Oncoscience最新文献

{"title":"Early success of the COCOON trial: Preventing dermatologic adverse events in first-line EGFR-mutant NSCLC.","authors":"Bishal Tiwari, Asmita Koirala","doi":"10.18632/oncoscience.648","DOIUrl":"10.18632/oncoscience.648","url":null,"abstract":"<p><p>Dermatologic adverse events (AEs) are a well-recognized complication of EGFR-targeted therapies, often emerging early during treatment and contributing to dose interruptions, patient discomfort, and reduced adherence. The combination of amivantamab, a bispecific EGFR-MET antibody, with lazertinib, a third-generation EGFR tyrosine kinase inhibitor, has demonstrated significant survival benefits in EGFR-mutant advanced non-small cell lung cancer (NSCLC). However, this therapeutic advancement brings with it an increased incidence of cutaneous toxicity. At the 2025 European Lung Cancer Congress, interim findings from the phase II COCOON trial were presented, offering timely insight into a proactive approach to managing these toxicities. This commentary summarizes and contextualizes the COCOON study, which investigated whether a structured dermatologic prophylaxis regimen could mitigate moderate-to-severe skin AEs in patients receiving first-line amivantamab plus lazertinib. The prophylactic protocol included oral doxycycline or minocycline, ceramide-based moisturization, chlorhexidine nail care, and topical clindamycin, initiated at specified intervals. Compared to standard reactive care, this strategy halved the incidence of grade ≥2 dermatologic AEs (38.6% vs. 76.5%) and reduced grade ≥3 events and treatment discontinuations. The COCOON results emphasize the clinical value of anticipating EGFR inhibitor-related toxicities through multidisciplinary supportive care. By implementing straightforward, low-cost interventions, clinicians can significantly improve tolerability and maintain dose intensity, maximizing therapeutic benefit. As this data informs future updates to clinical practice guidelines, it reinforces the need to integrate dermatologic prevention into first-line treatment planning for EGFR-mutant NSCLC. This commentary highlights COCOON's relevance as a model for supportive care innovation in targeted oncology.</p>","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"13 ","pages":"69-76"},"PeriodicalIF":0.0,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12998688/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147488924","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":"Associations among physical activity, diet, non-lifestyle characteristics and the gut microbiome of cancer patients: A scoping review and network analysis.","authors":"Jerry Armah, Sarah Alzahid, Qinglin Pei, Lakeshia Cousin, Dany Fanfan, Coy Heldermon, Debra Lyon","doi":"10.18632/oncoscience.651","DOIUrl":"10.18632/oncoscience.651","url":null,"abstract":"<p><p>Lifestyle factors, such as physical activity and dietary modifications can beneficially modulate the gut microbiome of cancer patients, however their effects are often shaped by non-modifiable variables. This review and network analysis aims to synthesize current evidence on how both lifestyle and non-lifestyle factors affect the gut microbiome in cancer patients. A systematic search was conducted on Scopus, CINAHL, PubMed and Web of Science to produce 51 eligible studies for this review. A chi-square test of independence indicated that the distribution of gut bacteria function categories was significantly associated with the category of influencing factor (Χ² = 390.87, <i>p</i> = 0.032). Across studies, high physical activity and healthy diets were associated with increased abundances of saccharolytic/short-chain fatty acids and lactic acid-producing bacteria, alongside decreased abundances of pathogenic or opportunistic bacteria. However, these associations may also be influenced by non-lifestyle characteristics such as chemotherapy, age, and cancer type or stage which could mask the benefits of lifestyle interventions. This study highlights the limited but growing evidence linking physical activity, diet and the gut microbiome in cancer populations. Progress in this field will require larger, more integrative designs that account for non-lifestyle confounders and apply advanced analytical approaches to capture complex interactions.</p>","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"13 ","pages":"85-103"},"PeriodicalIF":0.0,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12998689/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147488840","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":"Tumor-informed liquid biopsy detection of structural variants in high grade serous ovarian cancer.","authors":"Jian Li, Shiro Takamatsu, Allison L Brodsky, Thomas Welte, Katherine Calzoncinth, Veena K Vuttaradhi, Joseph Celestino, Barrett Lawson, R Tyler Hillman","doi":"10.18632/oncoscience.645","DOIUrl":"10.18632/oncoscience.645","url":null,"abstract":"<p><strong>Background: </strong>High grade serous ovarian cancer (HGSOC) recurs frequently and commercial tests have emerged for tumor-informed, cell-free DNA (cfDNA)-based detection of minimal residual disease. These tests are based on somatic single nucleotide variants prevalent in many cancers and thus are not well matched to HGSOC, which is dominated by structural genomic rearrangements. The purpose of this study was to evaluate the feasibility of a structural-variant (SV)-informed, cfDNA-based method for detecting clonal and subclonal HGSOC disease burden.</p><p><strong>Methods: </strong>A method was developed for detecting patient-specific SV breakpoints using digital droplet PCR (ddPCR) with custom tumor-informed primer/probe pairs. Test parameters were first estimated using synthetic cfDNA generated by ultrasonication of genomic DNA from ovarian cancer cell lines. The optimized workflow was implemented in which whole genome sequencing of multisite pre-treatment HGSOC biopsies performed and high confidence SVs were called by multiple published SV callers. Real-time PCR and ddPCR were used for assay development.</p><p><strong>Results: </strong>Following the optimized workflow, tumor-specific SV breakpoint-spanning primers/probe sets of four HGSOC patients' multisite biopsies were designed and validated by real-time PCR and ddPCR. Together with four HGSOCs, a total of 29 SVs breakpoints-spanning tumor-informed primers/probe sets were designed and validated in multisite biopsies. 15 validated tumor-specific SVs were selected for quantification in their corresponding liquid biopsies using the validated ddPCR, and 9 had measurements in liquid biopsies.</p><p><strong>Conclusions: </strong>Our result shows the detection of SVs from pre-treatment cfDNA using tumor-informed breakpoints-spanning ddPCR is feasible and may enable a novel and sensitive method for monitoring on-treatment disease burden.</p>","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"13 ","pages":"44-54"},"PeriodicalIF":0.0,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12981705/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147464447","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":"Massive calcified solid pseudopapillary neoplasm of the pancreatic head.","authors":"Faten Limaiem, Mohamed Hajri","doi":"10.18632/oncoscience.642","DOIUrl":"10.18632/oncoscience.642","url":null,"abstract":"<p><p>Solid pseudopapillary neoplasm (SPN) of the pancreas is an uncommon, low-grade malignant tumor, accounting for less than 3% of all exocrine pancreatic neoplasms. Although typically indolent, SPN poses significant diagnostic challenges and must be distinguished from other pancreatic tumors to guide appropriate management. We present the case of a 31-year-old woman with a two-year history of right upper abdominal pain which had recently worsened. Laboratory investigations, including tumor markers, were within normal limits. Imaging revealed a massive, lobulated pancreatic head tumor with solid, cystic, and calcified components. The mass was in close contact with the duodenum, the splenomesenteric confluence, and the right colic flexure, without evidence of invasion. The patient underwent a cephalic pancreaticoduodenectomy (Whipple procedure). Gross examination showed a well-encapsulated 12.5 × 9 × 8 cm mass with cystic degeneration, hemorrhage, and coarse calcifications. Histological examination revealed solid and pseudopapillary architecture with low mitotic activity and degenerative changes. Immunohistochemistry demonstrated positivity for β-catenin and CD10, confirming the diagnosis of SPN. Complete surgical resection is associated with an excellent prognosis, although rare aggressive behavior has been reported. This case underscores the diagnostic value of integrating imaging, histopathology, and immunohistochemistry. It also highlights the importance of considering SPN in the differential diagnosis of large, calcified pancreatic masses in young women.</p>","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"13 ","pages":"29-34"},"PeriodicalIF":0.0,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12931887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147313814","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":"Reduced immunogenicity of MYC amplified, metastatic prostate cancer.","authors":"Sunny Kahlon, Vayda R Barker, Mallika Varkhedi, Alex Y Wang, Taha I Huda, George Blanck","doi":"10.18632/oncoscience.644","DOIUrl":"10.18632/oncoscience.644","url":null,"abstract":"<p><strong>Objectives: </strong>Through a genomics-based approach analyzing gene expression levels and adaptive immune receptor recombinations, we sought to determine whether MYC amplification was associated with a worse outcome and reduced immunogenicity.</p><p><strong>Methods: </strong>MYC copy numbers and the presence of adaptive immune receptor (IR) recombination sequencing reads were quantified in genomics files representing prostate cancer samples.</p><p><strong>Results: </strong>Our results showed that increased MYC amplification was found in metastatic stages of prostate cancer. Furthermore, increased MYC amplification was not only associated with worse progression-free survival but also with reduced immunogenicity in metastatic tumors, as determined by the recovery of a reduced numbers of adaptive IR recombination sequencing reads from tumor RNAseq and tumor whole genome sequence files.</p><p><strong>Conclusions: </strong>MYC amplification is associated with reduced tumor immunogenicity as assessed by the recovery of IR recombination reads from prostate cancer genomics files.</p>","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"13 ","pages":"35-43"},"PeriodicalIF":0.0,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12931888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147291052","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":"Gastrointestinal toxicity of targeted cancer therapies in the United States: Clinicopathologic patterns, FDA safety frameworks, and implications for national patient protection.","authors":"Muhammad Moseeb Ali Hashim, Muhammad Ahsan, Muhammad Aizaz Mohsin Khan, Hafsa Hameed Thakur, Talha Kamran Khan, Kamran Zahoor, Sania Muzaffar, Feroza Fatima, Shamama Tu Zahra, Ammara Naeem, Mahima Gandhi, Muhammad Usama Ashraf, Pir Maroof Qureshi","doi":"10.18632/oncoscience.643","DOIUrl":"10.18632/oncoscience.643","url":null,"abstract":"<p><strong>Background: </strong>As precision oncology advances, non-immune checkpoint targeted therapies such as tyrosine kinase inhibitors (TKIs), antibody-drug conjugates (ADCs), and chimeric antigen receptor T-cell (CAR-T) therapies are increasingly used across gastrointestinal (GI) and non-GI malignancies. While these agents have transformed cancer treatment, they are also associated with a broad spectrum of GI toxicities that remain underrecognized in both clinical practice and pathology.</p><p><strong>Objective: </strong>This review comprehensively examines the mechanisms, clinicopathological features, and management strategies of GI toxicity induced by TKIs, ADCs, and CAR-T therapies, emphasizing the diagnostic role of pathologists in identifying treatment-related injury patterns.</p><p><strong>Methods: </strong>We synthesized data from pivotal clinical trials, FDA drug labeling, post-marketing surveillance (FAERS), and real-world histopathologic descriptions of GI adverse events. SEER data on GI malignancies treated with targeted therapies were also reviewed to highlight epidemiologic context.</p><p><strong>Results: </strong>TKIs may induce mucosal ischemia, apoptosis, or colitis-like inflammation due to angiogenesis inhibition and off-target effects. ADCs contribute to epithelial injury through cytotoxic payloads, while CAR-T therapy is associated with cytokine-mediated GI inflammation. Histological findings range from apoptotic enteropathy to ulcerative colitis and mimic infections, GVHD, or autoimmune disease. Misdiagnosis can lead to treatment delays or unnecessary dose reductions.</p><p><strong>Conclusions: </strong>The landscape of GI toxicity from targeted cancer therapies is expanding rapidly. Accurate recognition of characteristic pathology patterns and integration with clinical history are crucial for safe and effective management. Enhanced pharmacovigilance, pathology-oncology collaboration, and incorporation of national surveillance data (FAERS, SEER) are essential to advancing precision medicine and patient safety.</p>","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"13 ","pages":"10-28"},"PeriodicalIF":0.0,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12888886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146168614","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":"Dual targeting of oncogenic microtubules and mitochondria in PDAC.","authors":"Michael W Spinrad, Chun Cai, Lauren C Gattie, Rui Wang, Aman Bajwa, Wei Li, Evan S Glazer","doi":"10.18632/oncoscience.641","DOIUrl":"10.18632/oncoscience.641","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers. Microtubule inhibition is a promising therapeutic target as microtubule dynamics play a critical role in growth of metastases due to over expression of several β-tubulin subtypes compared to normal cells. Previous studies have shown that decreased expression of βIII- and βIVb-tubulin is associated with decreased PDAC cell growth. Bromodomain and Extra-Terminal domain (BET) proteins are transcription factors that regulate mitochondria proteins. In this study, we hypothesize that SB-216 and Veru-111 (related novel compounds) inhibit cell growth via suppression of oncogenic βIII- and βIVb-tubulin subtypes and mitochondria function via suppression of BRD4, the most active BET protein. PDAC cell growth was analyzed with the IncuCyte Live-Cell Analysis system. mRNA expression of βIII- and βIVb-tubulin was evaluated with quantitative real time PCR. Western blot analysis was performed for βIII, βIVb-tubulin, and BRD4 protein expression and expression of autophagy and mitophagy markers LC3B and p62/SQSTM1. Mitochondrial function/respiration was measured using a Seahorse XF-24 Flux Analyzer. Cell growth was greatly inhibited across all doses in multiple PDAC cell lines (<i>p</i> < .0001). mRNA expression of <i>TUBB3</i> (βIII subtype) and <i>TUBB4</i> (βIVb subtype) was significantly decreased (<i>p</i> < .05). BRD4 protein expression was reduced in with compensatory increase in mRNA expression. Treated PDCL had reduced mitochondrial respiration. Autophagy markers were increased in treated PDAC cells. Our data demonstrates that SB-216 effectively inhibits PDAC cell growth through inhibiting oncogenic microtubules and mitochondrial function. This novel approach simultaneously targets two hallmarks of cancer and patient demise.</p>","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"13 ","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12893626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146184108","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":"Solitary diffuse-type giant neurofibroma arising from the sciatic nerve in a 13-year-old: A rare occurrence.","authors":"Reshmi Sultana, Suryadevara Sailaja","doi":"10.18632/oncoscience.640","DOIUrl":"10.18632/oncoscience.640","url":null,"abstract":"<p><p>Giant solitary neurofibromas involving deep peripheral nerves, particularly the sciatic nerve, are exceptionally rare in pediatric patients and pose unique diagnostic and surgical challenges. They often remain asymptomatic due to their deep intermuscular location, which delays detection until significant growth occurs. We report a 13-year-old male with a painless posterior thigh swelling, incidentally noticed while playing. MRI revealed a 12.8 × 6.6 × 3.8 cm lobulated intermuscular mass along the sciatic nerve. Tru-cut biopsy suggested a cellular neurofibroma. The patient underwent function-preserving excision under microscopic magnification, with careful dissection of the tumor from individual sciatic nerve fascicles. Intraoperative neurophysiological monitoring (IONM) was not available, highlighting the challenges of ensuring nerve preservation without real-time feedback. Postoperatively, transient foot drop occurred but resolved completely with physiotherapy. Histopathology confirmed a diffuse-type cellular neurofibroma with patchy S100 and SOX10 positivity, focal CD34 expression, and low Ki-67, supporting a benign profile. This case underscores the importance of meticulous surgical technique, the potential value of IONM, and vigilant postoperative care in achieving optimal outcomes for deep-seated pediatric neurofibromas.</p>","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"12 ","pages":"231-235"},"PeriodicalIF":0.0,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12723959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145829402","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":"Necrotizing fasciitis of the head and neck - clinical features, diagnostics, and management strategies.","authors":"Anna Aydin, Lawik Revend, Doha Revend, Oliver Schuck, Florian Dudde","doi":"10.18632/oncoscience.639","DOIUrl":"10.18632/oncoscience.639","url":null,"abstract":"<p><strong>Background: </strong>Necrotizing fasciitis (NF) of the head and neck is a rare but rapidly progressive and life-threatening soft tissue infection that constitutes a true surgical emergency. Due to the complex anatomy of the cervicofacial region and the proximity to the upper airway, early diagnosis and management are particularly challenging, and delayed recognition is associated with high morbidity and mortality. This article aims to provide a concise and clinically oriented overview of the presentation, diagnostic pitfalls, and current management strategies for cervicofacial necrotizing fasciitis.</p><p><strong>Methods: </strong>A narrative review of the available literature was conducted and complemented by clinical experience from a tertiary referral center. Key aspects including etiology, risk factors, clinical features, imaging findings, laboratory parameters, microbiology, surgical management, airway control, and adjunctive therapies were synthesized and critically discussed.</p><p><strong>Results: </strong>Cervicofacial NF often presents with disproportionate pain, rapidly progressive swelling, and early systemic toxicity. Odontogenic infections represent the most common source, frequently in the presence of systemic comorbidities such as diabetes mellitus or immunosuppression. Contrast-enhanced computed tomography is the imaging modality of choice, whereas laboratory scoring systems such as the LRINEC score show limited sensitivity in head and neck infections. The cornerstone of treatment is immediate and aggressive surgical debridement combined with broad-spectrum intravenous antibiotics, early airway protection, and intensive care support. Repeated surgical interventions are frequently required. The role of adjunctive hyperbaric oxygen therapy remains controversial and cannot be routinely recommended based on current evidence.</p><p><strong>Conclusion: </strong>Necrotizing fasciitis of the head and neck requires a high index of suspicion, prompt imaging, and decisive multidisciplinary management. Early surgical intervention and airway control are critical determinants of outcome. Given the rarity of cervicofacial NF, further multicenter studies and registries are needed to refine diagnostic tools, identify prognostic factors, and optimize treatment strategies, particularly in high-risk populations such as immunocompromised and oncologic patients.</p>","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"12 ","pages":"219-225"},"PeriodicalIF":0.0,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12723960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145829470","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":"Silent toxicity: A rare case of 5-fluorouracil-induced hyperammonemic encephalopathy.","authors":"Areti Kalfoutzou, Cleopatra Rapti, Eleftheria Bagiokou, Vasileios Kolintzikis, Vasileios Ramfidis","doi":"10.18632/oncoscience.638","DOIUrl":"10.18632/oncoscience.638","url":null,"abstract":"<p><p>Hyperammonemic encephalopathy (HE) is a rare but serious neurological condition characterized by an acute alteration in mental status due to elevated serum ammonia levels, occurring in the absence of known liver disease. The build-up of ammonia, a by-product of protein metabolism, in the bloodstream leads to its crossing of the blood-brain barrier, where it acts as a neurotoxin, causing potentially reversible brain damage. Chemotherapeutic agents such as 5-fluorouracil (5-FU) are known to cause drug-induced HE. Our case reports a 63-year-old woman who presented with several episodes of reduced consciousness shortly after 5-FU administration, highlighting the necessity of monitoring serum ammonia levels in patients treated with 5-FU who develop neurological symptoms, and the need for expert consultation in attempting a 5-FU rechallenge.</p>","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"12 ","pages":"226-230"},"PeriodicalIF":0.0,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12723958/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145829391","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}