Cancer Chemotherapy and Pharmacology最新文献

{"title":"Impact of altitude on hemoglobin dynamics and prognosis in patients with advanced hepatocellular carcinoma receiving antiangiogenic TKIs: A propensity score matched study.","authors":"Mengyun Zhou, Xiang Zhao, Meng Zhang, Mao Peijing, Chilie Quncuo, Pubu Zhuoga, Bianba Qiongda, Meilang Chutso, Bian Ma Cuo, Bangchao Zhao, Guangfa Wang, Cheng Yuan","doi":"10.1007/s00280-025-04786-5","DOIUrl":"10.1007/s00280-025-04786-5","url":null,"abstract":"<p><strong>Purpose: </strong>Antiangiogenic tyrosine kinase inhibitors (TKIs) are associated with elevated hemoglobin [Hb] levels, potentially influencing prognosis in advanced hepatocellular carcinoma (HCC) patients. However, the impact of altitude on Hb dynamics and its prognostic significance remains underexplored. This study aimed to assess altitude-related Hb changes and their relationship with treatment outcomes in patients following TKI treatment.</p><p><strong>Methods: </strong>In this retrospective cohort study, medical data from two institutions in Tibet and Beijing were analyzed. Between 2016 and 2022, 128 advanced HCC patients treated with antiangiogenic TKIs were divided into high- and low-altitude groups based on their city of residence. Hematological parameters were retrieved at baseline and every 3 months for 9 months post-treatment initiation. Propensity score matching (PSM) was used to adjust for demographic and baseline differences. Hb percentage changes from baseline (no increase, increase < 15%, increase ≥ 15%) were evaluated at each time point as predictors of time to treatment failure (TTTF) using the Cox proportional hazards model.</p><p><strong>Results: </strong>After PSM, Hb trajectories differed between the altitude groups. The high-altitude patients exhibited progressive increases, while the low-altitude patients experienced a transient rise followed by a decline. We found no significant TTTF differences between the matched altitude groups (P = 0.33). However, in the high-altitude unmatched cohort, a ≥ 15% increase in Hb at 9 months was linked to a significantly lower risk of treatment failure (HR = 0.22 [95% CI = 0.06-0.83]; P = 0.03). Patients with increases < 15% showed a numerical trend toward prolonged TTTF (HR = 0.30 [0.08-1.15]).</p><p><strong>Conclusion: </strong>Antiangiogenic TKIs induce altitude-dependent Hb changes, with sustained increases at high altitudes and transient reversibility at low altitudes. A ≥ 15% increase in Hb at 9 months after TKI therapy may serve as a potential biomarker for identifying high-altitude populations likely to benefit more from TKI therapy. Future studies should validate these findings in larger cohorts.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"70"},"PeriodicalIF":2.7,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144567139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peptides derived from the POU domain of BRN2 show antitumor activity against murine melanoma model cells in vitro and in vivo.","authors":"Maria Carolina Mariano Cesar, Agnes Kobayashi Calvo de Sant'ana, Renato Arruda Mortara, Victória Santos Souza, Thaysa Paschoalin, Marco Antônio Soufen, Juliana Machado Anastácio, Erenildo F Macedo, Fernanda Fernandes Miranda da Cunha, Dayane Batista Tada, Denise Costa Arruda","doi":"10.1007/s00280-025-04790-9","DOIUrl":"https://doi.org/10.1007/s00280-025-04790-9","url":null,"abstract":"<p><p>The BRN2 transcription factor controls the protein expression involved in cell motility and is overexpressed in melanoma. Gene mutations involved in cell signaling pathways lead to BRN2 overexpression, tumor formation and metastasis. Peptides derived from the DNA binding domain of transcription factors can compete for the transcription binding and regulate protein expression. In this work, the antitumor activity in vitro and in vivo of the peptide E24G, derived from the DNA-binding POU domain of the BRN2 transcription factor was investigated. This peptide was fragmented into two smaller peptides E12F and A12G, their antitumor activities were characterized and compared with E24G. The E24G at 1 mM significantly reduced cell motility in vitro of B16F10-Nex2 melanoma cells. E12F peptide also inhibited cell motility at a concentration eight times smaller than E24G in murine and human melanoma cells. We observed that the antitumor activity of both E24G and E12F peptides depends on the macropinocytosis displayed by tumor cells. Also, the E24G and E12F peptides induced an increase of the CDH13 expression in 50%, however the treatment with E12F increased the expression already after 12 h by 100%. In vivo assays showed that both peptides reduced the development of metastatic lung nodules without presenting toxicity to normal organs. Our results indicate that E12F and E24G peptides can restore normal expression of BRN2 target genes at the molecular level, inhibiting the cell motility. In addition, we confirmed that the peptide binds to the DNA binding site of the BRN2 transcription factor. Further studies will elucidate their mechanisms of antitumor activity, so far our results pointed out the potential application of E12F and E24G peptides as innovative treatments for metastatic melanoma.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"67"},"PeriodicalIF":2.7,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ETV1 genetic polymorphisms as a candidate prognosis biomarker of Gastrointestinal stromal tumor.","authors":"Wei Zhuang, Minju Jo, Haibo Qiu, Wanlong Lin, Min Huang, Xueding Wang","doi":"10.1007/s00280-025-04789-2","DOIUrl":"https://doi.org/10.1007/s00280-025-04789-2","url":null,"abstract":"<p><strong>Purpose: </strong>While imatinib is effective for treating Gastrointestinal Stromal Tumors (GISTs), significant variability in patient outcomes exists, highlighting the need for reliable prognostic biomarkers. ETV1, a key transcription factor involved in GIST progression, is implicated in disease biology, but the role of ETV1-related single nucleotide polymorphisms (SNPs) in predicting prognosis remains unclear.</p><p><strong>Methods: </strong>This study included 75 GIST patients. We focused on identifying tag SNPs in the ETV1 gene and examined their association with clinical outcomes. Patient characteristics, somatic mutations, and imatinib concentration were also analyzed in a multivariate model. ETV1 expression was assessed using immunohistochemistry, and miRNA interactions with ETV1 transcripts were investigated via the dual-luciferase reporter assay system.</p><p><strong>Results: </strong>We found that the rs3735343 SNP, located in the 3' untranslated region of ETV1, was significantly associated with progression-free survival (PFS) in GIST patients receiving imatinib (P = 0.008). Multivariate analysis identified tumor size (P = 0.032, Hazard Ratio [HR] = 4.173, 95% CI: 1.127-15.454) and rs3735343 (P = 0.009, HR = 8.995, 95% CI: 1.712-47.255) as independent predictors of PFS. The rs3735343 risk allele also correlated with elevated ETV1 expression in GIST tissue (P = 0.04). Additionally, miR-4311 was found to specifically and negatively regulate ETV1 mRNA levels associated with the rs3735343 risk allele in vitro.</p><p><strong>Conclusion: </strong>This study reported ETV1 rs3735343 as a novel prognostic candidate biomarker for GISTs treated with Imatinib, providing a potential biomarker for risk assessment of GIST. Additionally, our findings suggest that rs3735343 may act as a miRNA-regulated SNP, with miR-4311 playing a key role in its regulation.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"68"},"PeriodicalIF":2.7,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trends in renal function following vascular endothelial growth factor inhibitor administration in patients with cancer and diabetes mellitus.","authors":"Yuma Shibutani, Miki Hayakawa, Mayu Ishizaka","doi":"10.1007/s00280-025-04793-6","DOIUrl":"https://doi.org/10.1007/s00280-025-04793-6","url":null,"abstract":"<p><strong>Background: </strong>Vascular endothelial growth factor (VEGF) inhibitors are associated with a high incidence of proteinuria. In patients with diabetes, increased proteinuria is closely associated with decreased renal function; however, the impact of increased proteinuria on renal function in patients with cancer and diabetes mellitus undergoing VEGF inhibitor therapy remains unknown.</p><p><strong>Methods: </strong>The incidence of proteinuria and renal function in patients with cancer and a history of diabetes who were treated with VEGF inhibitors at the National Cancer Center Hospital East between January 2018 and December 2019 was retrospectively investigated.</p><p><strong>Results: </strong>Among the 49 patients included, 21 (43%) developed proteinuria ≥ 3 + after VEGF inhibitor treatment. In all patients, a decreasing trend in the estimated glomerular filtration rate (eGFR) was observed beginning 2 years after treatment initiation. The decrease in eGFR from baseline was - 6.6% at 1 year, -11% at 2 years, and - 13% at 4 years. Patients who developed proteinuria ≤ 2 + showed no significant decrease in eGFR from baseline to either the end of treatment (p = 0.91) or the latest value during the observation period (p = 0.64). Similarly, no significant decrease in eGFR was observed in those with proteinuria ≥ 3+ (end of treatment, p = 0.91; latest value during the observation period, p = 0.18).</p><p><strong>Conclusions: </strong>In patients with cancer and diabetes mellitus, increased proteinuria after VEGF inhibitor therapy suggested that it was not associated with a significant decline in renal function.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"69"},"PeriodicalIF":2.7,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacokinetics, safety, and tolerability of fedratinib in adults with moderate and severe hepatic impairment: results from the phase 1 FEDR-CP-001 trial.","authors":"Yizhe Chen, Richard A Preston, Thomas Marbury, William B Smith, Massimo Attanasio, Mark Thomas, Michael Thomas, Bing He, Yongjun Xue, Atalanta Ghosh, Gopal Krishna, Ken Ogasawara","doi":"10.1007/s00280-025-04785-6","DOIUrl":"10.1007/s00280-025-04785-6","url":null,"abstract":"<p><strong>Purpose: </strong>The FEDR-CP-001 (NCT03983161) trial evaluated the pharmacokinetics (PK) and safety of a single dose of fedratinib in adults with moderate or severe hepatic impairment (HI) compared with matched healthy participants with normal hepatic function.</p><p><strong>Methods: </strong>This was a non-randomized, open-label, multicenter, phase 1 trial. Participants were aged 18-75 years and had a BMI of 18-40 kg/m². HI was determined by Child-Pugh score. Participants were placed into 1 of the following groups: group 1, moderate HI; group 2, healthy participants matched to group 1; group 3, severe HI; and group 4, healthy participants matched to group 3. Participants received a single dose of fedratinib 300 mg (groups 1 and 2) or 200 mg (groups 3 and 4) and were followed for 21 days.</p><p><strong>Results: </strong>All participants (N = 38; groups 1, 3, and 4 [n = 8 each], group 2 [n = 14]) completed the trial. Peak and total fedratinib exposures (C_max, AUC_0-∞) were similar between moderate HI versus matched healthy participants. In participants with severe HI, there were lower total exposures compared to the matched healthy participants where the ratios of geometric means for C_max, and AUC_0-∞ were 0.897 and 0.660, respectively, and with large inter-participant variability. Ten participants experienced a treatment-emergent adverse event (all were considered mild), which were evenly distributed across groups.</p><p><strong>Conclusion: </strong>These data indicate that reducing fedratinib starting doses is not necessary for patients with moderate or severe HI, and support clinicians in regular monitoring of patients with HI taking fedratinib.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"65"},"PeriodicalIF":2.3,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pazopanib and antacids: insights from the WHO pharmacovigilance database.","authors":"Kazuki Nishida, Yao Liang, Osamu Maeda, Angélique Da Silva, Yuichi Ando, Basile Chrétien","doi":"10.1007/s00280-025-04792-7","DOIUrl":"https://doi.org/10.1007/s00280-025-04792-7","url":null,"abstract":"<p><p>Pazopanib, a multi-targeted tyrosine kinase inhibitor, is used for advanced renal cell carcinoma and soft tissue sarcoma. However, it is associated with dose-dependent adverse events (AEs), including hypertension, and gastrointestinal issues. Antacids like proton pump inhibitors (PPIs) and histamine-2 receptor antagonists (H2RAs) are often co-administered, raising concerns about potential drug interactions. Pazopanib's solubility and absorption are pH-dependent, with increased gastric pH potentially reducing its bioavailability. In this study, we analyzed VigiBase^® data using multivariate logistic regression models and found significant interactions between pazopanib and antacids (PPIs, H2RAs, and others), suggesting reduced serious AE reporting, possibly due to lower pazopanib exposure. A secondary analysis of CYP3A4 inhibitors showed a non-significant trend for higher serious AEs, aligning with expected pharmacokinetic effects. These findings emphasize the need for caution when combining antacids with pazopanib, as it may reduce both toxicity and efficacy.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"66"},"PeriodicalIF":2.7,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting insulin-like growth factor-1 (IGF-1) by using metformin in non-diabetic metastatic breast cancer female patients: a randomized controlled trial.","authors":"Hager Salah, Hoda Rabea, Mostafa S Sheemy, Alshaimaa Ibrahim Rabie, Hebatallah Ahmed Mohamed Moustafa, Ahmed A Elberry, Ahmed Hassan","doi":"10.1007/s00280-025-04791-8","DOIUrl":"10.1007/s00280-025-04791-8","url":null,"abstract":"<p><strong>Purpose: </strong>Insulin-like growth factor-1 (IGF-1) may play a role in breast cancer (BC) development. Metformin was found to exert anti-cancer function in several studies, partly by interference with the IGF-1 signaling pathway and reducing its blood levels. Therefore, our study aimed primarily to find out how metformin affected both IGF-1 levels and clinical outcomes in metastatic breast cancer patients (MBC) and secondarily to identify the correlation between post-treatment IGF-1 decline rates and BC prognosis and metastasis.</p><p><strong>Methods: </strong>Fifty MBC female patients were randomly assigned to either the control group (who were administered conventional chemotherapy) and the intervention group (treated with metformin plus chemotherapy). An enzyme-linked immunosorbent assay (ELISA) was used to detect IGF-1 levels at baseline and three months post-treatment.</p><p><strong>Results: </strong>IGF-1 levels in the metformin group were significantly lower than in the control group (p = 0.011). Furthermore, the percentage of post-treatment drop in IGF-1 levels differed significantly between the control and metformin groups (p = 0.001). Patients whose IGF-1 levels increased after treatment had a statistically significant occurrence of progressive disease (disease progression) in the control group higher than in the metformin group (92.9% versus 87.5%).</p><p><strong>Conclusion: </strong>The co-administration of metformin with chemotherapy significantly inhibited the IGF-1 signaling pathway, which reduced progressive diseases and reduced mortality in non-diabetic MBC patients. However, while metformin exerts a robust IGF-1 lowering effect, combination chemotherapy and low metastasis burden may further enhance this effect.</p><p><strong>Trail registration: </strong>Our trial was registered at clinicaltrials.gov (ID no. NCT04143282).</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"64"},"PeriodicalIF":2.7,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144511602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential anticancer effects of sodium-glucose cotransporter protein 2 (SGLT2) inhibitors Canagliflozin and Dapagliflozin.","authors":"Weiyu Dong, Yanyan Wang, Shaohua Fan","doi":"10.1007/s00280-025-04788-3","DOIUrl":"https://doi.org/10.1007/s00280-025-04788-3","url":null,"abstract":"<p><p>The use of sodium-glucose cotransporter protein 2 (SGLT2) inhibitors, specifically canagliflozin and dapagliflozin, has expanded from diabetes treatment to promising anticancer applications. Epidemiological links between diabetes and certain cancers highlight the potential of these agents in oncology, as SGLT2 is highly expressed in various tumor types. By inhibiting glucose uptake, canagliflozin and dapagliflozin disrupt glycolysis-dependent tumor growth, promoting apoptosis and reducing proliferation across multiple cancer models, including liver, prostate, and lung cancers. Key pathways involved in these effects include PI3K/AKT, mTOR, and AMPK signaling. Importantly, the combination of SGLT2 inhibitors with chemotherapy or radiotherapy has been shown to enhance antitumor efficacy and reduce treatment resistance, underscoring their potential as adjunctive therapies. However, adverse effects, such as increased risk of infection, and the need for more comprehensive mechanistic studies limit current applications. Future research should focus on expanding the understanding of these mechanisms, evaluating efficacy in additional tumor types, and optimizing combination therapies to mitigate side effects. SGLT2 inhibitors thus represent a novel class of metabolic modulators with potential for significant impact in cancer therapeutics.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"63"},"PeriodicalIF":2.7,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical relevance of Nectin-4 downregulation and biological changes caused by cytotoxic chemotherapy in bladder cancer.","authors":"Makito Miyake, Takuya Owari, Kota Iida, Sayuri Onishi, Nobutaka Nishimura, Tomomi Fujii, Cynthia N Jinno, Hideki Furuya, Yuki Oda, Tatsuki Miyamoto, Mitsuru Tomizawa, Takuto Shimizu, Kenta Onishi, Shunta Hori, Yosuke Morizawa, Daisuke Goto, Yasushi Nakai, Nobumichi Tanaka, Noriyoshi Miura, Tadahiko Kikugawa, Takashi Saika, Charles Rosser, Kiyohide Fujimoto","doi":"10.1007/s00280-025-04783-8","DOIUrl":"https://doi.org/10.1007/s00280-025-04783-8","url":null,"abstract":"<p><strong>Introduction: </strong>Mechanism underlying resistance to enfortumab vedotin (EV) and prognostication of Nectin-4 expression in muscle-invasive bladder cancer (MIBC) remains unclear.</p><p><strong>Methods: </strong>We generated gemcitabine-resistant HT-1376 and cisplatin-resistant HT-1376 cells generated from parental HT1376 cells (derived from MIBC). Transcriptome analysis was conducted to explore the biological function of differentially expressed genes detected in chemoresistant HT-1376 cells compared to parental HT-1376. In 70 patients with MIBC undergoing radical cystectomy, unsupervised hierarchical clustering was performed using immunohistochemical staining pattern with GATA3, KRT20, KRT5/6, KRT14, and Nectin-4 expression derived from the gene expression-based Nectin-4-modified NanoString molecular classification: Luminal-Nec4-High, Luminal-Nec4-Low, Basal-Nec4-High, and Basal-Nec4-Low subgroups.</p><p><strong>Results: </strong>We found significant downregulation of Nectin-4 expression along with epithelial-to-mesenchymal transition in chemoresistant HT-1376 cells. Exogenous expression of NECTIN4 in chemoresistant HT-1376 cells partially restored sensitivity to EV. RNA seq identified differentially expressed genes, including Nectin-4 and small proline-rich proteins, downregulated in chemoresistant HT-1376 cells. Over-representation analysis using GO and KEGG revealed upregulation of gene sets enriched for ribosome biogenesis-related pathways in chemoresistant HT-1376 cells. Nectin-4-modified molecular subtype resulted in better stratification of survival-the Luminal-Nec4-High subgroup had the best and the Basal-Nec4-Low subgroup had the worst prognosis. Comparing molecular subtypes of MIBC cells between transurethral resection specimens and matched radical cystectomy specimens revealed that 43% of neoadjuvant chemotherapy-treated patients with luminal subtype tumors showed a marked shift to the basal subtype in the cystectomy specimens.</p><p><strong>Conclusion: </strong>The clinical utility of Nection-4, associated molecules, and Nectin-4-modified molecular subtype need to be studied for better management strategies for MIBC.</p>","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"62"},"PeriodicalIF":2.7,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144483220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel desensitization protocol utilizing conventional formulations to mitigate Temozolomide-Related skin hypersensitivity.","authors":"Morgan E Cantley, Clyde Coleman, Rachael M Morgan, Niharika Reddy, Sarah A Sertich, John L Villano","doi":"10.1007/s00280-025-04782-9","DOIUrl":"10.1007/s00280-025-04782-9","url":null,"abstract":"","PeriodicalId":9556,"journal":{"name":"Cancer Chemotherapy and Pharmacology","volume":"95 1","pages":"61"},"PeriodicalIF":2.7,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}