tamsulosin (tamsulosin WOWTAB / Harnal D)

NK and CIK Cells in Hematologic Malignancies: Comparative Mechanisms, Clinical Evidence, and Translational Perspectives.

Mosadegh Manshadi Shiva S, Sankanian Ghazaleh G, Moshari Mohammadreza M, Hajifathali Abbas A et al.

Hematologic malignancies remain a major cause of morbidity and mortality despite advances in chemotherapy, targeted therapies, and hematopoietic stem cell transplantation. Adaptative cell therapy has emerged as a promising approach, in which natural killer (NK) and cytokine-induced killer (CIK) cells appear as potentially complementary effective platforms. This review critically compares NK and CIK cells as two adaptive cellular immunotherapy platforms for hematologic malignancies, focusing on their biological properties, antitumor mechanisms, production strategies, clinical evidence, safety profiles, and translational limitations. NK and CIK cells were comparatively evaluated with respect to their biological properties, antitumor mechanisms, production strategies, clinical evidence, safety profiles, and translational limitations. NK cells, through the release of perforin-granzyme, death receptor pathways, and antibody-dependent cytotoxicity, perform rapid tumor clearance, allowing for immediate tumor volume reduction, but with limited persistence in vivo. In contrast, in vitro-expanded CIK cells (CD3+CD56+) show robust proliferation and sustained cytotoxicity, with an overall low, but not entirely zero, risk of graft-versus-host disease, supporting long-term immune surveillance. CAR engineering, cytokine-induced memory-like NK cells, and DC-CIK platforms may improve persistence, specificity, and metabolic fitness. Combination strategies with checkpoint inhibitors and standard therapies may enhance antitumor efficacy. However, most evidence is still preliminary and comes mainly from early-phase, single-arm, and heterogeneous studies. NK and CIK cells may offer complementary benefits rather than direct competitive approaches. Their distinct functional properties provide the biological rationale for future combination or sequential strategies. However, prospective clinical studies are needed to define their efficacy, safety, durability, and optimal clinical application in hematological malignancies.

Selective Uptake of Oral Extended-Release Hydromorphone After Formulary Listing in Cancer Care.

Kajiura Shinya S, Chikaoka Shingo S, Hayashi Ryuji R

Context-dependent roles of HtrA2/Omi in ovarian cancer: mitochondrial apoptotic function linking platinum sensitivity and acquired chemoresistance-a narrative review.

Wu Yao Y, Gu Yu Y, Wang Xuemei X, Cheng Hongjing H

Epithelial ovarian cancer often responds to platinum therapy but frequently relapses with acquired chemoresistance. HtrA2/Omi is a mitochondrial serine protease that can promote apoptosis after cytosolic release. This narrative review synthesizes ovarian-cancer-specific and mechanistic evidence and asks whether HtrA2/Omi is better understood as a static expression marker or as a stress-activated apoptotic effector linked to platinum response. PubMed, Web of Science, Scopus, and reference lists were searched through April 30, 2026 and updated through June 25, 2026 using terms related to HtrA2/Omi, PRSS25, ovarian cancer, platinum resistance, apoptosis, X-linked inhibitor of apoptosis protein (XIAP), mitochondrial release, cytosolic release and invasion. A structured narrative approach was used because the ovarian HtrA2/Omi literature is limited, heterogeneous, and unsuitable for pooled quantitative synthesis. This review proposes a two-layer model. Baseline HtrA2/Omi abundance is context dependent and varies with histotype, assay platform, treatment state, and compartment resolution. In contrast, under platinum or mitochondrial stress, cytosolic HtrA2/Omi release more consistently supports XIAP relief, caspase activation, apoptosis, and platinum sensitivity. Persistent post-treatment HtrA2/Omi loss may mark an apoptosis-deficient resistant state. HtrA2/Omi should not be framed as a simple oncogene or tumor suppressor in ovarian cancer. Its clearest value is as a candidate response-linked, compartment-aware marker of platinum-induced apoptotic competence. Clinical use requires longitudinal, histotype-stratified and microenvironment-aware validation before treatment selection.

Formaldehyde exposure risk assessment among fiberboard furniture manufacturing workers in Thailand: Comparison of TIS 2012 and EPA IRIS standards.

Thetkathuek Anamai A, Jaidee Wanlop W

Formaldehyde exposure in medium-density fiberboard furniture manufacturing is an important occupational health concern because formaldehyde-containing resins can release hazardous airborne emissions during production processes. The aim of this study was to evaluate and compare formaldehyde exposure risks among furniture manufacturing workers using the Thai Industrial Standard (TIS) 2012 semi-quantitative model and the United States Environmental Protection Agency Integrated Risk Information System (EPA IRIS) quantitative model, and to examine the concordance between the two frameworks. A cross-sectional study was conducted among 439 workers from ten departments in a medium-density fiberboard furniture factory in Chachoengsao Province, Thailand. Work characteristics and health symptoms were collected using structured questionnaires. Full-shift personal air sampling was performed in accordance with the National Institute for Occupational Safety and Health Method 5700, and samples were analyzed by high-performance liquid chromatography. Risk characterization was conducted using TIS 2012 based on exposure rating × health effect rating, while EPA IRIS was applied to estimate non-cancer risk using the hazard quotient and lifetime cancer risk using the inhalation unit risk. Non-cancer and lifetime cancer risks were assessed using HQ and inhalation unit risk. The mean formaldehyde concentration was 5.47 mg/m3 (0.70-11.55 mg/m3), peaking in the Clearing department (11.55 mg/m3). TIS 2012 classified 80% of departments as very high risk, compared with 50% under the EPA IRIS HQ model. The EPA IRIS model showed hazard quotients ranging from 6.59 to 87.99 and lifetime cancer risks ranging from 7.72×10-3 to 1.27×10-1, all exceeding the acceptable cancer risk threshold of 1×10-6. Concordance between the two models was 73%, with discrepancies observed in the Edging and Drilling departments. All departments had unacceptable cancer risks, indicating the need for immediate exposure-control measures. Integrating semi-quantitative and quantitative assessment frameworks is essential for comprehensive occupational risk management. Departments identified as very high risk by both models require urgent control measures and inclusion of cancer-risk assessment in routine occupational health surveillance.