Pancreatic cancer remains one of the most aggressive malignancies with limited treatment options and poor survival rates. Vitamin D deficiency has been suggested to influence cancer progression and survival outcomes in various malignancies.
Aim
This study aimed to investigate the association between Vitamin D deficiency and disease progression as well as survival in patients diagnosed with pancreatic cancer.
Methods
A retrospective cohort study was conducted, including 151 patients diagnosed with pancreatic cancer between 2012 and 2022. Serum Vitamin D levels at the time of diagnosis were measured. Disease progression was evaluated through radiological assessments and clinical reports. Survival outcomes, including overall survival (OS) and progression-free survival (PFS), were analyzed using Kaplan-Meier survival curves and Cox proportional hazards regression models.
Results
Of the 151 patients, 84 (56 %) were identified as Vitamin D deficient at the time of diagnosis. The deficient group exhibited a significantly higher frequency of advanced-stage disease (stages III and IV) compared to the non-deficient group (p < 0.05). During the follow-up period, 66 (78.6 %) of Vitamin d-deficient patients and 56 (84.8 %) of non-deficient patients experienced disease progression (p = 0.51). Moreover, Kaplan-Meier analysis showed a non-significant trend toward shorter median PFS (8.95 months vs. 9.27 months, p = 0.51) and OS (17.64 months vs. 19.05 months, p = 0.616) in the Vitamin d-deficient group.
Conclusion
Vitamin D deficiency is prevalent among patients with pancreatic cancer and appears to be associated with more advanced disease at diagnosis. Although a trend toward poorer survival outcomes was observed, the association between Vitamin D deficiency and OS/PFS did not reach statistical significance. Additional prospective studies are needed to confirm these findings and explore potential benefits of Vitamin D supplementation in pancreatic cancer management.
{"title":"Exploring the prognostic significance of vitamin D deficiency in pancreatic cancer: Disease progression and survival outcomes","authors":"Aladeen Alloubani, Baraa Abadalhaq, Amal Alshami, Diana Fakhory, Feras Abdalghani, Mallak Almasri, Maysa Alkouz","doi":"10.1016/j.ctarc.2025.100917","DOIUrl":"10.1016/j.ctarc.2025.100917","url":null,"abstract":"<div><h3>Background</h3><div>Pancreatic cancer remains one of the most aggressive malignancies with limited treatment options and poor survival rates. Vitamin D deficiency has been suggested to influence cancer progression and survival outcomes in various malignancies.</div></div><div><h3>Aim</h3><div>This study aimed to investigate the association between Vitamin D deficiency and disease progression as well as survival in patients diagnosed with pancreatic cancer.</div></div><div><h3>Methods</h3><div>A retrospective cohort study was conducted, including 151 patients diagnosed with pancreatic cancer between 2012 and 2022. Serum Vitamin D levels at the time of diagnosis were measured. Disease progression was evaluated through radiological assessments and clinical reports. Survival outcomes, including overall survival (OS) and progression-free survival (PFS), were analyzed using Kaplan-Meier survival curves and Cox proportional hazards regression models.</div></div><div><h3>Results</h3><div>Of the 151 patients, 84 (56 %) were identified as Vitamin D deficient at the time of diagnosis. The deficient group exhibited a significantly higher frequency of advanced-stage disease (stages III and IV) compared to the non-deficient group (<em>p</em> < 0.05). During the follow-up period, 66 (78.6 %) of Vitamin <span>d</span>-deficient patients and 56 (84.8 %) of non-deficient patients experienced disease progression (<em>p</em> = 0.51). Moreover, Kaplan-Meier analysis showed a non-significant trend toward shorter median PFS (8.95 months vs. 9.27 months, <em>p</em> = 0.51) and OS (17.64 months vs. 19.05 months, <em>p</em> = 0.616) in the Vitamin <span>d</span>-deficient group.</div></div><div><h3>Conclusion</h3><div>Vitamin D deficiency is prevalent among patients with pancreatic cancer and appears to be associated with more advanced disease at diagnosis. Although a trend toward poorer survival outcomes was observed, the association between Vitamin D deficiency and OS/PFS did not reach statistical significance. Additional prospective studies are needed to confirm these findings and explore potential benefits of Vitamin D supplementation in pancreatic cancer management.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"43 ","pages":"Article 100917"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143821500","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}
The optimal timing of radiotherapy (RT) for asymptomatic brain metastasis (aBM) in patients with non-small cell lung cancer (NSCLC) without targetable oncogenic drivers treated with immune checkpoint inhibitors (ICIs) remains unclear. This study aimed to assess the efficacy and safety of upfront (U)-RT combined with ICIs for aBM.
Methods
We retrospectively reviewed consecutive patients with aBM from NSCLC who received ICI-containing chemotherapy at National Cancer Center Hospital East between 2016 and 2021. The U-RT group was defined patients who received RT for aBM before or during the first ICI cycle, and the non-U-RT group otherwise.
Results
Of the 324 patients with NSCLC and aBM screened, 54 were enrolled, with 34 and 20 patients in the U-RT and non-U-RT groups, respectively. The median overall survival was 27.5 and 13.8 months (hazard ratio [HR] = 0.40, 95 % confidence interval [CI] 0.19–0.87), respectively, and median cranial progression-free survival was 9.2 and 6.0 months (HR = 0.50, 95 % CI 0.25–0.98), respectively, in the U-RT and non-U-RT groups. The U-RT group showed a significantly lower aBM progression rate than the non-U-RT group (P = 0.04). U-RT was an independent prognostic factor in the multivariate analysis using propensity score adjustment (HR = 0.42, 95 % CI 0.18–0.96). Although severe adverse events were observed in 47 % and 35 % of patients in the U-RT and non-U-RT groups, respectively, no treatment-related deaths occurred.
Conclusions
ICIs with U-RT demonstrated higher efficacy with acceptable tolerability for aBM than ICIs without U-RT. Our findings should be confirmed in future prospective trials.
对于接受免疫检查点抑制剂（ICIs）治疗的无靶向致癌驱动因素的非小细胞肺癌（NSCLC）患者无症状脑转移（aBM）的最佳放疗时间（RT）仍不清楚。本研究旨在评估先期(U)-RT联合ICIs治疗aBM的疗效和安全性。方法回顾性分析2016年至2021年在国家癌症中心东医院连续接受含ici化疗的非小细胞肺癌aBM患者。U-RT组定义为在第一个ICI周期之前或期间接受aBM放疗的患者，而非U-RT组则相反。结果在筛选的324例NSCLC和aBM患者中，54例入组，其中U-RT组和非U-RT组分别为34例和20例。U-RT组和非U-RT组的中位总生存期分别为27.5个月和13.8个月（风险比[HR] = 0.40, 95%可信区间[CI] 0.19-0.87），中位无颅进展生存期分别为9.2个月和6.0个月（HR = 0.50, 95% CI 0.25-0.98）。U-RT组aBM进展率明显低于非U-RT组（P = 0.04）。在使用倾向评分调整的多变量分析中，U-RT是一个独立的预后因素（HR = 0.42, 95% CI 0.18-0.96）。尽管在U-RT组和非U-RT组中分别有47%和35%的患者观察到严重不良事件，但没有发生与治疗相关的死亡。结论与未加U-RT的ICIs相比，联合U-RT的ICIs对aBM具有更高的疗效和可接受的耐受性。我们的发现应该在未来的前瞻性试验中得到证实。
{"title":"Efficacy and safety of upfront radiotherapy with immune checkpoint inhibitors for brain metastasis in non-small cell lung cancer","authors":"Yu Tanaka , Hiroki Izumi , Eri Sugiyama , Tetsuya Sakai , Yuji Shibata , Kaname Nosaki , Hibiki Udagawa , Shigeki Umemura , Yoshitaka Zenke , Shingo Matsumoto , Kiyotaka Yoh , Tetsuo Akimoto , Koichi Goto","doi":"10.1016/j.ctarc.2025.100937","DOIUrl":"10.1016/j.ctarc.2025.100937","url":null,"abstract":"<div><h3>Introduction</h3><div>The optimal timing of radiotherapy (RT) for asymptomatic brain metastasis (aBM) in patients with non-small cell lung cancer (NSCLC) without targetable oncogenic drivers treated with immune checkpoint inhibitors (ICIs) remains unclear. This study aimed to assess the efficacy and safety of upfront (U)-RT combined with ICIs for aBM.</div></div><div><h3>Methods</h3><div>We retrospectively reviewed consecutive patients with aBM from NSCLC who received ICI-containing chemotherapy at National Cancer Center Hospital East between 2016 and 2021. The U-RT group was defined patients who received RT for aBM before or during the first ICI cycle, and the non-U-RT group otherwise.</div></div><div><h3>Results</h3><div>Of the 324 patients with NSCLC and aBM screened, 54 were enrolled, with 34 and 20 patients in the U-RT and non-U-RT groups, respectively. The median overall survival was 27.5 and 13.8 months (hazard ratio [HR] = 0.40, 95 % confidence interval [CI] 0.19–0.87), respectively, and median cranial progression-free survival was 9.2 and 6.0 months (HR = 0.50, 95 % CI 0.25–0.98), respectively, in the U-RT and non-U-RT groups. The U-RT group showed a significantly lower aBM progression rate than the non-U-RT group (<em>P</em> = 0.04). U-RT was an independent prognostic factor in the multivariate analysis using propensity score adjustment (HR = 0.42, 95 % CI 0.18–0.96). Although severe adverse events were observed in 47 % and 35 % of patients in the U-RT and non-U-RT groups, respectively, no treatment-related deaths occurred.</div></div><div><h3>Conclusions</h3><div>ICIs with U-RT demonstrated higher efficacy with acceptable tolerability for aBM than ICIs without U-RT. Our findings should be confirmed in future prospective trials.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"43 ","pages":"Article 100937"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143935133","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}
Pub Date : 2025-01-01DOI: 10.1016/j.ctarc.2025.100964
Meaghan Polack , Gabi W. van Pelt , Augustinus S.L.P. Crobach , Lioe-Fee de Geus-Oei , Rob A.E.M. Tollenaar , J.Han J.M. van Krieken , Wilma E. Mesker
Background: Colorectal cancer is highly prevalent. The stromal tumour microenvironment significantly influences tumour behaviour, and cancer-associated fibroblasts (CAFs), as major component of tumour stroma, are increasingly studied. Specifically, CAF-marker fibroblast activation protein (FAP) is gaining interest as tracer for imaging using radiolabelled FAP-inhibitor (FAPI). We describe patterns of FAP-expression, and associations to intratumoural stroma amount, establishing a biological background and potential future reference to pathology assessment.
Materials and methods: Archival histological material from 125 stage-II/III CRC patients was collected. Haematoxylin-and-eosin staining was performed to determine the tumour-stroma ratio (TSR), indicating stromal percentages in primary tumours, lymph nodes (LNs) and biopsies. On immunohistochemistry stains, FAP-expression was semiquantitatively scored as little-no, heterogeneous, or moderate-high expression. Correlation of TSR and FAP-expression with Chi-square testing was assessed. Other patterns were also described, e.g. tumour epithelial FAP-expression.
Results: In total, 93 patients (40 stage-III colon [CC], 53 stage-II/III RC) were included. Correlation between 41 (44 %) stroma-high CRC (18/40 CC, 45 %; 23/53 RC, 43 %) with high FAP-expression was not significant (P = 0.428 CRC; P = 0.470 CC; P = 0.615 RC). The majority of CRC had any FAP-expression (78 CRC, 84 %), mostly the invasive front, and in most associated LN metastases (87 % CRC tumour-positive LN). However, FAP-expression was often heterogeneous, even staining healthy colon and lymphoid tissue.
Conclusions: CRCs and LN metastases generally express FAP, but levels vary significantly between and within tumours and have no direct correlation with TSR. Care has to be taken translating FAPI-PET/CT results with e.g. disease extent and activity, emphasizing the importance of multidisciplinary approach.
{"title":"Fibroblast activation protein-expression in colorectal carcinomas and implications for clinical application","authors":"Meaghan Polack , Gabi W. van Pelt , Augustinus S.L.P. Crobach , Lioe-Fee de Geus-Oei , Rob A.E.M. Tollenaar , J.Han J.M. van Krieken , Wilma E. Mesker","doi":"10.1016/j.ctarc.2025.100964","DOIUrl":"10.1016/j.ctarc.2025.100964","url":null,"abstract":"<div><div>Background: Colorectal cancer is highly prevalent. The stromal tumour microenvironment significantly influences tumour behaviour, and cancer-associated fibroblasts (CAFs), as major component of tumour stroma, are increasingly studied. Specifically, CAF-marker fibroblast activation protein (FAP) is gaining interest as tracer for imaging using radiolabelled FAP-inhibitor (FAPI). We describe patterns of FAP-expression, and associations to intratumoural stroma amount, establishing a biological background and potential future reference to pathology assessment.</div><div>Materials and methods: Archival histological material from 125 stage-II/III CRC patients was collected. Haematoxylin-and-eosin staining was performed to determine the tumour-stroma ratio (TSR), indicating stromal percentages in primary tumours, lymph nodes (LNs) and biopsies. On immunohistochemistry stains, FAP-expression was semiquantitatively scored as little-no, heterogeneous, or moderate-high expression. Correlation of TSR and FAP-expression with Chi-square testing was assessed. Other patterns were also described, e.g. tumour epithelial FAP-expression.</div><div>Results: In total, 93 patients (40 stage-III colon [CC], 53 stage-II/III RC) were included. Correlation between 41 (44 %) stroma-high CRC (18/40 CC, 45 %; 23/53 RC, 43 %) with high FAP-expression was not significant (<em>P</em> = 0.428 CRC; <em>P</em> = 0.470 CC; <em>P</em> = 0.615 RC). The majority of CRC had any FAP-expression (78 CRC, 84 %), mostly the invasive front, and in most associated LN metastases (87 % CRC tumour-positive LN). However, FAP-expression was often heterogeneous, even staining healthy colon and lymphoid tissue.</div><div>Conclusions: CRCs and LN metastases generally express FAP, but levels vary significantly between and within tumours and have no direct correlation with TSR. Care has to be taken translating FAPI-PET/CT results with e.g. disease extent and activity, emphasizing the importance of multidisciplinary approach.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"44 ","pages":"Article 100964"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144661963","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}
Pub Date : 2025-01-01DOI: 10.1016/j.ctarc.2025.101020
Djordje Marina , August Nielsen , Kristian Buch-Larsen , Michael Andersson , Åse Krogh Rasmussen , Peter Schwarz
Purpose
Aromatase inhibitors are commonly used in adjuvant therapy for breast cancer. However, their impact on thyroid function remains unclear. This study aimed to evaluate thyroid function in postmenopausal women with oestrogen-receptor-positive early-stage breast cancer one and two years after initiating aromatase inhibitors.
Methods
This prospective controlled study involved 59 postmenopausal women with early-stage breast cancer and 39 healthy controls. All participants underwent chemotherapy and aromatase inhibitor treatment, with 35 receiving locoregional radiotherapy. The primary outcomes included evaluation of thyroid hormones and thyroid-binding globulin post-chemotherapy, at one-year and two-year follow-ups after initiation of aromatase inhibitors. Secondary outcomes included thyroid autoantibodies and weight/body mass index.
Results
There were no significant differences in thyroid parameters between the patients and healthy controls pre-chemotherapy. During treatment, free-thyroxine levels increased at both visits (p < 0.01), and total thyroxine increased at the two-year visit (p = 0.02), while triiodothyronine decreased (p < 0.01 and p = 0.03). No changes in thyroid-stimulating hormone or thyroid-binding globulin were observed, but albumin increased after one year (p < 0.01). Weight change was insignificant, and autoimmune thyroiditis prevalence was low (≤15 %). No differences in thyroid function between women with or without locoregional radiotherapy/trastuzumab were found.
Conclusions
This study suggests that, despite statistically significant changes in peripheral thyroid hormones, there were no obvious clinically important effects observed in patients with early-stage breast cancer during the two-year treatment with aromatase inhibitors. The changes were not associated with thyroid autoimmunity, non-thyroidal illness, radiotherapy, trastuzumab therapy, or high-dose corticosteroids. Further research is needed to better understand the long-term impact of aromatase inhibitors on thyroid function in this population.
Clinical trial registration
This study is registered at clinicaltrials.gov (NCT03784651).
{"title":"Impact of aromatase inhibitors on thyroid function in postmenopausal women with early-stage breast cancer: a prospective controlled study","authors":"Djordje Marina , August Nielsen , Kristian Buch-Larsen , Michael Andersson , Åse Krogh Rasmussen , Peter Schwarz","doi":"10.1016/j.ctarc.2025.101020","DOIUrl":"10.1016/j.ctarc.2025.101020","url":null,"abstract":"<div><h3>Purpose</h3><div>Aromatase inhibitors are commonly used in adjuvant therapy for breast cancer. However, their impact on thyroid function remains unclear. This study aimed to evaluate thyroid function in postmenopausal women with oestrogen-receptor-positive early-stage breast cancer one and two years after initiating aromatase inhibitors.</div></div><div><h3>Methods</h3><div>This prospective controlled study involved 59 postmenopausal women with early-stage breast cancer and 39 healthy controls. All participants underwent chemotherapy and aromatase inhibitor treatment, with 35 receiving locoregional radiotherapy. The primary outcomes included evaluation of thyroid hormones and thyroid-binding globulin post-chemotherapy, at one-year and two-year follow-ups after initiation of aromatase inhibitors. Secondary outcomes included thyroid autoantibodies and weight/body mass index.</div></div><div><h3>Results</h3><div>There were no significant differences in thyroid parameters between the patients and healthy controls pre-chemotherapy. During treatment, free-thyroxine levels increased at both visits (<em>p</em> < 0.01), and total thyroxine increased at the two-year visit (<em>p</em> = 0.02), while triiodothyronine decreased (<em>p</em> < 0.01 and <em>p</em> = 0.03). No changes in thyroid-stimulating hormone or thyroid-binding globulin were observed, but albumin increased after one year (<em>p</em> < 0.01). Weight change was insignificant, and autoimmune thyroiditis prevalence was low (≤15 %). No differences in thyroid function between women with or without locoregional radiotherapy/trastuzumab were found.</div></div><div><h3>Conclusions</h3><div>This study suggests that, despite statistically significant changes in peripheral thyroid hormones, there were no obvious clinically important effects observed in patients with early-stage breast cancer during the two-year treatment with aromatase inhibitors. The changes were not associated with thyroid autoimmunity, non-thyroidal illness, radiotherapy, trastuzumab therapy, or high-dose corticosteroids. Further research is needed to better understand the long-term impact of aromatase inhibitors on thyroid function in this population.</div></div><div><h3>Clinical trial registration</h3><div>This study is registered at clinicaltrials.gov (NCT03784651).</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"45 ","pages":"Article 101020"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145412633","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}
Pub Date : 2025-01-01DOI: 10.1016/j.ctarc.2025.101026
Kevin M. Levine , Natalie F. Uy , Ted A. Gooley , Jenna Voutsinas , Micah Tratt , Keith D. Eaton , Rafael Santana-Davila , Alice H. Berger , Christina S. Baik
Resistance to osimertinib, a third-generation EGFR tyrosine kinase inhibitor, remains a key challenge in the treatment of EGFR-mutated non-small cell lung cancer (NSCLC). Although retreatment with earlier-generation EGFR tyrosine kinase inhibitors has been studied, data on osimertinib rechallenge are limited. We conducted a single institution retrospective analysis of patients with EGFR-mutated NSCLC who were rechallenged with osimertinib following progression on prior osimertinib and interim systemic therapy, including chemotherapy. Seventeen patients met inclusion criteria, all with adenocarcinoma histology and either EGFR exon 19 deletions or L858R mutations. Median interval between osimertinib treatments was 10.5 months. Osimertinib retreatment resulted in a partial response in 18 % (3/17) and stable disease in 35 % of patients (6/17), for a disease control rate of 53 % (9/17). Median retreatment duration was 4.3 months, and median overall survival following retreatment initiation was 8.9 months. Among patients with central nervous system involvement, several experienced intracranial stability without additional radiation. Duration of initial osimertinib therapy did not strongly predict retreatment benefit. These findings suggest that osimertinib rechallenge may provide clinically meaningful disease control in a subset of patients, especially given its tolerability and oral formulation. Further research is needed to identify biomarkers of sensitivity and to optimize patient selection for osimertinib retreatment following interval chemotherapy.
{"title":"Osimertinib retreatment for patients with advanced EGFR-mutated non-small cell lung cancer","authors":"Kevin M. Levine , Natalie F. Uy , Ted A. Gooley , Jenna Voutsinas , Micah Tratt , Keith D. Eaton , Rafael Santana-Davila , Alice H. Berger , Christina S. Baik","doi":"10.1016/j.ctarc.2025.101026","DOIUrl":"10.1016/j.ctarc.2025.101026","url":null,"abstract":"<div><div>Resistance to osimertinib, a third-generation EGFR tyrosine kinase inhibitor, remains a key challenge in the treatment of EGFR-mutated non-small cell lung cancer (NSCLC). Although retreatment with earlier-generation EGFR tyrosine kinase inhibitors has been studied, data on osimertinib rechallenge are limited. We conducted a single institution retrospective analysis of patients with EGFR-mutated NSCLC who were rechallenged with osimertinib following progression on prior osimertinib and interim systemic therapy, including chemotherapy. Seventeen patients met inclusion criteria, all with adenocarcinoma histology and either EGFR exon 19 deletions or L858R mutations. Median interval between osimertinib treatments was 10.5 months. Osimertinib retreatment resulted in a partial response in 18 % (3/17) and stable disease in 35 % of patients (6/17), for a disease control rate of 53 % (9/17). Median retreatment duration was 4.3 months, and median overall survival following retreatment initiation was 8.9 months. Among patients with central nervous system involvement, several experienced intracranial stability without additional radiation. Duration of initial osimertinib therapy did not strongly predict retreatment benefit. These findings suggest that osimertinib rechallenge may provide clinically meaningful disease control in a subset of patients, especially given its tolerability and oral formulation. Further research is needed to identify biomarkers of sensitivity and to optimize patient selection for osimertinib retreatment following interval chemotherapy.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"45 ","pages":"Article 101026"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145412635","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}
Pub Date : 2025-01-01DOI: 10.1016/j.ctarc.2025.101014
Dong Woog Yoon , Soohyun Hwang , Boram Lee , Yeong Jeong Jeon , Junghee Lee , Dong Wook Shin , Byeong-Ho Jeong , Seong Yong Park , Hong Kwan Kim , Yong Soo Choi , Jong Ho Cho
Background
Invasive mucinous adenocarcinoma (IMA) is genetically distinct from non-mucinous adenocarcinoma, commonly characterized by KRAS mutations. However, studies exploring molecular co-alterations alongside KRAS mutations in IMA remain limited.
Methods
We reviewed 84 patients with surgically resected IMAs from 2015 to 2023 who underwent NGS using TruSight™ Oncology 500 or CancerSCAN assays. Overall survival (OS) and disease-free survival (DFS) were assessed using Cox regression, and log-rank tests were used to evaluate the prognostic role of each molecular alteration.
Results
Among the 84 patients, driver alterations were identified in KRAS (67.9 %, n = 57), ERBB2 (10.7 %, n = 9), and NRG-1 (7.1 %, n = 6), while concurrent mutations were found in TP53 (31 %, n = 26), NKX2–1 (23.8 %, n = 20), CDKN2A (15.5 %, n = 13), and PIK3CA (10.7 %, n = 9). Among the overall cohort, survival analysis demonstrated that TP53 alterations were associated with worse OS (p = 0.03), while NKX2–1 alterations were linked to better DFS (p = 0.03). In the KRAS-mutant subgroup, TP53 alterations were associated with worse OS (p < 0.01) and DFS (p < 0.01), while NKX2–1 mutations were associated with better OS (p = 0.05). Multivariate analysis identified TP53 alterations as independent prognostic factors for OS (HR,11.32; 95 % CI,2.18–58.75) and DFS (HR,4.33; 95 % CI,1.84–10.2) in patients with KRAS mutations.
Conclusion
Concurrent TP53 mutations have significant prognostic implications in KRAS-mutant IMAs. This finding underscores the potential role of TP53 mutations in guiding personalized treatment approaches to improve patient outcomes.
Micro abstract
In a retrospective cohort of 84 resected pulmonary invasive mucinous adenocarcinomas, next-generation sequencing was performed and genomic alterations were correlated with prognosis. KRAS was the predominant driver (∼68 %), and concurrent TP53 mutations (∼32 %) independently predicted worse overall and disease-free survival within KRAS-mutant IMA. TP53 co-mutation serves as a practical risk stratifier to inform closer post-surgical surveillance and potential adjuvant strategies.
背景：侵袭性粘液腺癌（IMA）在基因上不同于非粘液腺癌，通常以KRAS突变为特征。然而，探索IMA中KRAS突变的分子共改变的研究仍然有限。方法：我们使用TruSight™Oncology 500或CancerSCAN分析，回顾了2015年至2023年接受NGS手术切除的84例ima患者。使用Cox回归评估总生存期（OS）和无病生存期（DFS），并使用log-rank检验评估每种分子改变的预后作用。结果：84例患者中，KRAS （67.9%, n = 57）、ERBB2 （10.7%, n = 9）和NRG-1 （7.1%, n = 6）发生了驱动突变，而TP53 （31%, n = 26）、NKX2-1 （23.8%, n = 20）、CDKN2A （15.5%, n = 13）和PIK3CA （10.7%, n = 9）发生了同步突变。在整个队列中，生存分析显示TP53改变与较差的OS相关（p = 0.03），而NKX2-1改变与较好的DFS相关（p = 0.03）。在kras突变亚组中，TP53突变与较差的OS （p < 0.01）和DFS （p < 0.01）相关，而NKX2-1突变与较好的OS相关（p = 0.05）。多因素分析发现，TP53改变是KRAS突变患者OS （HR,11.32; 95% CI,2.18-58.75）和DFS （HR,4.33; 95% CI,1.84-10.2）的独立预后因素。结论：并发TP53突变对kras突变型ima具有重要的预后影响。这一发现强调了TP53突变在指导个性化治疗方法以改善患者预后方面的潜在作用。摘要：在84例肺浸润性粘液腺癌的回顾性队列中，我们进行了下一代测序，基因组改变与预后相关。KRAS是主要的驱动因素（~ 68%），同时发生的TP53突变（~ 32%）独立预测KRAS突变IMA患者的总生存率和无病生存率更差。TP53共突变可作为实际的风险分层，为更密切的术后监测和潜在的辅助策略提供信息。
{"title":"Clinical significance of concurrent TP53 mutations in KRAS-mutant invasive mucinous adenocarcinoma patients undergoing curative-intent lung surgery","authors":"Dong Woog Yoon , Soohyun Hwang , Boram Lee , Yeong Jeong Jeon , Junghee Lee , Dong Wook Shin , Byeong-Ho Jeong , Seong Yong Park , Hong Kwan Kim , Yong Soo Choi , Jong Ho Cho","doi":"10.1016/j.ctarc.2025.101014","DOIUrl":"10.1016/j.ctarc.2025.101014","url":null,"abstract":"<div><h3>Background</h3><div>Invasive mucinous adenocarcinoma (IMA) is genetically distinct from non-mucinous adenocarcinoma, commonly characterized by <em>KRAS</em> mutations. However, studies exploring molecular co-alterations alongside <em>KRAS</em> mutations in IMA remain limited.</div></div><div><h3>Methods</h3><div>We reviewed 84 patients with surgically resected IMAs from 2015 to 2023 who underwent NGS using TruSight™ Oncology 500 or CancerSCAN assays. Overall survival (OS) and disease-free survival (DFS) were assessed using Cox regression, and log-rank tests were used to evaluate the prognostic role of each molecular alteration.</div></div><div><h3>Results</h3><div>Among the 84 patients, driver alterations were identified in <em>KRAS</em> (67.9 %, <em>n</em> = 57), <em>ERBB2</em> (10.7 %, <em>n</em> = 9), and <em>NRG-1</em> (7.1 %, <em>n</em> = 6), while concurrent mutations were found in <em>TP53</em> (31 %, <em>n</em> = 26), <em>NKX2–1</em> (23.8 %, <em>n</em> = 20), <em>CDKN2A</em> (15.5 %, <em>n</em> = 13), and <em>PIK3CA</em> (10.7 %, <em>n</em> = 9). Among the overall cohort, survival analysis demonstrated that <em>TP53</em> alterations were associated with worse OS (<em>p</em> = 0.03), while <em>NKX2–1</em> alterations were linked to better DFS (<em>p</em> = 0.03). In the <em>KRAS</em>-mutant subgroup, <em>TP53</em> alterations were associated with worse OS (<em>p</em> < 0.01) and DFS (<em>p</em> < 0.01), while <em>NKX2–1</em> mutations were associated with better OS (<em>p</em> = 0.05). Multivariate analysis identified <em>TP53</em> alterations as independent prognostic factors for OS (HR,11.32; 95 % CI,2.18–58.75) and DFS (HR,4.33; 95 % CI,1.84–10.2) in patients with <em>KRAS</em> mutations.</div></div><div><h3>Conclusion</h3><div>Concurrent <em>TP53</em> mutations have significant prognostic implications in <em>KRAS</em>-mutant IMAs. This finding underscores the potential role of <em>TP53</em> mutations in guiding personalized treatment approaches to improve patient outcomes.</div></div><div><h3>Micro abstract</h3><div>In a retrospective cohort of 84 resected pulmonary invasive mucinous adenocarcinomas, next-generation sequencing was performed and genomic alterations were correlated with prognosis. KRAS was the predominant driver (∼68 %), and concurrent TP53 mutations (∼32 %) independently predicted worse overall and disease-free survival within KRAS-mutant IMA. TP53 co-mutation serves as a practical risk stratifier to inform closer post-surgical surveillance and potential adjuvant strategies.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"45 ","pages":"Article 101014"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145306902","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}
Pub Date : 2025-01-01DOI: 10.1016/j.ctarc.2025.100967
Xiongbing Lu , Ke Chen , Jiaqi Mei , Hua Hao , Yihe Li , Linxing Duan , Yun Yi , Yuanqiao He
Objective
To develop a patient-derived xenograft model (PDX) of Scrotal Paget's disease (SPD), providing an experimental tool for the screening of therapeutic drugs and the development of new drugs for SPD treatment.
Methods
SPD tumor tissues were implanted into the subcutaneous area of the right scapula in male NOD-Scid mice to establish a PDX model. PDX tissues were characterized using H&E staining, immunohistochemistry, and PCR. Cisplatin chemotherapy's antitumor effects were assessed through ex vivo histoculture drug sensitivity test (HDST) with patient tumor tissues and in vivo experiments with the PDX model.
Results
The patient-derived SPD tissues were tumorigenic in male NOD-Scid mice and remained stable upon serial passage. H&E staining confirmed the preservation of morphological features from the patient's tumor tissues. Immunohistochemistry showed protein expression patterns consistent with clinical presentation. PCR ruled out spontaneous murine lymphoma. HDST experiments indicated cisplatin sensitivity in the patient's tumor tissues. In vivo experiments demonstrated significant tumor growth inhibition in SPD PDX mice with cisplatin, without affecting mouse body weight.
Conclusion
A SPD PDX model was successfully established, the PDX tumors maintained the characteristics of the patient’s original tumors.
{"title":"Establishment and characterization of patient-derived xenograft of scrotal Paget's disease","authors":"Xiongbing Lu , Ke Chen , Jiaqi Mei , Hua Hao , Yihe Li , Linxing Duan , Yun Yi , Yuanqiao He","doi":"10.1016/j.ctarc.2025.100967","DOIUrl":"10.1016/j.ctarc.2025.100967","url":null,"abstract":"<div><h3>Objective</h3><div>To develop a patient-derived xenograft model (PDX) of Scrotal Paget's disease (SPD), providing an experimental tool for the screening of therapeutic drugs and the development of new drugs for SPD treatment.</div></div><div><h3>Methods</h3><div>SPD tumor tissues were implanted into the subcutaneous area of the right scapula in male NOD-Scid mice to establish a PDX model. PDX tissues were characterized using H&E staining, immunohistochemistry, and PCR. Cisplatin chemotherapy's antitumor effects were assessed through ex vivo histoculture drug sensitivity test (HDST) with patient tumor tissues and in vivo experiments with the PDX model.</div></div><div><h3>Results</h3><div>The patient-derived SPD tissues were tumorigenic in male NOD-Scid mice and remained stable upon serial passage. H&E staining confirmed the preservation of morphological features from the patient's tumor tissues. Immunohistochemistry showed protein expression patterns consistent with clinical presentation. PCR ruled out spontaneous murine lymphoma. HDST experiments indicated cisplatin sensitivity in the patient's tumor tissues. In vivo experiments demonstrated significant tumor growth inhibition in SPD PDX mice with cisplatin, without affecting mouse body weight.</div></div><div><h3>Conclusion</h3><div>A SPD PDX model was successfully established, the PDX tumors maintained the characteristics of the patient’s original tumors.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"45 ","pages":"Article 100967"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144920317","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}
Plasma-based testing with circulating cell-free DNA (cfDNA) is an active area of biomarker exploratory studies in patients with non-small cell lung cancer (NSCLC) harboring EGFR mutations. The Exosome-focused Translational Research for Afatinib study prospectively explored novel plasma biomarkers for afatinib monotherapy in patients with NSCLC harboring EGFR mutations using genomics, proteomics, epigenomics, and metabolomics. Herein, we present the results of the genomics part.
Materials and Methods
Clinical data of afatinib were matched with next generation sequencing (NGS)-based genomics data of cfDNA (n = 101) and extracellular vesicle DNA (evDNA) (n = 99) from pretreatment plasma samples.
Results
The detection sensitivity of cfDNA and evDNA mutations was 86 % (87/101) and 37 % (37/99), respectively. When cfDNA mutations were classified into tissue-matched (any EGFR mutations consistent with those identified in tissue) (n = 28), tissue-unmatched (n = 59), and mutation-undetected (n = 14) groups, cfDNA mutation status was a predictor of progression-free survival (PFS) (p < 0.01) and overall survival (OS) (p < 0.01). EvDNA mutation status was a predictor of OS (p < 0.01) rather than PFS (p = 0.48). When the tissue-unmatched cfDNA group was subclassified into EGFR-related (n = 49) and EGFR-unrelated (n = 10) groups, the EGFR-unrelated group had a median PFS and 3-year OS rate of 31.2 months and 80.0 %, respectively. EGFR-unrelated and mutation-undetected cfDNA groups (n = 24) exhibited a median PFS and 3-year OS rate of >30 months and >80 %, respectively, with afatinib monotherapy.
Conclusion
This is the first large-scale prospective study of NGS-based concurrent testing for plasma cfDNA and evDNA mutations. The findings suggest that cfDNA mutation status is a promising plasma biomarker for afatinib monotherapy.
{"title":"Plasma biomarkers for afatinib monotherapy in EGFR-mutated non-small cell lung cancer: Novel insights from companion genomics analysis of the EXTRA study","authors":"Tomonori Makiguchi , Hisashi Tanaka , Kei Morikawa , Aya Hirata , Hidetoshi Itani , Shigeru Tanzawa , Kageaki Watanabe , Hiroyuki Yasuda , Kazuya Horiuchi , Hideyuki Nakagawa , Yoshitaka Seki , Yoshiro Nakahara , Kentaro Hayashi , Nobumasa Takahashi , Takeo Endo , Akihiro Bessho , Tetsuya Okano , Kiyoshi Takeyama , Akikazu Kawase , Makoto Endo , Nobuhiko Seki","doi":"10.1016/j.ctarc.2025.100952","DOIUrl":"10.1016/j.ctarc.2025.100952","url":null,"abstract":"<div><h3>Objectives</h3><div>Plasma-based testing with circulating cell-free DNA (cfDNA) is an active area of biomarker exploratory studies in patients with non-small cell lung cancer (NSCLC) harboring <em>EGFR</em> mutations. The Exosome-focused Translational Research for Afatinib study prospectively explored novel plasma biomarkers for afatinib monotherapy in patients with NSCLC harboring <em>EGFR</em> mutations using genomics, proteomics, epigenomics, and metabolomics. Herein, we present the results of the genomics part.</div></div><div><h3>Materials and Methods</h3><div>Clinical data of afatinib were matched with next generation sequencing (NGS)-based genomics data of cfDNA (<em>n</em> = 101) and extracellular vesicle DNA (evDNA) (<em>n</em> = 99) from pretreatment plasma samples.</div></div><div><h3>Results</h3><div>The detection sensitivity of cfDNA and evDNA mutations was 86 % (87/101) and 37 % (37/99), respectively. When cfDNA mutations were classified into tissue-matched (any <em>EGFR</em> mutations consistent with those identified in tissue) (<em>n</em> = 28), tissue-unmatched (<em>n</em> = 59), and mutation-undetected (<em>n</em> = 14) groups, cfDNA mutation status was a predictor of progression-free survival (PFS) (<em>p</em> < 0.01) and overall survival (OS) (<em>p</em> < 0.01). EvDNA mutation status was a predictor of OS (<em>p</em> < 0.01) rather than PFS (<em>p</em> = 0.48). When the tissue-unmatched cfDNA group was subclassified into <em>EGFR</em>-related (<em>n</em> = 49) and <em>EGFR</em>-unrelated (<em>n</em> = 10) groups, the <em>EGFR</em>-unrelated group had a median PFS and 3-year OS rate of 31.2 months and 80.0 %, respectively. <em>EGFR</em>-unrelated and mutation-undetected cfDNA groups (<em>n</em> = 24) exhibited a median PFS and 3-year OS rate of >30 months and >80 %, respectively, with afatinib monotherapy.</div></div><div><h3>Conclusion</h3><div>This is the first large-scale prospective study of NGS-based concurrent testing for plasma cfDNA and evDNA mutations. The findings suggest that cfDNA mutation status is a promising plasma biomarker for afatinib monotherapy.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"44 ","pages":"Article 100952"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144203122","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}
Pub Date : 2025-01-01DOI: 10.1016/j.ctarc.2025.100948
Mihaela T Dimitrova , Celine Tabche
Background
Breast cancer ranks as one of the most common cancer types in the world, and in Bulgaria, it represents a quarter of all malignant diagnoses in women. Breast cancer screening in Bulgaria is the lowest among all European Union (EU) countries. Existing literature on breast cancer care in Bulgaria is scarce. This study aims to explore the current trends, patterns, and gaps in breast cancer care in Bulgaria.
Methods
This study is a scoping review from peer-reviewed databases and grey literature. The results were screened against the SPIDER methodology's inclusion and exclusion criteria. Covidence was used in screening and full-text review. The study included 39 sources.
Results
Breast cancer is the leading cause of cancer mortality in Bulgaria and the incidence remains lower than the European average due to underreporting. Bulgaria lacks a structured breast cancer screening programme, leading to low service use, although essential prophylactic exams are covered by the National Health Insurance Fund. Barriers like the underuse of treatment and significant delays in reimbursement of new cancer therapies exist. with lower survival rates compared to the rest of the EU. While policies focus on increasing screening and improving prevention, practical steps towards achieving this have not yet been taken.
Conclusion
There is low screening and underreporting of breast cancer rates in Bulgaria. The lack of full reimbursement of diagnostic methods, limited adoption of the multidisciplinary approach, and complex market access processes are barriers to developing efficient treatment plans. Efficient screening and prevention are crucial for positive outcomes.
{"title":"Mapping the landscape of breast cancer care in Bulgaria: a scoping review","authors":"Mihaela T Dimitrova , Celine Tabche","doi":"10.1016/j.ctarc.2025.100948","DOIUrl":"10.1016/j.ctarc.2025.100948","url":null,"abstract":"<div><h3>Background</h3><div>Breast cancer ranks as one of the most common cancer types in the world, and in Bulgaria, it represents a quarter of all malignant diagnoses in women. Breast cancer screening in Bulgaria is the lowest among all European Union (EU) countries. Existing literature on breast cancer care in Bulgaria is scarce. This study aims to explore the current trends, patterns, and gaps in breast cancer care in Bulgaria.</div></div><div><h3>Methods</h3><div>This study is a scoping review from peer-reviewed databases and grey literature. The results were screened against the SPIDER methodology's inclusion and exclusion criteria. Covidence was used in screening and full-text review. The study included 39 sources.</div></div><div><h3>Results</h3><div>Breast cancer is the leading cause of cancer mortality in Bulgaria and the incidence remains lower than the European average due to underreporting. Bulgaria lacks a structured breast cancer screening programme, leading to low service use, although essential prophylactic exams are covered by the National Health Insurance Fund. Barriers like the underuse of treatment and significant delays in reimbursement of new cancer therapies exist. with lower survival rates compared to the rest of the EU. While policies focus on increasing screening and improving prevention, practical steps towards achieving this have not yet been taken.</div></div><div><h3>Conclusion</h3><div>There is low screening and underreporting of breast cancer rates in Bulgaria. The lack of full reimbursement of diagnostic methods, limited adoption of the multidisciplinary approach, and complex market access processes are barriers to developing efficient treatment plans. Efficient screening and prevention are crucial for positive outcomes.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"44 ","pages":"Article 100948"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144263807","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}
Thyroid transcription factor-1 (TTF-1) is expressed in the thyroid gland, lungs, and brain, and has also been reported in thymomas. While some studies have suggested TTF-1 as a specific marker for type AB thymoma, others have noted significant variability, often due to small case numbers. In this study, TTF-1 expression was evaluated in 50 cases of type A and AB thymomas using three distinct clones (8G7G3/1, SPT24, and SP141), and quantified with a four-grade scale. Additionally, CD20 expression and GTF2I mutation status were analyzed.
TTF-1 expression analyses with the SPT24 and SP141 clones yielded a score of 3 (defined as positivity in >50 % of cells) in 20 % and 18 % of thymomas, respectively. In contrast, the 8G7G3/1 clone showed a score of 0 (positivity in <1 % of cells) across all tumors. There were no differences in score 3 positivity between type A and type AB thymomas for either the SPT24 or SP141 clones. Additionally, no statistically significant associations were identified between clinicopathological characteristics or GTF2I mutations and score 3 versus score ≤2 cases for both clones. Tumors with a CD20 score of 3 demonstrated a tendency towards higher SPT24 or SP141 expression. Different expressions by TTF-1 clone may be diagnostic challenges in type A/AB thymomas, and pathologists should be aware of aberrant TTF-1 expression using SPT24 and SP141 clone in thymomas.
{"title":"Immunohistochemical analysis of thyroid transcription factor-1 in type A and AB thymomas comparing multiple primary antibody clones","authors":"Ayaka Mitsui , Jumpei Kashima , Satsuki Kishikawa , Shun-ichi Watanabe , Yasushi Goto , Yasushi Yatabe","doi":"10.1016/j.ctarc.2025.101045","DOIUrl":"10.1016/j.ctarc.2025.101045","url":null,"abstract":"<div><div>Thyroid transcription factor-1 (TTF-1) is expressed in the thyroid gland, lungs, and brain, and has also been reported in thymomas. While some studies have suggested TTF-1 as a specific marker for type AB thymoma, others have noted significant variability, often due to small case numbers. In this study, TTF-1 expression was evaluated in 50 cases of type A and AB thymomas using three distinct clones (8G7G3/1, SPT24, and SP141), and quantified with a four-grade scale. Additionally, CD20 expression and <em>GTF2I</em> mutation status were analyzed.</div><div>TTF-1 expression analyses with the SPT24 and SP141 clones yielded a score of 3 (defined as positivity in >50 % of cells) in 20 % and 18 % of thymomas, respectively. In contrast, the 8G7G3/1 clone showed a score of 0 (positivity in <1 % of cells) across all tumors. There were no differences in score 3 positivity between type A and type AB thymomas for either the SPT24 or SP141 <em>clon</em>es. Additionally, no statistically significant associations were identified between clinicopathological characteristics or <em>GTF2I</em> mutations and score 3 versus score ≤2 cases for both clones. Tumors with a CD20 score of 3 demonstrated a tendency towards higher SPT24 or SP141 expression. Different expressions by TTF-1 clone may be diagnostic challenges in type A/AB thymomas, and pathologists should be aware of aberrant TTF-1 expression using SPT24 and SP141 clone in thymomas.</div></div>","PeriodicalId":9507,"journal":{"name":"Cancer treatment and research communications","volume":"45 ","pages":"Article 101045"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145614396","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}
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