Chemotherapy-induced peripheral neuropathy (CIPN) is a prevalent and debilitating complication of cancer treatment, characterized by neuropathic pain, sensory disturbances, and functional impairment that can substantially reduce quality of life. Neurotoxicity induced by chemotherapeutic agents affects peripheral nerves, dorsal root ganglia, and supporting structures, contributing to persistent pain and neurological dysfunction. This systematic review evaluated the efficacy and safety of antidepressants, particularly duloxetine and amitriptyline, in the management of CIPN-related pain. Following PRISMA guidelines and registration in PROSPERO (CRD42024608551), a systematic search of PubMed, Scopus, and Web of Science was conducted for studies published between November 2019 and October 2025. This time frame was selected to capture contemporary evidence and recent developments in multimodal treatment strategies, while acknowledging that foundational studies establishing the efficacy of duloxetine predate this period. Clinical and observational studies involving adult patients with CIPN were included. Of 892 records identified, 11 studies met the eligibility criteria. Duloxetine demonstrated clinically meaningful reductions in neuropathic pain, as assessed by VAS, NRS, and CTCAE measures. Topical amitriptyline also showed promising analgesic effects, although the available evidence remains limited. Combination therapies involving duloxetine and agents such as tapentadol, pregabalin, mirogabalin, or amitriptyline were associated with additional reductions in pain intensity; however, current evidence remains insufficient to establish additive or synergistic effects. Overall, antidepressant therapy was generally well tolerated, with predominantly mild and manageable adverse events. Current evidence supports antidepressants, particularly duloxetine, associated with reductions in pain intensity in heterogeneous studies, whereas evidence for CIPN prevention remains inconclusive. These findings support their continued use in clinical practice and highlight the need for larger, well-designed randomized controlled trials to optimize treatment strategies and further define the role of combination therapies in CIPN management.

Phthalazine derivatives are nitrogen-containing heterocyclic compounds that have gained considerable attention in medicinal chemistry due to their pharmacological potential. This review briefly outlines the biological properties and clinical application of five- and six-membered heterocycles. The main focus is placed on the recent advances in the development and biological evaluation of the phthalazine derivatives. A particular emphasis is put on their PARP and VEGFR inhibitory activity, which has been investigated in clinical trials for cancer treatment, ultimately leading to the market launch of some of these compounds. Furthermore, the recent studies on numerous phthalazine derivatives that demonstrate promising anticancer activity in vitro are presented. Finally, this review combines the previously developed synthesis strategies and possible improvements that could be implemented in the future with clinically oriented summary focused on the application of these compounds in oncology, thereby complementing current literature.

To report a rare case of recurrent intestinal perforation caused by primary intestinal extranodal NK/T-cell lymphoma (ENKTL), analyze the diagnostic challenges of this rare and aggressive malignancy, and raise clinical awareness for its early identification and optimal management in patients with unexplained gastrointestinal perforation.

A 31-year-old female presented with 3 days of persistent hypogastric abdominal pain and a 1-day history of high fever up to 39 ℃. She had undergone emergency surgery for jejunal perforation 20 months prior, with a postoperative pathological diagnosis of Epstein-Barr virus (EBV)-associated T- and NK-cell lymphoproliferative disorders. Multiple follow-up colonoscopies and bone marrow aspiration examinations failed to confirm the diagnosis of ENKTL, due to negative immunohistochemical staining of cluster of differentiation (CD)56 and EBV-encoded small RNA (EBER) in biopsy specimens. Abdominal contrast-enhanced computed tomography on this admission confirmed intestinal perforation, and emergency partial ileectomy was performed. Histopathological examination of the resected specimen showed diffuse full-thickness intestinal infiltration of atypical lymphoid cells, with positive immunohistochemical staining for CD2, CD3, CD56, T‑cell intracellular antigen‑1 (TIA-1) and EBER, and a Ki-67 proliferation index of approximately 70%. The final diagnosis of ENKTL (Ann Arbor stage IVA) was confirmed, and the patient received systemic chemotherapy with a regimen of methotrexate, etoposide, dexamethasone and pegaspargase after surgery.

The patient's general condition improved significantly after combined surgical intervention and systemic chemotherapy. During the 26-month continuous follow-up, the patient remained in good general condition, with no recurrence of abdominal pain, intestinal perforation, disease progression, or severe treatment-related adverse events.

Primary intestinal ENKTL is a rare and highly aggressive subtype of non-Hodgkin lymphoma, whose non-specific clinical and imaging manifestations pose major challenges for early diagnosis, which may lead to delayed treatment and unfavorable prognosis. This disease should be included in the core differential diagnosis for young patients, especially Asian populations, presenting with unexplained gastrointestinal perforation. Repeated deep tissue biopsy, EBER detection combined with comprehensive imaging evaluation are essential for early definitive diagnosis, and timely surgical intervention combined with standardized systemic chemotherapy can effectively improve the clinical outcomes of affected patients.

The American Association of Bronchology and Interventional Pulmonology (AABIP) Essential Knowledge in Interventional Pulmonology Series aims to provide clinicians with concise, up-to-date reviews of key topics in the field, presented on a 3-year rotating cycle. The 2025 series focused on advanced diagnostic bronchoscopy. In this article, we provide an update on the bronchoscopic approach to malignant disease, examining whether navigational bronchoscopy has closed the diagnostic gap with transthoracic needle biopsy for peripheral pulmonary lesions, how advanced bronchoscopic technologies enable integrated diagnosis and mediastinal staging workflows, and whether these clinical benefits translate into meaningful economic value. These reviews are designed to complement the Essential Knowledge in Interventional Pulmonology Lecture Series delivered at the 2025 AABIP Annual Conference, which is available for viewing on the AABIP website: https://aabip.memberclicks.net/essential-knowledge-in-interventional-pulmonology-series.

Familial cerebral cavernous malformation (CCM) is an autosomal dominant vascular disorder with age-dependent penetrance and marked intrafamilial variability. KRIT1 loss-of-function variants are the most common genetic cause, but pediatric genotype-phenotype correlations remain limited.

Clinical, radiological, histopathological, and molecular findings of a pediatric family with suspected familial CCM were reviewed. Brain and spinal MRI, calvarial histopathology, whole-exome sequencing, segregation analysis, and targeted literature review were performed.

The index patient was a 14-year-old boy presenting with focal seizure and a progressively enlarging right parietal calvarial mass. MRI revealed multiple cerebral and cerebellar CCMs with a cervical intramedullary cavernous malformation. The calvarial lesion was excised and confirmed as hemangioma. Whole-exome sequencing identified a previously unreported heterozygous KRIT1 initiation-region duplication, NM_004912.4: c.2dup, predicted to result in p.(Met1IlefsTer31) with loss of all major functional domains. The same variant was detected in the clinically asymptomatic sibling with MRI-confirmed multiple CCMs, whereas the mother was negative. The father had died from intracerebral hemorrhage, but genetic testing was unavailable.

This report expands the KRIT1 mutational spectrum and illustrates the wide clinical range of familial CCM, from asymptomatic radiological disease to epilepsy and fatal hemorrhage within one family. These findings support early molecular diagnosis, cascade screening, and susceptibility-sensitive MRI surveillance.

Efficient diagnostic biomarkers enable early detection of hepatocellular carcinoma (HCC), which improves survival. Circulating extracellular vesicles (EVs) in plasma, as a noninvasive diagnostic carrier, have caused widely concern. Here, a novel oxylipidomic profiling was used to analysis the HCC patients' tissue-derived EVs (TD-EVs) cargo and revealing differentially expressed oxylipins (vs. adjacent tissues, p<0.05), which undetected in bulk tissues. The hub oxylipins 13(S)-HODE discovered in TD-EVs was validated in plasma derived EVs (PD-EVs) by using single-molecule analysis platform, showing superior efficacy in AFP-negative HCC patients (AUC = 0.8474 vs. 0.7627 in AFP-positive). Clinically, machine learning integrating EV-derived 13(S)-HODE with routine clinical parameters of HCC patients was developed to optimize diagnostic classification. The machine learning model, LightGBM, achieved outstanding performance: AUC_mean = 0.962, Sensitivity = 0.933 (0.660-0.997), Specificity: 0.957(0.760-0.998), 95%CI: 0.958-1.000 in multi-group classification of HCC diagnostics, demonstrating the enhanced diagnostic efficiency of 13(S)-HODE positive EV subpopulation with other clinical data. This study firstly establishes EV-derived 13(S)-HODE as a concordantly biomarker across tissue and plasma sources. Furthermore, single-molecule analysis platform offers it a highly sensitive diagnostic performance for HCC, particularly valuable for AFP-negative HCC subgroup.

Gastric cancer (GC) is a heterogeneous disease characterized by diverse molecular profiles and distinct histological subtypes, each with differing prognoses and therapeutic responses. Melanoma-associated antigen-A (MAGEA) genes encode cancer testis antigens frequently expressed in tumor tissue and in limited amounts in normal tissues, making them a promising target for cancer immunotherapy. While therapies targeting MAGEA family members have demonstrated promise across various cancers, clinical trials have been limited by substantial toxicities, underscoring the need to precisely identify patient subgroups most likely to benefit from MAGEA-targeted treatments. We performed gene expression analysis of MAGEA3, 6 and 12 in an Australian-based multicenter cohort of 100 GC patients, including 49 intestinal-type GC cases accrued between 1999 and 2009, and compared expression profiles with those of the Cancer Genome Atlas (TCGA) cohort. Expression patterns were determined in histological and TCGA molecular subtypes of GC. Progression-free survival was examined using the log-rank test and Cox proportional hazards modeling. MAGEA3, 6, and 12 were mainly expressed in intestinal-type GC and were not associated with other clinicopathological variables. Multivariate analyses revealed that elevated expression of these MAGEA members was prognostic of poorer survival in intestinal-type GC patients. In the TCGA cohort, higher MAGEA3, 6, and 12 expression was observed in intestinal-type GC and the chromosomal instability (CIN) subtype, and associations of poorer progression-free survival with high expression were found. Our findings highlight the differences in GC subtype biology and suggest a potential role for MAGEA3, 6, and 12 as biomarkers and targets for intestinal-type GC immunotherapy; however, the relatively small intestinal-type GC sample size warrants validation in larger cohorts.

The NCCN guidelines recommend a chest computed tomography (CT) scan every 6 months for 2-3 years for patients with early-stage non-small cell lung cancer (NSCLC). This study aimed to evaluate whether multi-location CT scans offer a survival benefit.

This study collected clinical data for NSCLC patients who underwent curative intent surgery between 2014 and 2018. Patients were grouped by surveillance CT type: chest CT only (Group CC) or combined chest-abdominal CT (Group CA). The primary outcomes include all-cause mortality, the risk of NSCLC recurrence, and the risk of developing a second primary cancer. Multivariable time-varying Cox models adjusted for clinical factors (age, sex, stage, hospital) and six covariates, including comorbidities, smoking, MVPA, CT frequency, time since surgery, and post-op cancer diagnosis.

Of 32,426 patients, 23,501 were analyzed after exclusions; 22,097 were in Group CC and 1,404 in Group CA. Group CC had a higher recurrence rate (18.7% vs. 14.4%), while Group CA had higher all-cause mortality (19.7% vs. 18.0%). Adjusted Cox analysis showed higher recurrence detection in Group CA (HR 1.80, 95% CI: 1.60-2.01) and lower mortality (HR 0.82, 95% CI: 0.71-0.94) vs. Group CC among patients with recurrence or second cancers. Subgroup analysis showed higher recurrence detection in Group CA for both stages. Mortality was reduced in regional stage (HR 0.77, 95% CI: 0.64-0.93), but not in local stage (HR 1.03, 95% CI: 0.78-1.35).

Multi-location CT surveillance after curative surgery in early-stage NSCLC, especially regional-stage, was associated with lower mortality, recurrence, and second primary cancer risk.

Reports of immune checkpoint inhibitor (ICI) therapy-associated immune-related adverse events (irAEs) exhibit considerable heterogeneity, particularly when comparing data from clinical trials and real-world observational studies.

We conducted a systematic review of real-world observational studies (case reports and series) reporting cardiovascular irAEs in PubMed and Embase from inception to April 1, 2024. We analyzed 116 case reports from 115 studies and highlighted the commonest irAEs, treatments instituted, and ensuing outcomes.

Myocarditis was the most common, accompanied frequently by pericarditis and heart failure. Treatment typically included corticosteroids and discontinuation of ICI therapy. Higher doses of corticosteroids appeared promising. Refractory cases benefited from plasmapheresis, intravenous immunoglobulin, mycophenolate, tacrolimus, or infliximab. Rechallenging ICI therapy after irAEs resulted in mixed outcomes.

Given the heterogeneity of data, analysis of aggregated data from central repositories like Side Effect Registry Immuno-Oncology (SERIO) would be invaluable.

Colorectal cancer (CRC) is a prevalent malignant neoplasm characterized by high incidence and mortality rates. Currently, the role of microRNAs (miRNAs) in CRC is increasingly recognized. In this study, we aim to investigate the prognostic value of miR-363-5p and its associated molecular mechanisms.

A total of 156 paired samples were collected from patients with CRC. The levels of miR-363-5p in the samples were detected by RT-qPCR. KM curves and multivariable Cox regression models evaluated the prognostic value of miR-363-5p. Flow cytometry, CCK-8 assay and Transwell assay examined the effects of miR-363-5p on cellular malignant phenotypes. Dual-luciferase reporter assays validated the targeting relationship.

The expression level of miR-363-5p was declined in CRC, and patients with TNM stage III + IV exhibited lower miR-363-5p expression compared to those with TNM stage I + II. Furthermore, individuals with low miR-363-5p expression demonstrated shorter overall survival than those with high expression, and miR-363-5p was confirmed as an independent protective factor for CRC. In vitro, miR-363-5p suppressed cellular malignant phenotypes, primarily manifested by miR-363-5p mimic promoting apoptosis while inhibiting proliferation, migration and invasion. Mechanistically, we identified MEIS3 as a direct target of miR-363-5p, and rescue experiments confirmed that MEIS3 overexpression attenuated the tumor-suppressive effects of miR-363-5p.

Downregulated miR-363-5p were involved in CRC progression and associated with poor patient prognosis. Mechanistically, upregulated miR-363-5p suppressed the malignant cellular phenotype by negatively regulating MEIS3, thereby inhibiting the progression of CRC.