{"title":"Nasolabial flap in head & neck reconstruction: a historical workhorse with modern relevance","authors":"Latha P Rao, Dency Hansalia, Akshay Kantha, Meenu Singh, Manoj Pandey","doi":"10.1016/j.ctarc.2026.101387","DOIUrl":"10.1016/j.ctarc.2026.101387","url":null,"abstract":"<div><h3>Background</h3><div>Reconstructive specialists face substantial hurdles when managing head and neck impairments caused by birth defects, injuries, or cancer surgeries, which affect both aesthetics and physiological performance. The nasolabial flap, a highly adaptable pedicle flap, has remained a foundational element in head and neck repair since its early documentation in ancient records like the Sushruta Samhita around 600 BC.</div></div><div><h3>Methods</h3><div>A comprehensive narrative review of peer-reviewed literature from databases including PubMed and Scopus was performed to analyze the chronological development, surgical structure, clinical usage, procedural methods, benefits, drawbacks, and contemporary technological innovations associated with the nasolabial flap.</div></div><div><h3>Results</h3><div>The nasolabial flap's clinical dependability, visual results, and tissue flexibility make it an excellent choice for repairs that are too extensive for primary closure yet insufficient to warrant microvascular free tissue transfer. Recent integrations of modern structural tools further enhance outcomes.</div></div><div><h3>Conclusion</h3><div>Regardless of structural constraints such as dimensions and the risk of complications like partial necrosis, the nasolabial flap is an essential component of the reconstructive hierarchy. Its traditional baseline is now highly refined by modern tools like 3D printing and computational fluid dynamics, optimizing functional and aesthetic patient outcomes.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"49 ","pages":"Article 101387"},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148811782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mylene J.C. Duivenvoorden, Vineet Kurisunkal, Gerjon Hannink, Michael Parry, Lee Jeys, Floortje G.M. Verspoor
{"title":"Temporal changes in Denosumab use among patients with giant cell tumour of bone at a specialist oncology centre: a retrospective cohort study","authors":"Mylene J.C. Duivenvoorden, Vineet Kurisunkal, Gerjon Hannink, Michael Parry, Lee Jeys, Floortje G.M. Verspoor","doi":"10.1016/j.ctarc.2026.101380","DOIUrl":"10.1016/j.ctarc.2026.101380","url":null,"abstract":"<div><h3>Objectives</h3><div>Denosumab, a RANKL inhibitor, has transformed the management of giant cell tumor of bone (GCTB). This study evaluates evolving patterns of Denosumab therapy, associated outcomes, and adverse events in a large cohort.</div></div><div><h3>Design</h3><div>A retrospective review was conducted on all GCTB patients who were treated at the Royal Orthopaedic Hospital, Birmingham, UK, between 2000 and 2023. Patients who received Denosumab as part of their management were included. Data was stratified by tumour location (axial skeleton vs. extremities) and treatment period (before or after 2018).</div></div><div><h3>Results</h3><div>Among 155 eligible patients (median age 34 years, IQR 25–47; 52% female), Denosumab treatment patterns changed markedly over time. Prior to 2018, short-course neoadjuvant Denosumab before intralesional curettage was common but was associated with high local recurrence rates (37% in extremities, 10% in axial skeleton). After 2018, Denosumab was used more selectively for long-term disease control, especially in complex or inoperable cases. Adverse events occurred in 18% of patients, and were categorized as serious (14/155, 9%), moderate (7/155, 5%), or mild (7/155, 5%). Respectively they occurred after median 45 weeks (IQR 8–100), 45 weeks (IQR 22–94) and 130 weeks (IQR 89–220). The adverse events occurred more frequently on a monthly Denosumab regime(16%, 25/155) when compared to 2-monthly(3%, 2/59) and 3-monthly (3%, 1/31).</div></div><div><h3>Conclusions</h3><div>These findings reveal a change in Denosumab use for GCTB, moving away from short-course neoadjuvant therapy due to high recurrence risk, and towards long-term treatment in select patients. A standardized Denosumab dosing regimen is recommended to achieve consistent international treatment outcomes, safely reduce dosage, and potentially lower the risk of adverse events. Our results support a tailored, multidisciplinary approach with careful monitoring for adverse events and ongoing research studies to refine treatment protocols.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"49 ","pages":"Article 101380"},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148825425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Saeb Younis Abdul-Rahman , Abdulkareem Shareef , S. Renuka Jyothi , Priya Priyadarshini Nayak , J. Bethanney Janney , Gurjant Singh , Aashna Sinha , Sitora Tilyavova , Hayder Naji Sameer , Ahmed Yaseen , Rasim M. Salih , Mohaned Adil
{"title":"miR-155 and the orchestration of cell-death evasion and chemoresistance in cancer: Isoform-specific mechanisms and therapeutic opportunities","authors":"Saeb Younis Abdul-Rahman , Abdulkareem Shareef , S. Renuka Jyothi , Priya Priyadarshini Nayak , J. Bethanney Janney , Gurjant Singh , Aashna Sinha , Sitora Tilyavova , Hayder Naji Sameer , Ahmed Yaseen , Rasim M. Salih , Mohaned Adil","doi":"10.1016/j.ctarc.2026.101198","DOIUrl":"10.1016/j.ctarc.2026.101198","url":null,"abstract":"<div><div>MicroRNA-155 (miR-155) is a crucial miRNA that connects inflammation signaling with epigenetic regulation, impacting programmed cell death (PCD) and influencing chemotherapy resistance. It inhibits apoptosis by targeting pro-apoptotic factors and adjusts autophagy via PDK1/AKT–mTOR activation or downregulating ATG5, helping cells cope with stress. In many solid and hematologic cancers, the predominant pattern involves promoting resistance, mainly through miR-155–5p-driven suppression of pro-apoptotic or checkpoint regulators, involving PI3K/AKT, NF-κB, and STAT3 pathways. Conversely, some studies indicate chemosensitizing or tumor-suppressive roles in specific contexts, such as miR-155–3p/MYD88 signaling in breast cancer, miR-155/XIAP in ovarian cancer, and miR-155/CD47–TNFAIP8 in multiple myeloma. miR-155 also influences autophagy depending on the context, either promoting protective autophagy by targeting mTOR pathway regulators or enhancing chemosensitivity by suppressing key autophagy components like ATG5. New findings associate miR-155 with pyroptosis, necroptosis, and immune clearance via phagocytosis, though the mechanisms vary across pathways. In the tumor microenvironment, exosomal miR-155 spreads resistance traits, such as epithelial–mesenchymal transition, stemness, and survival signaling in adjacent cells. Therapeutic approaches include inhibition or restoration, tailored to isoform, tumor type, and network, with growing support for oligonucleotide-based therapies, nanoparticle delivery, and combination treatments. Overall, miR-155 is a powerful biomarker for chemoresistance and a promising therapeutic target, especially when strategies are isoform- and context-specific. This review adopts a mechanism-first approach to distinguish common resistance modules from true context-dependent exceptions, highlighting isoform specificity and translational relevance.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"47 ","pages":"Article 101198"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147632486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jeanette Bæhr Georgsen , Maria Vad Jakobsen , Peter Meldgaard , Johanne Lade-Keller , Peter Jepsen , Patricia Switten Nielsen , Lena Dyrborg , Torben Steiniche
{"title":"Mapping the mutational terrain of lung adenocarcinoma: A Danish cohort study of 880 patients","authors":"Jeanette Bæhr Georgsen , Maria Vad Jakobsen , Peter Meldgaard , Johanne Lade-Keller , Peter Jepsen , Patricia Switten Nielsen , Lena Dyrborg , Torben Steiniche","doi":"10.1016/j.ctarc.2026.101202","DOIUrl":"10.1016/j.ctarc.2026.101202","url":null,"abstract":"<div><h3>Background</h3><div>In this population-based cohort, we examined the prevalence of targetable genomic alterations and characterized <em>KRAS</em> subtypes in relation to co-mutations, PD-L1 expression, treatment, and survival.</div></div><div><h3>Materials and methods</h3><div>A total of 880 patients diagnosed with lung adenocarcinoma in Central Denmark in 2020–2021 underwent reflex next-generation sequencing using a 22-gene panel.</div></div><div><h3>Results</h3><div><em>KRAS</em> mutations were present in 383/880 tumors (43.5 %), of which <em>KRAS</em> G12C accounted for 174 cases (19.8 % of the total cohort). Overall, targetable alterations were identified in 327/880 tumors (37.2 %). <em>KRAS</em> G12C mutations were more frequent in females and smokers. <em>KRAS</em> mutations were largely mutually exclusive with other targetable driver alterations. TP53 mutations were more common in <em>KRAS</em> wild-type tumors, whereas non-G12C <em>KRAS</em> mutations were associated with <em>SMAD4</em> mutations. PD-L1 ≥50 % occurred most frequently in tumors with <em>KRAS</em> G12C.</div><div><em>KRAS</em> mutation status was not associated with overall survival in unadjusted analyses. After adjustment for clinical covariates, non-G12C <em>KRAS</em> mutations showed a modest association with increased mortality. Among 628 patients with available treatment data, survival differed across treatment modalities. Among patients receiving systemic first-line treatment (n = 183), survival was significantly better with immune checkpoint inhibitors or targeted therapy than with chemotherapy (p < 0.001). <em>KRAS</em> mutation status was not associated with treatment-specific survival in any treatment group.</div></div><div><h3>Conclusion</h3><div>Lung adenocarcinomas are characterized by a high prevalence of targetable alterations, with <em>KRAS</em> G12C representing the most frequent alteration. <em>KRAS</em> mutation status showed limited prognostic relevance. These findings support routine molecular testing and integration of genomic and clinical data to guide personalized treatment.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"47 ","pages":"Article 101202"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147637727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Integrating the Silva pattern into clinical practice: a prognostic tool for tailoring surgery and adjuvant therapy in cervical adenocarcinoma","authors":"Xinmei Wang, Juan Xu, Hongyuan Zhang, Pengpeng Qu","doi":"10.1016/j.ctarc.2026.101187","DOIUrl":"10.1016/j.ctarc.2026.101187","url":null,"abstract":"<div><h3>Objective</h3><div><strong>:</strong> To establish an intelligent risk-stratification framework by validating the Silva pattern system in endocervical adenocarcinoma (ECA), enabling personalized treatment decisions.</div></div><div><h3>Methods</h3><div>Clinicopathological data from 178 ECA patients (2017–2023) were retrospectively analyzed. Silva patterns were assessed by two gynecologic pathologists using the Silva pattern system criteria. The 178 patients were followed-up for 48–102 months.Machine-learning-ready morphometric features were extracted. Survival analysis employed Kaplan-Meier/Cox regression.</div></div><div><h3>Results</h3><div><strong>:</strong> There were significant differences in clinicopathological characteristics among different Silva subtypes, and the highest rates of tumor diameter ≥4 cm, pelvic lymph node metastasis (PLNM), lymphovascular space invasion (LVSI), and deep stromal invasion were found in Silva pattern C group (<em>P</em> < 0.05).The progression-free survival (PFS) and overall survival (OS) of the patients were as follows: Silva mode <em>A</em>>Silva mode <em>B</em> >Silva mode C group (<em>P</em> < 0.05).FIGO stage, tumor diameter, PLNM, depth of stromal invasion, LVSI, Sliva subtypes were the risk factors affecting the prognosis of ECA(<em>P</em> < 0.05).</div></div><div><h3>Conclusion</h3><div><strong>:</strong> The Silva system offers strong prognostic stratification. Pattern A supports conservative management; pattern C warrants radical therapy; pattern B requires individualized approaches. Silva-based strategy reduces overtreatment, and integration with molecular biomarkers could further refine prognostication.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"47 ","pages":"Article 101187"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147650093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Bioinformatics and experimental insights into LINC01605 and the miR-101–3p/BIRC5 axis in oral squamous cell carcinoma pathogenesis and clinical outcomes","authors":"Roghayeh Abbasalipourkabir , Somayeh Aslani , Saman Morovat , Nasrin Ziamajidi , Elham Akrami , Shiva Pourvahdani , Mahdi Bahmani , Amirnader Emami Razavi , Ashkan Kalantary-Charvadeh","doi":"10.1016/j.ctarc.2026.101212","DOIUrl":"10.1016/j.ctarc.2026.101212","url":null,"abstract":"<div><h3>Background</h3><div>LncRNAs modulate several druggable and non-druggable genes through miRNAs sequestering in oral squamous cell carcinoma (OSCC). This study evaluates LINC01605 expression and its potential interaction with the miR-101–3p/BIRC5 axis in OSCC development.</div></div><div><h3>Methods</h3><div>The OSCC sequencing data were downloaded from The Cancer Genome Atlas database. Different online databases, along with correlation analysis, were employed to predict lncRNAs downstream miRNAs and mRNAs. Further protein-protein interaction network and functional analysis were conducted to discover the role of target genes. The expression analysis through RT-qPCR, western blotting, and immunofluorescence, as well as correlation analysis of the axis, was studied in 30 paired OSCC and margin tissues. ROC, Kaplan-Meier, and Chi-square analyses were used to estimate the diagnostic, prognostic, and histopathological utility of this axis, respectively.</div></div><div><h3>Results</h3><div>After novelty checking and downstream finding, LINC01605/miR-101–3p/BIRC5 was selected. RT-qPCR showed upregulation of LINC01605, alongside the downregulation of miR-101–3p. The mRNA and protein levels of BIRC5 exhibited elevated expression in OSCC tissues. Significant positive correlation between LINC01605 and <em>birc5</em>, along with negative correlations between LINC01605-miR-101–3p, and miR-101–3p-<em>birc5</em> was found. The combined ROC curve demonstrated a high discriminating potential of this axis in OSCC tissue diagnosis. Moreover, patients with high LINC01605 and low miR-101–3p levels had a significantly poorer survival, and this was associated with perineural invasion and invasion depth.</div></div><div><h3>Conclusion</h3><div>This study reveals a new axis related to OSCC and may provide beneficial diagnostic, prognostic, and potential therapeutic targets in this cancer.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"47 ","pages":"Article 101212"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147739757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"BRAF mutation predicts survival after immunotherapy across multiple cancer types","authors":"Shaojun Zhou , Weiting Ge , Wen Cai","doi":"10.1016/j.ctarc.2026.101215","DOIUrl":"10.1016/j.ctarc.2026.101215","url":null,"abstract":"<div><div>Recently studies in selected tumors suggested that <em>BRAF</em> mutation may associates with survival benefit from immune checkpoint inhibitor (ICI) therapy. To broadly investigate this association at a pan-cancer level, we analyzed two independent ICI treatment cohorts (MSKCC: <em>n</em> = 1630, and Dana-Farber: <em>n</em> = 249). Patients with <em>BRAF</em>-mutant tumors exhibit better overall survival in the MSKCC cohort (Hazard ratio [HR] = 0.55, 95% confidence interval [CI]: 0.43–0.72; <em>P</em> < 0.001) and the result is validated by the Dana-Farber cohort (HR = 0.68, 95% CI: 0.46–0.99; <em>P</em> = 0.045). A multivariate analysis adjusting tumor mutational burden, mismatch repair status, cancer type, age and sex confirmed the results (adjusted HR = 0.58, 95% CI = 0.43–0.78; <em>P</em> < 0.001). Immunogenomic features analysis of TCGA dataset indicated that patients may respond to immunotherapy in various mechanisms. This finding substantially improves the therapeutic prospects for a sizeable fraction of patients who benefit from immunotherapy.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"47 ","pages":"Article 101215"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147739758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Moustafa A. Mansour, M. Wahid, Mohamed A.S. El Molla, Mohamed H. Helmy, Taha Mohammed Adel, Mohamed Said Elsanafiry, Hamdi Nabawi Mostafa
{"title":"The parasitic synapse: How gliomas hijack the connectome for malignant gain","authors":"Moustafa A. Mansour, M. Wahid, Mohamed A.S. El Molla, Mohamed H. Helmy, Taha Mohammed Adel, Mohamed Said Elsanafiry, Hamdi Nabawi Mostafa","doi":"10.1016/j.ctarc.2026.101438","DOIUrl":"10.1016/j.ctarc.2026.101438","url":null,"abstract":"<div><div>Gliomas, the most prevalent primary intrinsic tumors of the central nervous system, have historically been conceptualized as autonomous, space-occupying lesions that compromise neurological function through mass effect, tissue destruction, and peritumoral edema. However, contemporary research spanning molecular neuro-oncology, systems neuroscience, and clinical neurology has precipitated a fundamental paradigm shift, revealing that gliomas engage in complex, bidirectional, and dynamic interactions with the functional architecture of the brain. This review synthesizes a vast body of evidence to interrogate the provocative question of whether gliomas exert or aid brain functions. We systematically examine the evidence for glioma integration at synaptic, circuit, and large-scale network levels, scrutinize proposed mechanisms of neuron-glioma communication, and evaluate the clinical manifestations of this integration. A critical analysis concludes that while high-grade and low-grade gliomas demonstrate a remarkable capacity to integrate into and exploit the brain's structural and functional circuitry for proliferative advantage, there exists no substantive evidence that this integration confers any net beneficial or supportive function to the host brain. Instead, the apparent \"functional integration\" represents a sophisticated form of ecological niche adaptation and co-option of neurodevelopmental programs, characterized by direct synaptic coupling, activity-dependent paracrine signaling, and dynamic network remodeling. This refined understanding carries profound implications for developing novel therapeutic paradigms that target the tumor-brain interface, moving beyond cytotoxic strategies to include circuit-modulating and network-preserving approaches that disrupt the malignant synergy between neural activity and glioma progression while strategically bolstering the brain's innate capacity for functional resilience.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"49 ","pages":"Article 101438"},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148966007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yazan K. Barqawi, Krishna Rekha Moturi, Neda Hashemi-Sadraei, Melissa H. Roberts, Todd A. Thompson, Mohammad T. Alashqar, Matthew E. Borrego
{"title":"Racial and ethnic disparities in metabolic syndrome care among prostate cancer patients on androgen deprivation therapy","authors":"Yazan K. Barqawi, Krishna Rekha Moturi, Neda Hashemi-Sadraei, Melissa H. Roberts, Todd A. Thompson, Mohammad T. Alashqar, Matthew E. Borrego","doi":"10.1016/j.ctarc.2026.101440","DOIUrl":"10.1016/j.ctarc.2026.101440","url":null,"abstract":"<div><h3>Introduction</h3><div>Androgen deprivation therapy (ADT) is used for prostate cancer (PCa) but increases metabolic syndrome risk factors (MSRF). Guidelines recommend MSRF screening and treatment during ADT; however, adherence and disparities remain unclear. We evaluated racial and ethnic differences in MSRF screening and treatment rates among PCa patients initiating ADT.</div></div><div><h3>Methods</h3><div>We included 803 PCa patients initiating ADT at the University of New Mexico Comprehensive Cancer Center, 2010–2021. Guideline-concordant screening, based on the 2010 AHA/ACS/AUA scientific advisory committee, required primary care or completion of blood pressure, glucose, and lipid testing, with treatment continuation or initiation when indicated within six months of ADT initiation. Logistic regression assessed predictors of screening.</div></div><div><h3>Results</h3><div>Only 23.5% of patients received guideline-concordant screening. Rates were 26.8% (122/455) among NHW, 17.8% (43/242) Hispanic, 30.6% (15/49) African American, 14.6% (6/41) AI/AN/HN, and 18.8% (3/16) Asian patients. Compared with NHW patients, adjusted odds (aOR) were lower among Hispanic (aOR 0.40; 95% CI, 0.20–0.60; p = 0.0001), AI/AN/HN (aOR 0.20; 95% CI, 0.07–0.70; p = 0.007), and Asian patients (aOR 0.20; 95% CI, 0.04–0.90; p = 0.04). Guideline-concordant treatment occurred in 76.9% of eligible patients. Baseline dyslipidemia (aOR 3.10; 95% CI, 2.00–4.70; p < 0.0001) and oncologist experience >20 years versus <10 years (aOR 2.90; 95% CI, 1.40–6.30; p = 0.006) were associated with higher screening odds.</div></div><div><h3>Discussion</h3><div>MSRF screening was suboptimal, with significant racial and ethnic disparities. Estimates for AI/AN/HN and Asian subgroups warrant caution because of small sample sizes. Continuous provider education, standardized protocols, and improved access may reduce cardiometabolic risks and inequities.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"49 ","pages":"Article 101440"},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148976137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Tissue factor-targeted antibody-drug conjugates in cervical cancer: Focus on tisotumab vedotin","authors":"Mengyuan Xie, Qing Li","doi":"10.1016/j.ctarc.2026.101400","DOIUrl":"10.1016/j.ctarc.2026.101400","url":null,"abstract":"<div><div>Cervical cancer remains a major global health burden, and treatment options after progression of recurrent or metastatic disease remain limited. Tisotumab vedotin (TV) is a tissue factor-directed antibody–drug conjugate that delivers monomethyl auristatin E after target binding and internalization. In innovaTV 204, TV achieved an objective response rate of 24.0% and a median duration of response of 8.4 months; innovaTV 301 subsequently demonstrated superior overall survival, progression-free survival, and response rate versus investigator’s choice chemotherapy. In this review I examine the biological rationale for the use of TV, the design of TV and its clinical use, the clinical evidence for its use, as well as how toxicity is managed with treatment with TV, and I discuss unresolved issues surrounding TV, specifically as they pertain to the very limited clinical data that have been published regarding resistance mechanisms for the TV treatment modality. I also discuss the important need for the development of predictive biomarkers for TV and the development of rational combinations with other agents for use in combination with TV.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"49 ","pages":"Article 101400"},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}