented to increase social support for patients with lower socioeconomic status to mitigate financial toxicity.

Moderate-to-severe fatigue commonly occurs in patients with cancer. Given the numerous roles that epigenetic processes may play in the development and severity of fatigue, the purposes of this study were to (1) use a data-driven discovery approach to evaluate for mechanisms underlying morning fatigue in a group of oncology patients receiving chemotherapy and (2) identify common biological mechanisms associated with morning fatigue severity across these independent epigenetic evaluations.

Patients completed questionnaires during the week prior to their chemotherapy treatment. Severity of morning fatigue was evaluated using the Lee Fatigue Scale. Associations between morning fatigue severity and epigenetic aging acceleration (EAA), immune cell type compositions, and differential methylation of expression-associated loci (eCpGs) in distal regions (i.e., upstream of a gene on the same chromosome) were evaluated. These results were then evaluated for common biological mechanisms.

High morning fatigue was associated with older epigenetic age, positive EAA, and higher levels of EAA. Patients of the "Fast ager" type were more likely to have high morning fatigue. Higher morning fatigue was associated with lower (CD4 memory, CD8 memory, and NK) and higher (neutrophil and T regulatory) estimated proportions of cell types. Morning fatigue severity was associated with one differentially methylated distal region containing five eCpGs mapping to three genes (i.e., CILP, ONECUT1, SLCO3A1). Preliminary support was found for the role of Inflammaging as a common biological mechanism for morning fatigue.

This study provides an epigenetic characterization of morning fatigue in patients receiving chemotherapy. The findings suggest that biological aging, gene regulatory, and inflammatory processes may contribute to morning fatigue and provide future targets for therapeutic interventions.

Prophylactic cranial irradiation (PCI) is part of standard treatment for patients with limited disease small cell lung cancer (LD-SCLC), treated with curative intent. However, doubt has been raised about the efficacy of PCI in a modern clinical setting. Therefore, we examined factors impacting PCI receival, the cumulative incidence of symptomatic brain metastases, and overall survival (OS) with and without PCI. Patient/material and methods: Records of 190 patients with LD-SCLC consecutively treated between 2012 and 2021 at our institution were reviewed. Patients were grouped based on whether they received PCI (PCI, n = 119) or not (no PCI, n = 71). Baseline characteristics, Kaplan-Meier estimates of OS, and cumulative incidence of symptomatic brain metastases were compared for the two groups.

PCI no patients were older, had a poorer performance status, were more often treated in 2018-2021 and had more frequently a brain magnetic resonance imaging (MRI) at the time of diagnosis. No PCI median OS was 19 months compared to 24 months for PCI, not significantly different (p = 0.40). During follow-up 54 patients (28.4%) developed symptomatic brain metastases, with no statistically significant difference in the numbers of patients with, and cumulative incidence of, symptomatic brain metastases between the two groups (p = 0.35 and p = 0.21, respectively).

Despite patients not receiving PCI being older and in poorer performance status, no statistically significant difference in OS or cumulative incidence of brain metastasis were observed compared to patients who received PCI. This supports uncertainty regarding the role of PCI.

Investigating real-world outcomes of moderately hypofractionated radiotherapy (hypoRT) in elderly and multimorbid stage IIB-IIIC non-small-cell lung cancer (NSCLC) patients ineligible for concurrent chemoradiation.

We retrospectively analysed 70 patients with primary or recurrent stage IIB-IIIC NSCLC (TNM, 8th edition). HypoRT was administered to a total dose of 38-56 Gy in 10-17 fractions (2.5-3.8 Gy/fraction). Patterns of recurrence, survival outcome, and toxicity were assessed.

Seventy patients, with a median age of 76.4 years (range: 51.6-88.2 years), who received hypoRT between August 2015 and September 2022, were reviewed. At baseline, the median Charlson Comorbidity Index (CCI) with oncological diagnosis was 8 (range: 3-13). With a median follow-up post-radiotherapy of 63.9 months (95% Confidence Interval [CI]: 34.8-93.1 months), median progression-free survival (PFS) was 7.6 months (95% CI 6.0-11.0 months), and the median overall survival (OS) was 20.7 months (95% CI 16.7-30.7 months). Competing risk analysis revealed 12-month cumulative incidences of locoregional and distant failure in 41% (95% CI 30-53%) and 14% (95% CI 6-23%) of patients, respectively. Following disease progression, 45 patients received subsequent therapy: 25 underwent additional radiotherapy, 22 received systemic treatment (including immunotherapy), and 19 were referred for best supportive care. Treatment was well tolerated; only 3 patients (4%) developed grade 3 pneumonitis. No adverse events of grade > 3 were reported.

Moderately hypoRT is a safe, feasible, and effective treatment option for elderly and multimorbid patients with stage IIB-IIIC NSCLC, offering encouraging survival outcomes and low toxicity rates. Future prospective studies are needed to validate these findings and optimise treatment strategies for this high-risk population.

Cancer is among the major causes of death after heart transplant (HTx). Risk factors for cancer occurrence in this setting are not well established. This was a retrospective observational study of patients who underwent HTx between 2006 and 2019 and were followed up until May 2024. Clinical variables possibly associated with cancer were assessed with univariable and multivariable analyses. Survival analysis was carried out drawing Kaplan Meier curves and a Cox regression with time-varying covariates were performed to overcome the immortal-time-bias. Three-hundred-thirty-five HTx recipients were included, of whom 42 (12.5%) developed cancer after a median of 6.3 years. In univariable analysis, older age at HTx, smoking history, alcohol use, male sex, ischemic heart disease before HTx, use of cyclosporine rather than tacrolimus, and increased length of follow-up were associated with cancer. Upon multivariable analysis, ischemic heart disease (OR 2.70 [1.19-6.11], p = 0.017) and length of follow-up (OR 1.02 [1.00-1.04], p = 0.007) were independently associated with cancer occurrence. Cox regression revealed a higher risk of mortality among patients with cancer (HR 3.400, [2.026-5.709], p < 0.001). HTx recipients with prior ischemic cardiomyopathy and a longer survival time after transplant show a higher risk of developing cancer. Cancer significantly impairs post-transplant survival.

Colorectal cancer (CRC) remains a significant global health concern, being the third most common cancer and the second leading cause of cancer-related death. A colonoscopy examination is central to CRC prevention, enabling screening and adenoma removal. Nevertheless, the emergence of post-colonoscopy colorectal cancer (PCCRC), which is a CRC diagnosed after a colonoscopy that initially found no malignancy, highlights the critical gaps in the quality of current colonoscopy practices. Missed lesions, particularly those with a non-polypoid morphology or in the proximal colon, are the leading cause of PCCRC, accounting for approximately 80% of cases. Efforts to combat PCCRC focused on enhancing the colonoscopy quality through measurable indicators and developing novel technologies to improve the colonoscopy performance. Evidence of how these interventions are associated with the PCCRC risk is critical for endoscopists to obtain the best efficacy from colonoscopy screening. This review summarizes current clinical studies regarding this issue, focusing on randomized control trials and cohort studies to identify the future direction of clinical research on preventing PCCRC.

Chicken ovalbumin upstream promoter‑transcription factor II (COUP‑TFII), also known as nuclear receptor subfamily 2 group F member 2, is an orphan nuclear receptor that controls various biological processes, including development, angiogenesis, metabolism and tissue homeostasis. Structurally, COUP‑TFII comprises a DNA‑binding domain and a ligand‑binding domain, facilitating its interaction with various signaling pathways, and thereby exerting diverse biological effects. Alterations of the expression or transcriptional activity of COUP‑TFII are associated with various diseases, including cardiovascular diseases (CVDs) and different types of cancer such as colorectal cancer (CRC). In the context of CVDs, COUP‑TFII serves a key role in the development and function of the vascular system. Dysregulation of COUP‑TFII leads to aberrant angiogenesis and vascular remodeling, contributing to the pathogenesis of various CVDs. In CRC, COUP‑TFII acts as either a tumor suppressor or a tumor promoter, depending on the cellular context. The present review explores the structure and regulatory mechanisms of COUP‑TFII, its functions and molecular mechanisms in CVDs and CRC, and its emerging role in linking these diseases, offering insights into potential treatments and future research directions.

While consolidation immunotherapy after chemoradiotherapy (CRT) improves survival in limited-stage small cell lung cancer (LS-SCLC), some patients develop out-of-field progression during consolidation. Optimal management in such cases remains undefined.

We describe a 49-year-old male with LS-SCLC who developed supraclavicular lymph node metastasis during consolidation immunotherapy following definitive CRT. The patient underwent concurrent chemoradiotherapy targeting the recurrent node, followed by continued consolidative immunotherapy. This approach led to complete response of both the primary tumor and the metastatic lymph node, with minimal toxicity.

This case highlights the potential role of combining salvage radiotherapy with continued immunotherapy in managing isolated nodal recurrence during consolidation. Further studies are warranted to validate this individualized strategy.

Myeloproliferative neoplasms (MPNs) are a group of clonal hematopoietic stem cell disorders characterized by proliferation of one or more myeloid lineages in the bone marrow, resulting in an increased number of mature and immature cells in the peripheral blood and bone marrow. Chronic myeloid leukaemia (CML) is one of the commonest clonal myeloproliferative neoplasms encountered in clinical practice. It is characterized by a reciprocal rearrangement and fusion of the BCR genes on chromosome 22 and the ABL gene on chromosome 9.  Materials and methods: A cross-sectional study on the clinicohematological profile of chronic myeloid leukemia patients was conducted over five years in the hematology section of the pathology department in a tertiary care centre in North India. Detailed clinical history and examination, laboratory investigations of all the patients, along with molecular and cytogenetic studies, were noted from the patients' file records and bone marrow request forms. Peripheral blood film (PBF), bone marrow aspiration (BMA), clot section, and bone marrow biopsy slides were studied in detail. Frequencies and proportions were calculated based on all the above parameters, with relevant statistical analysis and final diagnosis were made and classified according to the WHO 2016 classification.

There were a total of 76 patients with CML, out of which 52 (69%) were in the chronic phase, 6 (8%) in the accelerated phase, and 18 (24%) in blast crisis. Leucocytosis with myeloid predominance was seen both on peripheral blood film as well as in bone marrow aspiration and biopsy slides in all of the cases. Cytogenetic studies showed BCR-ABL1 positivity in the majority of the patients (82.8%; n=63).

Most of the data available on MPNs is from studies in developed countries. There is only limited literature in India due to a lack of a centralized registry. The present study was an attempt to categorize CML as a group based on symptoms, morphology, and cytogenetics at a tertiary care hospital in a real-world setting.

Building upon the established role of P21 Activated Kinase 6 (PAK6) in tumor progression and chemoresistance pathways, we postulate its potential as a dual-function biomarker for small cell lung cancer (SCLC). This investigation aims to conduct a comprehensive evaluation of PAK6's diagnostic validity and prognostic significance through comparative analysis of PAK6 serological levels across distinct clinical cohorts to determine diagnostic thresholds, and its clinical correlation with therapeutic responsiveness.

This study included 109 patients diagnosed with SCLC, 92 patients with non-small cell lung cancer (NSCLC), 85 patients with pulmonary nodules (PN), and 94 healthy individuals undergoing routine physical examinations as the normal control group (NC). Serum PAK6 concentrations were measured using enzyme-linked immunosorbent assay (ELISA). Additionally, levels of neuron-specific enolase (NSE), carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA19-9), and pro-gastrin-releasing peptide (ProGRP) were quantified via chemiluminescence assays. Progression-free survival (PFS) data for SCLC patients were collected through case review and telephone follow-up.

Serum PAK6 levels were significantly higher in the SCLC group compared to the other three groups (p < 0.01). Similarly, NSE and ProGRP levels were markedly elevated in the SCLC group compared to the other groups (p < 0.01). Correlation analysis revealed a positive association between PAK6 and variables such as gender, VA (Veteran's Administration Lung Cancer Study Group) stage, age, smoking status, CEA, CA19-9, NSE, and ProGRP. The serum tumor markers (STMs) PAK6, NSE, and ProGRP exhibited superior diagnostic performance, with AUCs of 0.892, 0.834, and 0.935, respectively (95% confidence interval (CI) [0.857-0.927], [0.778-0.890], and [0.909-0.960]), compared to CEA and CA19-9 (AUCs = 0.676 and 0.611, respectively; 95% CI [0.622-0.731] and [0.547-0.675]) (p < 0.01). Furthermore, PAK6, NSE, and ProGRP levels significantly decreased after three months of treatment, while CEA and CA19-9 showed no significant changes. Survival analysis demonstrated that higher PAK6 levels were associated with poorer SCLC prognosis. Increased serum PAK6 expression correlated with shorter PFS (HR = 2.02 [1.33-3.07], P = 0.001).

Serum PAK6 holds significant clinical value for the diagnosis, treatment monitoring, and prognosis evaluation of SCLC and may serve as a potential therapeutic target for the disease.