Anticancer research最新文献

{"title":"Caffeic Acid Phenethyl Ester Inhibits Metastatic Properties of Acid-adapted Gastric Cancer Cells.","authors":"Sung-Chul Lim, Tae-Bum Lee, Song Iy Han","doi":"10.21873/anticanres.17534","DOIUrl":"https://doi.org/10.21873/anticanres.17534","url":null,"abstract":"<p><strong>Background/aim: </strong>The acidic tumor microenvironment promotes cancer invasiveness, epithelial-mesenchymal transition, and therapeutic resistance. This study aimed to investigate the long-term effects of acidic adaptation on gastric cancer cells and evaluate the anticancer properties of caffeic acid (CA) and caffeic acid phenethyl ester (CAPE) in this context.</p><p><strong>Materials and methods: </strong>SNU601 gastric cancer cells were cultured in prolonged acidic conditions (pH 6.7) to establish an acid-adapted subline (SNU601-6.7). Invasion assays and qPCR were used to assess invasive potential and the expression of matrix metalloproteinases (MMPs). The effects of CA and CAPE on viability, apoptosis, invasion, and β-catenin expression were evaluated.</p><p><strong>Results: </strong>SNU601-6.7 cells exhibited increased invasiveness, along with upregulation of MMP2, MMP7, and MMP9. Both CA and CAPE reduced cell viability and invasion, with CAPE exerting a significantly stronger effect and inducing moderate apoptosis. Mechanistic studies revealed that CAPE decreased total and nuclear β-catenin levels, and inhibited AKT and GSK3β phosphorylation. Further, pharmacological inhibition of AKT pathway confirmed its role in β-catenin accumulation and cell invasiveness.</p><p><strong>Conclusion: </strong>These findings identify CAPE as a potent inhibitor of invasion in acid-adapted gastric cancer cells by targeting the AKT/β-catenin pathway, highlighting its potential as a therapeutic candidate for gastric cancer in acidic tumor microenvironments.</p>","PeriodicalId":8072,"journal":{"name":"Anticancer research","volume":"45 4","pages":"1525-1534"},"PeriodicalIF":1.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742034","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":"Cardioprotective Effect of Pegfilgrastim on Chemotherapy-induced Cardiotoxicity in Preoperative Chemotherapy for Breast Cancer.","authors":"Takaaki Fujii, Yuko Nakazawa, Mayu Aoki, Keiko Tanabe, Misato Ogino, Sayaka Obayashi, Ken Shirabe","doi":"10.21873/anticanres.17551","DOIUrl":"https://doi.org/10.21873/anticanres.17551","url":null,"abstract":"<p><strong>Background/aim: </strong>Chemotherapy for breast cancer, particularly with anthracyclines and trastuzumab, is known to induce cardiotoxicity. Pegfilgrastim, a granulocyte colony-stimulating factor analog used to prevent chemotherapy-induced neutropenia, has shown potential myocardial protective effects. This study investigated pegfilgrastim's effect on preoperative chemotherapy-induced cardiotoxicity.</p><p><strong>Patients and methods: </strong>We retrospectively reviewed 110 patients who underwent preoperative chemotherapy from 2010 to 2019 and whose cardiac function was evaluated before and after chemotherapy. All patients received either Adriamycin or Fluorouracil, Epirubicin, and Cyclophosphamide as anthracyclines; in HER2-positive breast cancer, taxanes were combined with anti-HER2 therapy. Cardiac function was evaluated by ultrasound before and after chemotherapy.</p><p><strong>Results: </strong>Sixty-one patients treated with pegfilgrastim were compared to 49 non-treated patients. Cardiac function did not change with chemotherapy in the pegfilgrastim group; however, the ejection fraction with chemotherapy in the non-pegfilgrastim group decreased significantly (<i>p</i>=0.027).</p><p><strong>Conclusion: </strong>Pegfilgrastim may reduce chemotherapy-induced cardiotoxicity in addition to preventing febrile neutropenia.</p>","PeriodicalId":8072,"journal":{"name":"Anticancer research","volume":"45 4","pages":"1707-1712"},"PeriodicalIF":1.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742035","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":"Association Between Kita-kyushu Lung Cancer Antigen-1 Expression in Gastric Cancer and <i>Helicobacter pylori</i>-infection Status.","authors":"Nobue Futawatari, Takashi Fukuyama, Yusuke Akimoto, Junji Maehara, Daisuke Hihara, Yosuke Okamoto, Yuki Yokouchi, Kei Takahashi, Manabu Watanabe, Yoshihisa Saida","doi":"10.21873/anticanres.17541","DOIUrl":"https://doi.org/10.21873/anticanres.17541","url":null,"abstract":"<p><strong>Background/aim: </strong>Kita-kyushu lung cancer antigen-1 (KK-LC-1), a cancer/testis antigen (CTA), is frequently expressed in tumor and non-tumor sites of the stomach in patients with gastric cancer (GC). Additionally, KK-LC-1 has been associated with <i>Helicobacter pylori</i> (<i>Hp</i>) infection. Currently, the association between <i>Hp</i> eradication and GC incidence is unclear. This study aimed to investigate the association between KK-LC-1 expression and <i>Hp</i> eradication in GC.</p><p><strong>Patients and methods: </strong>This study included 124 patients treated for gastric cancer. Pathological tissue from resected specimens was used to investigate KK-LC-1 expression in tumor and non-tumor sites. The association between 14 clinicopathological factors, including <i>Hp</i> infection and eradication, and KK-LC-1 expression was investigated and analyzed by Fisher's exact test and multivariable regression analysis.</p><p><strong>Results: </strong>KK-LC-1 expression rate in cancerous tissues from patients with GC was 74.2%. The expression of KK-LC-1 was associated with older age, mucosal layer depth of invasion, differentiated type, no lymph node metastasis, <i>Hp</i> eradication, previous <i>Hp</i> infection, and multiple cancers.</p><p><strong>Conclusion: </strong>KK-LC-1 expression was high in GC cases with previous Hp infection and successful eradication. KK-LC-1 expression pattern suggests that it may be associated with GC independently of <i>Hp</i> infection.</p>","PeriodicalId":8072,"journal":{"name":"Anticancer research","volume":"45 4","pages":"1599-1606"},"PeriodicalIF":1.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742031","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":"Real-world Data of the Lung Cancer Compact Panel™ in Non-small Cell Lung Cancer Using Tissue Samples.","authors":"Yoshihiko Taniguchi, Akihiro Tamiya, Yukari Kamiyama, Hitoshi Sumitani, Yuki Iwahashi, Akihiro Tsukaguchi, Eiji Sugimoto, Yuji Inagaki, Keiko Nakao, Yoshinobu Matsuda, Maiko Takeda, Takahiko Kasai, Kyoichi Okishio, Shigeki Shimizu","doi":"10.21873/anticanres.17542","DOIUrl":"https://doi.org/10.21873/anticanres.17542","url":null,"abstract":"<p><strong>Background/aim: </strong>Multiple companion diagnostics are essential for detecting genetic alterations and guiding personalized treatment in patients with non-small cell lung cancer (NSCLC). The Lung Cancer Compact Panel™ (LCCP) is a newly developed multiple companion diagnostic tool designed to detect genetic mutations in NSCLC with high sensitivity, compatible with tissue and cytological samples. There has been no large-scale validation of the LCCP that includes tissue samples. This study analyzed LCCP data including tissue samples under real-world clinical conditions to examine its characteristics and usefulness.</p><p><strong>Patients and methods: </strong>We retrospectively analyzed consecutive NSCLC cases tested with the LCCP at a single institution between April 2023 and July 2024. Patient data, including histological type, genetic abnormalities, allele frequency, and program death ligand 1 expression, were collected from pathology records and electronic medical systems. Tissue specimens were used in cases where tumor content exceeded 5%.</p><p><strong>Results: </strong>Of the 317 cases, 154 (48.6%) harbored genetic abnormalities. The most common mutation was epidermal growth factor receptor (<i>EGFR</i>) major mutations (n=63). Among lung adenocarcinoma cases, 126 (70.0%) had genetic abnormalities. Fifteen patients had multiple coexisting genetic abnormalities. Notably, 13 patients had low allele frequencies (<2.5%). Nine variants were detected in 30 <i>EGFR</i> exon 19 deletion positive cases, three of which were undetectable by other multiple companion diagnostics. The LCCP demonstrated an ability to detect genetic abnormalities, even in cases with low tumor content (≥5%) compared to Oncomine DxTT and FoundationOne (≥30%), identifying rare <i>EGFR</i> exon 19 deletions and multiple coexisting mutations.</p><p><strong>Conclusion: </strong>These findings highlight LCCP's potential to improve personalized treatment strategies for NSCLC.</p>","PeriodicalId":8072,"journal":{"name":"Anticancer research","volume":"45 4","pages":"1607-1615"},"PeriodicalIF":1.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742059","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":"Fluoxetine Suppresses Osteosarcoma Progression <i>In Vivo</i> by Inducing Apoptosis and Inhibiting the AKT/mTOR/NF-κB Signaling Pathway.","authors":"Yu-Hsi Chen, Chi-Huan Li, Shih-Wei Liu, Fei-Ting Hsu, Ming-Chou Ku","doi":"10.21873/anticanres.17530","DOIUrl":"https://doi.org/10.21873/anticanres.17530","url":null,"abstract":"<p><strong>Background/aim: </strong>Osteosarcoma (OSCC) remains a significant health concern, necessitating novel therapeutic strategies. This study investigated the anti-tumor effects of fluoxetine in an <i>in vivo</i> OSCC model.</p><p><strong>Materials and methods: </strong>Mice inoculated with U-2 OS cells were treated with fluoxetine (10 or 20 mg/kg) to evaluate tumor growth, metastasis, and underlying molecular mechanisms.</p><p><strong>Results: </strong>Fluoxetine treatment resulted in a dose-dependent reduction in tumor volume and weight, without causing systemic toxicity, as confirmed by histopathological and biochemical analyses. Mechanistically, fluoxetine activated caspase-dependent apoptosis by up-regulating cleaved caspase-8, caspase-9, and caspase-3. It also inhibited OSCC metastasis by suppressing VEGF and MMP-9 expression, reducing epithelial-mesenchymal transition markers. Furthermore, fluoxetine significantly reduced the phosphorylation of AKT, PRAS40, mTOR, and NF-[Formula: see text]B, thereby disrupting key tumorigenic signaling pathways.</p><p><strong>Conclusion: </strong>Fluoxetine demonstrates promising anti-tumor activity in OSCC by inducing apoptosis, inhibiting metastasis, and targeting oncogenic signaling pathways. These findings suggest that fluoxetine may serve as a potential therapeutic agent for OSCC, warranting further investigation for clinical application.</p>","PeriodicalId":8072,"journal":{"name":"Anticancer research","volume":"45 4","pages":"1465-1480"},"PeriodicalIF":1.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143741826","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":"Increased Expression of DDX39 in Uveal Melanoma Is Associated With Patient Prognosis.","authors":"Shin-Nosuke Yamashita, Yoshiatsu Tanaka, Shajedul Islam, Takao Kitagawa, Kazuhiro Tokuda, Durga Paudel, Sarita Giri, Tohru Ohta, Fumiya Harada, Hiroki Nagayasu, Yasuhiro Kuramitsu","doi":"10.21873/anticanres.17547","DOIUrl":"https://doi.org/10.21873/anticanres.17547","url":null,"abstract":"<p><strong>Background/aim: </strong>Uveal melanoma is one of the most common primary intraocular tumors. It arises from melanocytes in the uvea and accounts for 3-5% of all melanomas. Uveal melanoma has a high metastatic potential. About half of the patients develop distant metastases including the liver, and the median survival time has been reported to be 4-5 months. Although the primary treatment for uveal melanoma has evolved from enucleation to eye-saving local treatment, there is no impact on the occurrence of distant metastases or overall survival. At least 50% of patients will develop metastases and the 3-year survival rate drops rapidly to 13%. Therefore, it is important to find prognostic biomarkers and therapeutic molecular targets that improve survival in patients with uveal melanoma. DDX39 is an Asp-Glu-Ala-Asp (DEAD) box RNA helicase required for mRNA transcription, splicing, and transport. There have been several reports of DDX39 over-expression in tumor tissues and cells, and we reported that patients with adrenocortical carcinoma with high DDX39 expression had a significantly worse prognosis. The clinicopathological involvement of DDX39 in uveal melanoma has not yet been documented.</p><p><strong>Materials and methods: </strong>We analyzed DDX39 mRNA expression and survival in patients with uveal melanoma using the GEPIA2 and UALCAN platforms.</p><p><strong>Results: </strong>DDX39 was found to be up-regulated in uveal melanoma tissues with increasing stage, and this up-regulated expression was inversely correlated with prolonged patient survival.</p><p><strong>Conclusion: </strong>DDX39 may be one of the potential prognostic biomarkers for patients with uveal melanoma.</p>","PeriodicalId":8072,"journal":{"name":"Anticancer research","volume":"45 4","pages":"1661-1666"},"PeriodicalIF":1.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143741881","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":"Inflammation-triggering Engineered Macrophages (MacTriggers) Are Promising Cell-based Therapeutic Avenues for Chemoresistant Solid Tumors.","authors":"Teruki Nii, Toma Yoshimi, Kenta Tanito, Shoichi Hijii, Haruka Takata, Akihiro Kishimura, Takeshi Mori, Tatsuhiro Ishida, Yoshiki Katayama","doi":"10.21873/anticanres.17525","DOIUrl":"https://doi.org/10.21873/anticanres.17525","url":null,"abstract":"<p><strong>Background/aim: </strong>Chimeric antigen receptor T-cell therapy has shown efficacy against chemoresistant B-cell leukemia and lymphoma but is limited in solid tumors. This study proposes using inflammation-triggering engineered macrophages (MacTriggers) to target chemoresistant tumors. Intravenous MacTriggers infiltrate tumors, inducing inflammation <i>via</i> tumor necrosis factor-alpha (TNF-α), converting the immunosuppressive microenvironment into an immuno-active state, and enhancing anti-tumor immune responses.</p><p><strong>Materials and methods: </strong>DOX-resistant murine colon cancer cells (DOX-Resi) were established by repeated <i>in vivo</i> exposure to DOX. IC₅₀ values and mRNA expression of Abcb1a (encoding P-gp) in WT or DOX-Resi cells were evaluated by qPCR. MacTriggers were engineered to release TNF-α upon sensing tumor-associated arginase 1 (Arg1) activity. BALB/c mice with subcutaneous DOX-Resi tumors received intravenous MacTriggers or DOX. Tumor growth, histological changes, and side effects, including cardiotoxicity, were assessed via tumor volume monitoring, immunohistochemistry, and serum cardiac troponin-I measurement.</p><p><strong>Results: </strong>DOX-Resi cells had an IC₅₀ value approximately 2.5 times higher than WT cells, with significantly higher Abcb1a expression. MacTriggers significantly suppressed DOX-Resi tumor growth, while DOX showed limited efficacy. MacTrigger administration did not cause severe side effects, unlike DOX, which induced cardiotoxicity.</p><p><strong>Conclusion: </strong>MacTriggers offer a novel, effective, and safer therapeutic approach for chemoresistant solid tumors, addressing chemotherapy limitations and improving outcomes in drug-resistant cancers.</p>","PeriodicalId":8072,"journal":{"name":"Anticancer research","volume":"45 4","pages":"1395-1405"},"PeriodicalIF":1.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143741884","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":"Characteristics and Mortality of Patients With Cancer Diagnosed With SARS-CoV-2 in Northern Portugal.","authors":"José Taveira-Barbosa, Teresa Garcia, Ana Lebre, Filipa Fontes, Mariana Brandão, Rita Calisto, Rubén Turé, Maria José Bento, Nuno Lunet, Samantha Morais, Luísa Lopes-Conceição","doi":"10.21873/anticanres.17555","DOIUrl":"https://doi.org/10.21873/anticanres.17555","url":null,"abstract":"<p><strong>Background/aim: </strong>Patients with cancer have been found to be at higher risk of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, which may negatively affect their prognosis. This study aimed to compare sociodemographic and clinical characteristics, as well as mortality, between cancer patients with and without SARS-CoV-2 infection.</p><p><strong>Patients and methods: </strong>Patients with tumors of the esophagus, stomach, colon and rectum, pancreas, lung, skin-melanoma, breast, cervix, non-Hodgkin lymphoma, and leukemia diagnosed between March 2019 and March 2021, and followed at the Portuguese Oncology Institute of Porto (IPO-Porto) were identified. Patients with SARS-CoV-2 infection between March 2020 and September 2021 were compared to patients without infection. Vital status was assessed up to March 2024. Cox proportional hazards regression was used to estimate crude, age- and stage-adjusted hazard ratios (HRs) and 95% confidence intervals (95%CIs) for mortality.</p><p><strong>Results: </strong>During follow-up, one-third of patients who had SARS-CoV-2 died (<i>vs</i>. one-fourth), corresponding to an adjusted HR (95%CI) of 1.39 (1.03-1.88). Significantly higher adjusted HRs were observed for residents outside Porto's Metropolitan Area (HR=1.94, 95%CI=1.22-3.09), patients with lung cancer (HR=2.02, 95%CI=1.12-3.66) and patients with surgery as the first cancer treatment received at IPO-Porto (HR=2.00, 95%CI=1.08-3.74).</p><p><strong>Conclusion: </strong>Cancer patients with SARS-CoV-2 infection had higher mortality compared to those without infection, and specific subgroups of patients at higher risk were identified.</p>","PeriodicalId":8072,"journal":{"name":"Anticancer research","volume":"45 4","pages":"1749-1760"},"PeriodicalIF":1.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742036","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":"Activation of <i>DCTN1-RET</i> Fusion Through Coiled-coil Domain as a Potential Target for RET Inhibitors.","authors":"Kohei Hayashi, Keiji Ishida, Masanori Kato, Shuichi Ohkubo, Yoshihiro Uto","doi":"10.21873/anticanres.17526","DOIUrl":"https://doi.org/10.21873/anticanres.17526","url":null,"abstract":"<p><strong>Background/aim: </strong>The REarranged during Transfection (<i>RET</i>) proto-oncogene fusion is a typical cancer driver gene frequently observed in thyroid and lung cancers. This study characterized the novel dynactin subunit 1 <i>(DCTN1)-RET</i> fusion gene and evaluated the efficacy of RET inhibitors against this fusion.</p><p><strong>Materials and methods: </strong>Thyroid cancer tissue DNA samples were sequenced to identify fusion genes, and an expression vector was generated using extracted RNA. Cell lines stably expressing DCTN1-RET variants, including those lacking the coiled-coil (CC) domain, were established. The functionality of these variants and therapeutic efficacy of RET inhibitors were examined both <i>in vitro</i> and <i>in vivo</i>.</p><p><strong>Results: </strong>The <i>DCTN1-RET</i> fusion gene contains the CC domain from DCTN1 and the kinase domain from RET. Deletion of the CC domain abrogated dimer formation and reduced RET and extracellular signal-regulated kinase phosphorylation. Cells expressing <i>DCTN1-RET</i> exhibited enhanced proliferation and tumorigenesis <i>in vivo</i>. The RET inhibitor TAS0286 effectively suppressed <i>DCTN1-RET</i>-mediated RET autophosphorylation and tumor growth in a mouse subcutaneous tumor model.</p><p><strong>Conclusion: </strong><i>DCTN1-RET</i> is a novel oncogenic fusion gene in thyroid cancer that promotes tumorigenesis through CC domain-mediated dimerization. It represents a potential therapeutic target for RET-specific inhibitors.</p>","PeriodicalId":8072,"journal":{"name":"Anticancer research","volume":"45 4","pages":"1407-1417"},"PeriodicalIF":1.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742013","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":"Chemotherapy Efficacy in Patients With Colorectal Cancer Experiencing Early Recurrence During or After Adjuvant Chemotherapy.","authors":"Dai Okemoto, Toshifumi Yamaguchi, Kanako Sugino, Nanako Matsuo, Makoto Sanomura, Shin Kameisihi, Toru Kadono, Hiroyuki Kodama, Hiroki Yukami, Elham Fakhrejahani, Hiroki Nishikawa","doi":"10.21873/anticanres.17550","DOIUrl":"https://doi.org/10.21873/anticanres.17550","url":null,"abstract":"<p><strong>Background/aim: </strong>Colorectal cancer (CRC) is the third most diagnosed malignancy worldwide. The efficacy of first-line chemotherapy for metastatic CRC with early recurrence after adjuvant therapy remains unclear; therefore, this study investigated its impact.</p><p><strong>Patients and methods: </strong>A retrospective evaluation was conducted on patients with early recurrence after adjuvant chemotherapy from three institutions between 2016 and 2021. Early recurrence was defined as recurrence during or within 1 year of completing adjuvant chemotherapy. Progression-free and overall survival, as well as the overall response rate, were endpoints, with analysis stratified by a recurrence-free interval (RFI) of 6 months.</p><p><strong>Results: </strong>Data from 455 patients treated with adjuvant therapy were reviewed, identifying 32 eligible patients. Twenty-eight patients (88%) received oxaliplatin-containing regimens, and four (12%) received fluoropyrimidine monotherapy. For palliative chemotherapy, oxaliplatin-based, irinotecan-based, or other regimens were administered to 13 (41%), 13 (41%), and 6 (18%) patients, respectively. Median progression-free and overall survival were 10.4 and 43.0 months, respectively. The overall response rate was 34.4%, and the disease control rate was 75.0%. Patients with RFI <6 months had a lower response rate (26% <i>vs</i>. 56%), shorter progression-free survival (10.4 <i>vs</i>. 17.8 months), and shorter overall survival (31.3 <i>vs</i>. 43.0 months); however, these differences were not statistically significant. Multivariate analysis suggested worse overall survival for patients with RFI <6 months than for those with RFI ≥6 months (hazard ratio=1.78, 95% confidence interval=0.35-8.98; <i>p</i>=0.49).</p><p><strong>Conclusion: </strong>Patients with CRC and RFI <6 months after adjuvant chemotherapy showed a trend toward poorer outcomes than those with RFI ≥6 months, suggesting a need for more intensive treatment strategies.</p>","PeriodicalId":8072,"journal":{"name":"Anticancer research","volume":"45 4","pages":"1695-1705"},"PeriodicalIF":1.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742037","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}