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  • American Association for Cancer Research (AACR)  (7)
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  • American Association for Cancer Research (AACR)  (7)
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  • 1
    Online-Ressource
    Online-Ressource
    Abstract 38: Large-scale study of NTRK fusions in Chinese solid tumors and using next generation sequencing: A multicenter study
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 16_Supplement ( 2020-08-15), p. 38-38
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 16_Supplement ( 2020-08-15), p. 38-38
    Kurzfassung: Background: NTRK gene fusions involving either NTRK1, NTRK2 or NTRK3 are oncogenic drivers of various solid tumor types but generally at a low frequency. TRK inhibitors such as LOXO-101, entrectinib, X396, AB-106, TL118 had remarkable and durable antitumor activities in patients (pts) with TRK fusion-positive cancers, regardless of age or tumor type. We assessed the frequency of NTRK fusions across 14, 491 advanced cancers to reveal the landscape in a wide variety of subtypes. Methods: A multicenter study in China was initiated from July 2013, and advanced cancer patients have been enrolled as of September 2018. We analyzed data from 14, 491 clinical advanced cancer cases, each of which had results from next-generation sequencing (NGS)-based 381 genes panel assay, analogous to the index patient. Results: Of this entire cohort [6837 lung cancer (47.18%), 1894 breast cancer (13.07%), 1325 colorectal cancer (9.14%), 312 soft tissue sarcoma (2.15%), 260 head and neck cancer (1.79%) and 1804 others (12.45%)], 40 patients were identified with NTRK fusions, including TPM3-NTRK1, LMNA-NTRK1, IRF2BP2-NTRK1, TPR-NTRK1, SQSTM1-NTRK1, C1orf111-NTRK1, NTRK1-CUL3, LIPI-NTRK1, NTRK1-C1orf61, TARDBP-NTRK1, LOC643387-NTRK1, NFASC-NTRK1, RFWD2-NTRK1, MSN-NTRK2, ATL2-NTRK2, AGTPBP1-NTRK2, ZCCHC7-NTRK2, CALR-NTRK2, ESRP1-NTRK2, ETV6-NTRK3. NTRK fusions were seen in 0.26% (18/6837) of lung cancer [C1orf111-NTRK1+TPM3-NTRK1(1), TPR-NTRK1(1), TPM3-NTRK1(2), SQSTM1-NTRK1+NTRK1-CUL3(1), LIPI-NTRK1(1), NTRK1-C1orf61(1), LMNA-NTRK1(1), MSN-NTRK2(1), TARDBP-NTRK1+LOC643387-NTRK1(1), IRF2BP2-NTRK1(1), ATL2-NTRK2 (1), NFASC-NTRK1(1), AGTPBP1-NTRK2(1), RFWD2-NTRK1(1), ZCCHC7-NTRK2(1), CALR-NTRK2(1) and ESRP1-NTRK2] ; 0.21%(4/1894) of breast cancer [ETV6-NTRK3(4)]; 0.37%(5/1325) of colorectal cancer [TPM3-NTRK1(1), ETV6-NTRK3(4)] ; 3.53%(11/312) of soft tissue sarcoma [LMNA-NTRK1(3), TPM3-NTRK1(1), ETV6-NTRK3(7)]; 0.38%(1/260) of head and neck cancer [ETV6-NTRK3(1)] and 0.05%(1/1804) of others [ETV6-NTRK3(1)]. Conclusion: NTRK fusions are a rare molecular subtype in Chinese solid tumors. The NTRK gene fusions more commonly occurred in NSCLC (0.3%), CRC (0.4%) and BC (0.2%), and may occur without other targetable alterations such as EGFR, ALK, ROS1. The clinical evidence for responsiveness of NTRK fusions driven solid tumors provides an opportunity to personalize treatments and improve clinical outcomes for patients (pts). Citation Format: Wen-xian Wang, Chun-wei Xu, Lei Lei, Xiao-jia Wang, You-cai Zhu, Yong Fang, Xiu-yu Cai, Rong-bo Lin, Li Lin, Hong Wang, Mei-yu Fang, Yin-bin Zhang, Shi-jie Lan, Xin Cai, Xin Liu, Xing-xiang Pu, Zong-yang Yu, Bing Wan, Jin-luan Li, Xian-bin Liang, Li-ping Wang, Wu Zhuang, Zi-yan Yang, Gang Chen, Tang-feng Lv, Yong Song. Large-scale study of NTRK fusions in Chinese solid tumors and using next generation sequencing: A multicenter study [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 38.
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2020-38
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2020
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 2
    Online-Ressource
    Online-Ressource
    Abstract 1597: Real-world large-scale study kinase domain duplications across diverse tumor types in Chinese populations
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Research Vol. 79, No. 13_Supplement ( 2019-07-01), p. 1597-1597
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 13_Supplement ( 2019-07-01), p. 1597-1597
    Kurzfassung: Background: Recently, kinase domain duplications (KDD) in BRAF, EGFR, MET and FGFR1 were reported, along with responses to tyrosine kinase inhibitors (TKI). However, its frequency and clinical outcomes in advanced cancer patients are larglely uncertain. We assessed the frequency of KDD across 14, 491 advanced cancers to reveal the landscape in a wide variety of subtypes. Methods: A multicenter study in China was initiated from July 2013, and advanced cancer patients have been enrolled as of September 2018. We analyzed data from 14, 491 clinical advanced cancer cases, each of which had results from next-generation sequencing (NGS)-based 381 genes panel assay, analogous to the index patient. Results: Of this entire cohort [6837 lung cancer (47.18%), 1894 breast cancer (13.07%), 1325 colorectal cancer (9.14%), 710 urinary system tumor (4.90%), 536 gynecological tumor (3.70%), 592 hepatobiliary cancer (4.09%), 221 gastric cancer (1.53%), 312 soft tissue sarcoma (2.15%), 260 head and neck cancer (1.79%) and 1804 others (12.45%)], 71 patients were identified with KDD, including EGFR (16), BRAF (12), MET (11), FGFR3 (8), RET (3), PDGFRA (3), ROS1 (3), FGFR1 (2), ERBB2 (2), SOX17 (2), ALK (2), KIT (1), NTRK1 (1), BAP1 (1), TMPRSS2 (1), ERBB4 (1), VHL (1), NTRK3 (1). KDD were seen in 0.39% (27/6837) of lung cancer [EGFR(9), BRAF (2), MET (6), FGFR3 (2), RET (1), PDGFRA (1), ROS1 (2), ERBB2 (1), ALK (1), NTRK1 (1), and ERBB4 (1)] ; 0.21%(4/1894) of breast cancer [BRAF (1), FGFR3 (2), FGFR1 (1)]; 0.60%(8/1325) of colorectal cancer [EGFR (1), BRAF (3), FGFR3 (2), RET (1), ROS1 (1)] ; 0.28%(2/710) of urinary system tumor [TMPRSS2(1), VHL (1)]; 0.19%(1/536) of gynecological tumor [SOX17 (1)] ; 0.17%(1/592) of hepatobiliary cancer [EGFR (1)]; 0.45%(1/221) of gastric cancer [ERBB2 (1)] ; 0.96%(3/312) of soft tissue sarcoma [EGFR (1), FGFR3 (1), PDGFRA (1)]; 0.77%(2/260) of head and neck cancer [BRAF (2)] ; and 1.22%(22/1804) of others [EGFR (4), BRAF (4), MET (5), FGFR3 (1), RET (1), PDGFRA (1), FGFR1 (1), SOX17 (1), ALK (1), KIT (1), BAP1 (1), and NTRK3 (1)]; KDD possibly related to target resistance were seen in ERBB2 amplification gastric cancer and ALK-related NSCLC. Conclusion: Diverse KDD are found across diverse tumor types and may underlie acquired resistance, and can benefit from matched targeted treatment. In addition, for short- or long-term responses to targeted treatment, we can use the NGS assay to explore differential gene alter in the future. Citation Format: Chun-wei Xu, Wen-xian Wang, Xiao-jia Wang, You-cai Zhu, Qu-xia Zhang, Yong Fang, Xiu-yu Cai, Yu Chen, Li Lin, Hong Wang, Mei-yu Fang, Yin-bin Zhang, Shi-jie Lan, Xin Liu, Xing-xiang Pu, Zong-yang Yu, Bing Wan, Jian-ying Li, Xian-bin Liang, Li-ping Wang, Wu Zhuang, Ling Lin, Gang Chen, Tang-feng Lv, Yong Song. Real-world large-scale study kinase domain duplications across diverse tumor types in Chinese populations [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1597.
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2019-1597
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2019
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 3
    Online-Ressource
    Online-Ressource
    Replication and Functional Genomic Analyses of the Breast Cancer Susceptibility Locus at 6q25.1 Generalize Its Importance in Women of Chinese, Japanese, and European Ancestry
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 4 ( 2011-02-15), p. 1344-1355
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 4 ( 2011-02-15), p. 1344-1355
    Kurzfassung: We evaluated the generalizability of a single nucleotide polymorphism (SNP), rs2046210 (A/G allele), associated with breast cancer risk that was initially identified at 6q25.1 in a genome-wide association study conducted among Chinese women. In a pooled analysis of more than 31,000 women of East-Asian, European, and African ancestry, we found a positive association for rs2046210 and breast cancer risk in Chinese women [ORs (95% CI) = 1.30 (1.22–1.38) and 1.64 (1.50–1.80) for the AG and AA genotypes, respectively, P for trend = 1.54 × 10−30], Japanese women [ORs (95% CI) = 1.31 (1.13–1.52) and 1.37 (1.06–1.76), P for trend = 2.51 × 10−4] , and European-ancestry American women [ORs (95% CI) = 1.07 (0.99–1.16) and 1.18 (1.04–1.34), P for trend = 0.0069]. No association with this SNP, however, was observed in African American women [ORs (95% CI) = 0.81 (0.63–1.06) and 0.85 (0.65–1.11) for the AG and AA genotypes, respectively, P for trend = 0.4027] . In vitro functional genomic studies identified a putative functional variant, rs6913578. This SNP is 1,440 bp downstream of rs2046210 and is in high linkage disequilibrium with rs2046210 in Chinese (r2 = 0.91) and European-ancestry (r2 = 0.83) populations, but not in Africans (r2 = 0.57). SNP rs6913578 was found to be associated with breast cancer risk in Chinese and European-ancestry American women. After adjusting for rs2046210, the association of rs6913578 with breast cancer risk in African Americans approached borderline significance. Results from this large consortium study confirmed the association of rs2046210 with breast cancer risk among women of Chinese, Japanese, and European ancestry. This association may be explained in part by a putatively functional variant (rs6913578) identified in the region. Cancer Res; 71(4); 1344–55. ©2011 AACR.
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-10-2733
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2011
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 4
    Online-Ressource
    Online-Ressource
    Abstract 3369: Mosaic chromosome X copy-number aberrations in leukocytes of never-smoking lung cancer patients: The Female Lung Cancer Consortium in Asia (FLCCA)
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Research Vol. 78, No. 13_Supplement ( 2018-07-01), p. 3369-3369
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 3369-3369
    Kurzfassung: Lung cancer (LC) is a global health burden that accounted for 1.69 million deaths worldwide in 2015. Asian women have high incidence rates of LC, with about half of all diagnoses occurring among never-smokers. Chromosomal copy-number (CN) aberrations can arise de novo in somatic cells with progressing age. These genomic alterations can change the dosage of critical genes and impact biological processes. Gains and losses of Chromosome X in a proportion of cells (ChrX mosaicism) are markers of genomic instability; however, their relationship with LC is unclear. We characterized leukocyte ChrX mosaicism among never-smoking Asian female LC patients and cancer-free controls. We investigated 5,137 LC cases (4,477 adenocarcinomas (AC) and 660 squamous cell carcinomas (SCC)) and 4,535 controls from 13 case-control studies and one cohort study in the Female Lung Cancer Consortium in Asia. Subjects were aged 19-91 years from China, Singapore, Taiwan, South Korea, and Japan. In case-control studies, blood was drawn after diagnosis and mostly before treatment. Leukocyte DNA was genotyped on Illumina 660W arrays, with a small subset on 610Q and 370K arrays. ChrX mosaicism was detected using normalized log R ratio (LRR) and B allele frequency (BAF) values from probes covering ChrX. ChrX was segmented for mosaic events (gains, losses, and copy-neutral) using circular binary segmentation on BAF values. Segments & lt;2 Mb were excluded. Event CN state was assigned based on LRR values. LRR deviations of 0.01 and −0.01 were used to classify events as gain and losses, respectively, for ChrX-spanning mosaic events; while thresholds of 0.05 and −0.05 were used for those spanning a portion of ChrX. Mosaic proportions were estimated using deviation from the expected BAF given the LRR-defined CN state. Fisher's Exact tests on 2x3 and 2x2 tables were used to compare ChrX mosaic events between LC cases and controls. Exact logistic regression was used to assess associations between combined gain and loss events and AC. We found 18 detectable mosaic ChrX events (0.19%) in 12 women. LC cases had 5 gains, 3 losses, and 4 copy-neutral mosaic events; while controls had no gains, 1 loss, and 5 copy-neutral events (p=9.8E-2). AC patients had significantly more combined gains and losses (n=7) and fewer copy-neutral events (n=0) compared to controls who had 1 combined gain and loss and 5 copy-neutral events (p=4.7E-3). Notably, all 5 gains were among AC and none among controls (p=3.5E-3). Women with combined gain and loss events had 7 times the odds of AC compared to those without them (p=3.8E-2). Our preliminary findings suggest a possible role of leukocyte ChrX mosaicism, particularly CN gains, in the biological mechanism of LC development. However, given the rarity of these events and possible disease-effect, larger studies are needed to further evaluate ChrX mosaicism as a risk factor for future occurrence of LC. Citation Format: Jason Y. Wong, Mitchell Machiela, Weiyin Zhou, Wei Jie Seow, Bryan Bassig, Jinming Zhang, Meredith Yeager, Wei Zheng, Xiao-Ou Shu, Hongbing Shen, Keitaro Matsuo, Chao Agnes Hsiung, Maria P. Wong, Yun-Chul Hong, Jiu-cun Wang, Yi-Long Wu, Baosen Zhou, Robert Klein, Zhihua Yin, Tangchun Wu, Pan-Chyr Yang, Yong-Bing Xiang, Adeline Seow, Yu-Tang Gao, Chen Wu, Jianjun Liu, Zhibin Hu, Laurie Burdett, Qiuyin Cai, Juncheng Dai, Dongxin Lin, Kexin Chen, Stephen Chanock, Nathaniel Rothman, Qing Lan. Mosaic chromosome X copy-number aberrations in leukocytes of never-smoking lung cancer patients: The Female Lung Cancer Consortium in Asia (FLCCA) [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 3369.
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2018-3369
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2018
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 5
    Online-Ressource
    Online-Ressource
    Abstract 2682: Analysis of polygenic risk score interaction with coal use and risk of lung adenocarcinoma among never-smoking women in Asia
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Research Vol. 79, No. 13_Supplement ( 2019-07-01), p. 2682-2682
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 13_Supplement ( 2019-07-01), p. 2682-2682
    Kurzfassung: Background: Accounting for approximately 1.76 million annual deaths worldwide, lung cancer is a significant global health burden. While smoking is the most common cause of lung cancer, up to 25% of all lung cancer patients worldwide are never smokers. Lung cancer is the leading cause of cancer mortality in China, where most women do not smoke, making women in Asia an ideal population to study. Previously conducted genome-wide association studies (GWAS) of lung cancer risk among never-smoking women in Asia identified 10 lung cancer susceptibility loci. Indoor air pollution from coal burned for home cooking and heating is known to contain lung carcinogens and has been found to be causally associated with lung cancer. In the current analysis, we evaluated gene-environment interaction between a polygenic risk score (PRS) and coal use in relation to lung adenocarcinoma. Methods: Three studies (Taiwan, Shanghai, Shenyang) from the Female Lung Cancer Consortium in Asia (FLCCA) were used for the primary analysis (1,419 cases; 1,446 controls). A replication study was conducted using samples from Xuanwei, China (159 cases; 572 controls), where lung cancer rates for never-smokers are among the highest in the world and attributed to widespread coal use. We calculated a PRS as the weighted sum of the risk allele counts across the 10 loci, and modeled PRS as a continuous variable scaled by the standard deviation in controls. Logistic regression was used to estimate the main effects of the PRS and coal use, and a likelihood ratio test was used to evaluate the interaction. Models were adjusted for age ( & lt;40, 40-49, 50-59, 60-69, ≥70 years), study, and significant eigenvectors. Results: Coal use was associated with an increased risk of lung adenocarcinoma (OR=1.31, 95% CI: 1.01-1.68). We observed an exposure-response relationship between PRS and lung adenocarcinoma (p-trend= 2x10-16) and found a significant multiplicative interaction between PRS and coal use (p-interaction= 0.005). The association between PRS and lung adenocarcinoma was significantly higher among the never coal users (OR=1.68, 95% CI: 1.52-1.86) compared to ever coal users in the three studies (OR=1.24, 95% CI: 1.03-1.50) (p-interaction=0.005), as well as between never coal users in the three studies and ever coal users in Xuanwei (OR=1.25, 95% CI: 1.04-1.49) (p-interaction=0.004). Conclusion: We observed an antagonistic interaction between PRS and coal use with lung adenocarcinoma, where the genetic effect was attenuated among those exposed to coal combustion in the home. We replicated the finding in Xuanwei. These results suggest that the pathogenesis of lung cancer among never-smoking women in Asia differs by exposure to coal combustion emissions and provides one of the few examples of sub-multiplicative gene-environment interactions in the cancer literature. Citation Format: Batel Blechter, Chao Agnes Hsiung, Zhihua Yin, Xiao-Ou Shu, H. Dean Hosgood, Jason Y.Y Wong, Jianxin Shi, Wei Hu, Bryan Bassig, Wei Jie Seow, Yu -ang Gao, Qiuyin Cai, Yong-Bing Xiang, I-Shou Chang, Baosen Zhou, Wei Zheng, Kyoung-Mu Lee, Stephen Chanock, Nilanjan Chatterjee, Nathaniel Rothman, Qing Lan. Analysis of polygenic risk score interaction with coal use and risk of lung adenocarcinoma among never-smoking women in Asia [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 2682.
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2019-2682
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2019
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 6
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    Online-Ressource
    Abstract LB-46: C/EBPα acts as tumor suppressor in lung cancer by inhibiting the proto-oncogene Bmi-1.
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. LB-46-LB-46
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. LB-46-LB-46
    Kurzfassung: C/EBPα gene expression is frequently lost in non-small cell lung cancer, suggesting it acts as a tumor suppressor. Here, we generated an inducible lung-specific mouse model of C/EBPα deletion (C/EBPαLung-Δ mice) that develops lung adenocarcinomas. We observed that C/EBPα excision results in upregulation of Bmi-1, and that tumor initiation strictly depends on Bmi-1 gene dosage, as C/EBPαLung-Δ mice carrying only one functional Bmi-1 allele escape tumorigenesis. Accordingly, C/EBPα negative human adenocarcinomas show elevated Bmi-1 expression, in line with our observation that C/EBPα acts as tumor suppressor in lung cells by directly inhibiting Bmi-1 transcription. Furthermore, pharmacological inhibition of Bmi-1 impairs the ability of C/EBPα null adenocarcinoma cells to form tumors in xenografts. Overall, we have identified Bmi-1 as a critical therapeutic target in those patients carrying abnormal C/EBPα function. Citation Format: Elena Levantini, Daniela S. Basseres, Wen Cai Zhang, Robert S. Welner, Meritxell Alberich-Jorda’, Kol Jia Yong, Bhavin M. Thakkar, Junyan Zhang, Chiara Battelli, Christopher J. Hetherington, Min Ye, Karen O'Brien, Maria Cristina Magli, Marie Loh, Min En Nga, Yin Huei Pang, Alain C. Borczuk, Lyuba Varticovski, Olivier Kocher, Pu Zhang, Ross A. Soo, Bing Lim, Balazs Halmos, Daniel G. Tenen. C/EBPα acts as tumor suppressor in lung cancer by inhibiting the proto-oncogene Bmi-1. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr LB-46. doi:10.1158/1538-7445.AM2013-LB-46
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2013-LB-46
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2013
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 7
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    Abstract P1-17-04: Hormone therapy (HT) brings more survival benefits than capecitabine (CAP) as maintenance therapy following the 1st-line chemotherapy in HR+/HER2-ABC/MBC: Update primary endpoint of OVERSTEP(ZJCHBC001)
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Research Vol. 82, No. 4_Supplement ( 2022-02-15), p. P1-17-04-P1-17-04
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 82, No. 4_Supplement ( 2022-02-15), p. P1-17-04-P1-17-04
    Kurzfassung: Background: OVERSTEP is a multicenter, randomized clinical trial of capecitabine (CAP) versus endocrine therapy (HT) as maintenance therapy after 1st-line CAP-based combination chemotherapy in HR+/HER2- ABC/MBC. At 2020 SABCS conference, we have reported the primary endpoint (progression-free survival, PFS) of the OVERSTEP (NCT02597868) trial. With a median follow-up of 24.3 months,Median PFS (mPFS) of HT cohort was significantly longer than that of CAP group (17.5 months vs. 12.2 months, HR=0.625, 95%CI: 0.429-0.909, P=0.013). In this annual meeting, we will report the update of mPFS and the secondary endpoint (overall survival, OS). Methods: HR+ and HER2- metastatic breast cancer were enrolled in this study. All patients were histologically confirmed and received at least 4 cycles of CAP-based combination regimen as 1st-line salvage chemotherapy. The patients who achieved CR, PR or durable SD by RECIST criteria entered into the maintenance therapy setting (MT), and randomly (1:1 ratio) assigned to either CAP single or HT group. Randomization was done centrally with stratification by endocrine sensitive or resistance and visceral or non-visceral metastasis. The primary endpoint was mPFS, and the secondary endpoint was overall survival (OS), safety, et al. The superiority test was performed in all patients who received at least one dose maintenance therapy. The last follow-up ended in June 30, 2021. The medium follow-up duration was 41.4 months and the OS event was mature. Results: A total of 181 eligible patients were enrolled in this study from Jun 5, 2013 to Jan 14, 2019. After combined chemotherapy, 75.14% (n=136) cases entered into the maintenance therapy setting, and 24.86% case were disease progressed (PD) during combined chemotherapy. After a median follow-up of 41.4 months (IQR 21.57-79.23), the update mPFS in HT group remained superior to CAP cohort (17.7 months vs. 12.2 months, P=0.011). In addition, the median maintenance duration of HT group was significantly longer than that of CAP group (13.8 months vs. 7.4 months, P= 0.008). For endocrine sensitive patients, mPFS was greatly prolonged in HT group compared to CAP cohort (29.3 months vs. 14.8 months, HR=0.515, 95%CI: 0.269-0.988, P=0.042). Besides, in non-visceral metastasis patients, median PFS of HT group was 25.3 months which was longer than CAP subgroup 17.0 months (HR=0.54, 95%CI: 0.300-0.972, P=0.037). However, in endocrine resistance patients, there was no significant difference between HT and CAP group (13.6 months vs. 12.0 months, HR=0.791, 95%CI: 0.499-1.253, P=0.314). There was no difference observed between HT and CAP group in visceral involved cases (14.3 months vs. 11.0 months, HR= 0.668, 95%CI: 0.410-1.089, P=0.101). The median OS was 51.7 months (95%CI: 36.614-66.786) in HT cohort and 39.8 months (95%CI:14.083-65.517) in CAP group, respectively (HR=0.882, 95%CI: 0.550-1.414, P=0.600). Conclusions: For HR+ and HER2- MBC, after 1st-line salvage combined chemotherapy, HT maintenance therapy demonstrated sustained better survival benefits than CAP, especially for hormone sensitive or non-visceral involved patients. The primary endpoint of this study was successfully reached and the median OS was prolonged by 11.9-months. Citation Format: Xiao-Jia Wang, Jian Huang, Xi-ying Shao, Li Cai, Yong-mei Yin, Li-li Zhang, Peng Shen, Yan-xia Shi. Hormone therapy (HT) brings more survival benefits than capecitabine (CAP) as maintenance therapy following the 1st-line chemotherapy in HR+/HER2-ABC/MBC: Update primary endpoint of OVERSTEP(ZJCHBC001) [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Sympos ium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P1-17-04.
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.SABCS21-P1-17-04
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2022
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Standort Signatur Einschränkungen Verfügbarkeit
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