Oncology Reviews最新文献

Breast cancer (BC) remains a leading cause of cancer-related morbidity and mortality worldwide. Its marked heterogeneity - encompassing molecular subtypes, histological characteristics, and variable therapeutic responses - continues to pose persistent clinical challenges Although advances in surgery, hormone therapy, chemotherapy, and targeted therapies have significantly improved patient outcomes, issues such as therapeutic resistance and disease relapse are still common, underscoring the need for novel molecular targets. Within this context, non-coding RNAs (ncRNAs) have emerged as pivotal regulators of breast cancer biology and hold promise as diagnostics and therapeutic agents. These non-protein-coding RNA molecules include diverse subclasses, such as long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and small non-coding RNAs (sncRNAs), each characterized by distinct structural features and biological functions. Mounting evidence implicates ncRNAs in key oncogenic processes - such as tumor initiation, progression, metastasis, immune evasion, and treatment resistance - often in a subtype-specific manner. Importantly, ncRNA expression profiles differ significantly across BC subtypes, and their stability in body fluids underscores their potential utility in liquid biopsy-based diagnostics. This review provides an integrated overview of the multifaceted roles of ncRNAs in BC, emphasizing their mechanisms of action, contributions to tumor heterogeneity, and translational potential as both biomarkers and therapeutic targets. Understanding ncRNAs complexity and context-specific functions may pave the way toward more precise, personalized interventions for BC patients.

Radiation-induced intestinal injury (RIII) poses a significant clinical challenge for patients undergoing pelvic or abdominal radiotherapy, characterized by dual features of acute symptoms (diarrhea, abdominal pain, rectal bleeding) and chronic complications (stricture, fistula, chronic pain), profoundly impacting quality of life. Despite high clinical prevalence, the molecular and cellular mechanisms underlying RIII remain poorly defined, hindering therapeutic development. Current diagnostic modalities (imaging, endoscopy) lack sensitivity and specificity for early detection or real-time monitoring. While biomarkers offer promise for non-invasive assessment and prognosis, existing candidates face limitations in reproducibility and clinical applicability. Therapeutic options, ranging from pharmaceuticals to surgery, show variable efficacy, underscoring the need for optimized strategies. This review systematically explores RIII pathogenesis, emphasizing radiation-induced immune dysregulation, epigenetic alterations, and gut microbiota dysbiosis. We discuss potential biomarkers, such as miRNA, fatty acid binding proteins (FABPs), etc. We categorize therapies into radioprotectors (pre-radiation use) and radiomitigators (post-radiation intervention), highlighting natural plant-derived compounds and traditional Chinese medicine (TCM) for their multi-target effects, alongside emerging approaches like stem cell and microbiota transplantation, with discussions on their therapeutic potential and clinical challenges. Crucially, we exclusively summarize recent clinical translation advances to accelerate drug development. Through critical evaluation of evidence, we propose future directions to refine risk stratification, enable timely intervention, and improve long-term outcomes for irradiated patients. This integrative analysis aims to bridge translational gaps and prioritize research avenues for RIII management.

Despite increases in prevalence, many cutaneous T-cell lymphoma (CTCL) patients still lack effective and safe therapies for their disease. The most prevalent subtype, mycosis fungoides is usually managed with skin directed treatments in early stages, while advanced stages are often targeted with systemic medications. These treatments are all symptomatic except for allogeneic hematopoietic stem cell transplantation, which is associated with its own risks of relapse and potentially fatal complications. A novel class of drugs termed "JAK inhibitors" (JAKi) has recently been developed primarily for chronic inflammatory diseases, but there is substantial evidence of JAK/STAT pathway overactivation also in CTCL. As of 1 December 2024, 14 JAKis have been collectively approved by the European Medicines Agency, the Food and Drug Administration and the Pharmaceutical and Medical Devices Agency of Japan. Despite some evidence from case reports, the efficacy and safety of JAKi in CTCL remains to be determined in controlled clinical trials. This review summarizes the current evidence on pathogenic JAK activation and its potential therapeutic inhibition in CTCL.

Methyltransferase-like 1 (METTL1) is a methyltransferase that modulates the RNA methylation process and has been increasingly investigated in cancer research over the past decade. The review aims to summarize the diverse roles of METTL1 in various cancers, focusing on the mechanisms underlying tumorigenesis, progression, and metastasis. Furthermore, the therapeutic value and targeting strategies for METTL1 are also discussed to provide the foundation for further development of METTL1-targeted therapies. The article integrates recent research findings to highlight significant discoveries regarding METTL1, emphasizing its potential as a therapeutic target in cancer treatment.

This article aims to critically evaluate the evidence for triplet therapy consisting of androgen deprivation therapy (ADT), docetaxel and a second-generation androgen receptor pathway inhibitor ([ARPI]; abiraterone, enzalutamide, darolutamide or apalutamide) in patients with metastatic hormone-sensitive prostate cancer (mHSPC), and what this evidence reveals regarding the use of these treatments in clinical practice. A search of PubMed, Medline, Embase, Cochrane, Scopus and Web of Science was conducted in April 2024 to identify relevant prospective and retrospective observational trials, randomized controlled trials (RCTs) and meta-analyses. The search identified 52 relevant articles: six full articles and 31 abstracts based on three RCTs, one observational study and 14 meta-analyses. Abiraterone- or darolutamide-containing triplet therapy was significantly better than ADT + docetaxel for improving overall survival in all study populations, particularly subgroups with high-volume and/or synchronous disease. The tolerability of ADT + docetaxel and triplet therapy were similar with most adverse events related to docetaxel. There were no data comparing triplet therapy with ADT + ARPI doublet therapy. Triplet therapy appears to be the most effective first-line regimen for men with mHSPC, good performance status and high-volume and synchronous metastases. Darolutamide-based triplet therapy may also be of benefit in other patients with high- or low-risk disease. Careful consideration of the risks and benefits are required to determine which patients can be spared from receiving docetaxel and rather be treated with alternative regimens.

This study presents a 5-year retrospective analysis of genetic counseling (GC) services for hereditary cancer syndromes (HCS) at a single center in Bulgaria. The aim is to describe the demographic and epidemiological characteristics of patients seeking GC, the uptake of genetic testing, and the spectrum of identified pathogenic variants. The results highlight an increasing trend in GC utilization. Key findings include differences in patient profiles between those seeking general HCS assessment and those undergoing tumor biomarker testing, the impact of financial accessibility on genetic testing uptake, and a pathogenic variant detection rate of 28% in tested individuals. The most frequently identified conditions were Hereditary Breast and Ovarian Cancer Syndrome and Lynch Syndrome, with pathogenic variants detected in genes such as BRCA1, MSH2, PALB2, and STK11. These findings underscore the need for enhanced awareness, improved financial access to testing, and the establishment of systematic cascade screening programs in Bulgaria.

This review aims to explore the mechanisms by which mitophagy contributes to treatment resistance in solid tumors. As advancements in cancer therapies continue to evolve, treatment resistance emerges as a significant barrier to successful tumor management. Mitophagy, a specific form of cellular autophagy, has been implicated in the survival, proliferation, and drug resistance of tumor cells. This article will summarize the latest research findings and analyze how mitophagy impacts the biological characteristics of solid tumors, thereby revealing its potential implications in cancer treatment strategies. By understanding the role of mitophagy in the context of treatment resistance, we may uncover new therapeutic targets and strategies to enhance the efficacy of existing cancer treatments.

Fibroblast Activation Protein (FAP) has emerged as a critical player in cancer biology, particularly in shaping the tumour microenvironment (TME) and influencing immunotherapy outcomes. FAP-positive cancer-associated fibroblasts (CAFs) play multiple roles in tumour progression and immune modulation. FAP, predominantly expressed on CAFs, contributes significantly to extracellular matrix remodelling, angiogenesis, and the creation of an immunosuppressive milieu. There are complex interactions between FAP-positive CAFs and various components of the immune system, highlighting their impact on T cell function and macrophage polarisation. This makes FAP a promising target for cancer therapy and potentially as a biomarker for immunotherapy treatment response. This review highlights the clinical challenges to target FAP and also addresses the heterogeneity of CAFs with the need for more refined characterisation to enhance therapeutic strategies and future research directions.

MET, a receptor tyrosine kinase proto-oncogene and the specific receptor for hepatocyte growth factor (HGF), plays a critical role in the initiation and progression of osteosarcoma (OS) through sustained pathway activation. Aberrant activation of MET has been shown to trigger multiple downstream signalling pathways, including RAS-ERK, PI3K-AKT, and STAT3, which are essential for OS cell proliferation, invasion, differentiation, and drug resistance. In recent years, significant progress has been made in the development of small-molecule inhibitors and specific antibodies targeting MET for OS therapy. The use of combination therapy as a treatment strategy involves the use of MET inhibitors in conjunction with chemotherapy, immunotherapy, and other targeted therapies. This approach has the potential to overcome resistance and improve therapeutic efficacy. This review summarises the mechanisms of MET signalling in OS, with a focus on the progress of MET-targeted therapies and their combination with other therapeutic strategies. The study provides valuable insights into future research directions, offering novel perspectives on the role of MET as a therapeutic target in OS.

Background: This study analyzed the nongenetic risk factors that contributed to colorectal cancer (CRC) incidence in the South Sulawesi population through a case-control study.

Methods: The sample consisted of 89 cases and 84 controls, aged between 19-86, with 99 males and 74 females from different ethnic groups. Univariate analysis was carried out using chi-square, Fisher's exact test, $t$ -test, and Mann-Whitney U test. Significant nongenetic risk factors were selected through the logit model L1 regularization, adjusted for age, gender, and ethnicity. The analyzed risk factors were the patient's weight, height, body mass index (BMI), defecation location, exercise habit, smoking habit, marital status, occupation, education level, and distance to the nearest health center. The estimated odds ratio from the logit model was used to analyze the significance of the selected risk factors.

Results: The significant risk factors from the logit model were smoking habit, education level, marital status, distance to the nearest health center, and weight. CRC cases were more likely to have lower education (OR = 1.819, 95% CI 1.354-2.443), residing in remote areas (OR = 1.44, 95% CI 1.17-1.772), experiencing decreasing weight (OR = 1.03, 95% CI 1.013-1.048). Controls were more likely to be non-smokers (OR = 0.325, 95% CI 0.149-0.707) and unmarried (OR = 0.161, 95% CI 0.036-0.716).

Conclusion: The study determined that other nongenetic risk factors, including education level, distance to the nearest health center, weight, smoking habit, and marital status, contributed to the CRC incidence within the South Sulawesi population. The study emphasized the importance in accounting for these risk factors for further, targeted CRC preventions.