Clinical Research (Excluding Clinical Trials)最新文献

{"title":"Abstract 404: A novel 4-gene score predict patient survival as well as pathologically complete (R0) resection in pancreatic cancer","authors":"M. Oshi, L. Le, Y. Tokumaru, A. Patel, R. Matsuyama, I. Endo, Li Yan, M. Katz, K. Takabe","doi":"10.1158/1538-7445.AM2021-404","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-404","url":null,"abstract":"BACKGROUND: Pancreatic cancer is one of the most aggressive cancers with a 5-year survival of less than 10%. Surgery is the only cure for pancreatic cancer but the majority of patients present with metastatic disease at the time of diagnosis. Systemic chemotherapy remains the primary treatment option. Given the insidious clinical presentation and poor treatment response, there is an urgent need to discover a predictive biomarker for appropriate patient selection. We hypothesized that the 4-gene score, which reflects tumor cell proliferation, is both a prognostic and predictive biomarker for pancreatic cancer. METHODS: The 4-gene score is derived from tumor expression of DOK4, HCCS, PGF, and SHCBP1 genes, which were identified based on differential mRNA expression analysis of a human breast cell line, its metastatic variant cells, and clinical outcome data of breast cancer patient cohorts, as previously reported. A total of 954 pancreatic cancer patients were analyzed for both discovery and validation of the 4-gene score from publicly available datasets to investigate the relationship between the score with clinical features such as metastasis, cancer aggressiveness, immune cell infiltration, patient survival, and resectability. RESULTS: We found that the 4-gene score correlation in pancreatic cancer was higher than in breast cancer cohorts, specifically in clinically aggressive parameters such as pathological grade and MKI67 expression. Also, the score in metastatic tumor cohorts was higher than in primary cancer cohorts (p CONCLUSION: The 4-gene score identified poor survival in pancreatic cancer and has potential as a predictive biomarker for R0 resection and treatment response in metastatic pancreatic cancer. Evaluating the degree of the 4-gene score could be a valuable potential prognostic tool. Citation Format: Masanori Oshi, Lan Le, Yoshihisa Tokumaru, Ankit Patel, Ryusei Matsuyama, Itaru Endo, Li Yan, Matthew H.G. Katz, Kazuaki Takabe. A novel 4-gene score predict patient survival as well as pathologically complete (R0) resection in pancreatic cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 404.","PeriodicalId":10518,"journal":{"name":"Clinical Research (Excluding Clinical Trials)","volume":"104 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86966296","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}

{"title":"Abstract 520: Potential role of serum proteome in predicting immune-related adverse events from immunotherapy in non-small cell lung cancer","authors":"M. Nam, L. Kim, William Cheng, W. Bae, J. Hwang, Y. Choi, Yeun Ho Lee, W. K. Hur, C. Jung, Heayoon S. Cho, Y. Chae","doi":"10.1158/1538-7445.AM2021-520","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-520","url":null,"abstract":"","PeriodicalId":10518,"journal":{"name":"Clinical Research (Excluding Clinical Trials)","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87066005","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}

{"title":"Abstract 354: Mucinous phenotype is associated with response to neoadjuvant chemotherapy in microsatellite instable resectable gastric cancer","authors":"H. Biesma, A.T.T.D. Soeratram, K. Sikorska, I. Caspers, H. F. Essen, J. Egthuijsen, A. Mookhoek, D. Hoek, W. Vos, H. Laarhoven, M. Nordsmark, D. L. Peet, F. Warmerdam, M. Geenen, O. Loosveld, J. Portielje, M. Los, E. Kranenbarg, H. Hartgrink, J. Sandick, C. V. D. Velde, M. Verheij, A. Cats, B. Ylstra, N. Grieken","doi":"10.1158/1538-7445.AM2021-354","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-354","url":null,"abstract":"Background: Epstein-Barr virus positivity (EBV+) and microsatellite instability (MSI-high) have been shown to be positive prognostic factors for long term survival in resectable gastric cancer (GC) in several studies. However, the benefit of perioperative treatment in patients with MSI-high tumors remains topic of discussion. Here, we present the clinicopathological outcome of patients with EBV+ and MSI-high GCs treated with surgery only in the Dutch D1/D2 trial, and treated with chemotherapy or chemoradiotherapy after preoperative chemotherapy and surgery in the CRITICS trial. Patients and methods: EBV was determined in tumor tissue using EBV-encoded RNA in situ hybridization (EBER-ISH). PCR and/or immunohistochemistry were performed to determine MSI status. Results were correlated to histopathological response, morphological tumor characteristics and survival. Results: In the Dutch D1/D2 trial 10.5% (47/447) of tumors were EBV+ and 10.5% (47/447) were MSI-high. In the CRITICS trial 5.5% (25/451) of tumors were EBV+ and 5.5% (25/451) were MSI-high tumors. In the Dutch D1/D2 trial, five-year overall survival probability was 51.1% for EBV+, 46.8% for MSI-high, and 42.5% for EBV-/MSS (P=0.19). In the CRITICS trial, five-year overall survival was 56.0% for EBV+, 47.3% for MSI-high, and 36.5% for EBV-/MSS (P=0.22). In the CRITICS trial, 3 (12.5%) MSI-high tumors showed moderate to complete histopathological response. Interestingly, all three showed a mucinous phenotype. Eight (36.4%) EBV+ and 114 (29.9%) EBV-/MSS tumors showed moderate to complete histopathological response. None of the EBV+ GCs showed mucinous differentiation. Conclusions: The favorable outcome of GC patients with resectable EBV+ or MSI-high tumors compared to EBV-/MSS tumors remains after perioperative chemotherapy. In MSI-high tumors significant histopathological response to neoadjuvant chemotherapy was found only in those with a mucinous phenotype. Citation Format: H.D. Biesma, A.T.T.D. Soeratram, K. Sikorska, I.A. Caspers, H.F. van Essen, J.M.P. Egthuijsen, A. Mookhoek, D.M. Hoek, W. Vos, H.W.M. van Laarhoven, M. Nordsmark, D.L. van der Peet, F.A.R.M. Warmerdam, M.M. Geenen, O.J.L. Loosveld, J.E.A. Portielje, M. Los, E. Meershoek - Klein Kranenbarg, H.H. Hartgrink, J. van Sandick, C.J.H. van de Velde, M. Verheij, A. Cats, B. Ylstra, N.C.T. van Grieken, On behalf of the CRITICS investigators. Mucinous phenotype is associated with response to neoadjuvant chemotherapy in microsatellite instable resectable gastric cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 354.","PeriodicalId":10518,"journal":{"name":"Clinical Research (Excluding Clinical Trials)","volume":"6 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90149471","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}

{"title":"Abstract 633: Thiopurines and mismatch repair deficiency cooperate to fuel TP53 mutagenesis and ALL relapse","authors":"Fan Yang, Samuel W. Brady, Huiying Sun, Chao Tang, L. Du, M. Barz, Xiaotu Ma, Yao Chen, Houshun Fang, Xiaomeng Li, Pandurang Kolekar, Omkar Pathak, J. Cai, Lixia Ding, Tianyi Wang, A. Stackelberg, S. Shen, C. Duan, C. Eckert, Hongzhuan Chen, Yu Liu, J. Klco, Hui Li, Ben-shang Li, Jinghui Zhang, R. Kirschner-Schwabe, Bin-Bing S. Zhou","doi":"10.1158/1538-7445.AM2021-633","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-633","url":null,"abstract":"Chemotherapy is curative for most children with acute lymphoblastic leukemia (ALL). Here we provide direct evidence that thiopurine chemotherapeutics can also directly induce drug resistance mutations leading to relapse. Using a large relapsed ALL cohort assembled from Chinese, US and German patients, we found that TP53 R248Q mutations were highly enriched at relapse compared to diagnosis. Relapse-specific TP53 R248Q was associated with the acquisition of MMR deficiency mutations in MSH2, MSH6, or PMS2 and a novel relapse-specific mutational signature. Using isogenic MCF10A cells with or without engineered MSH2 knockout, and the Nalm6 ALL cell line which has native MMR deficiency, we found that this novel signature was caused by a synergistic mutagenic interaction between thiopurine treatment and mismatch repair (MMR) deficiency (called the thio-dMMR signature) that contributes to a hypermutator phenotype and acquisition of TP53 R248Q in residual ALL during remission. Treatment-induced TP53-mutant clones then expand due to broad chemoresistance, leading to eventual relapse. Indeed, thiopurines preferentially induced C>T mutations at the center of NCG trinucleotides, which can lead to TP53 R248Q, and the thiopurine mutation rate was accelerated 2- to 10-fold in MMR-deficient ALL and cell lines. Thiopurine treatment induced C>T mutations preferentially on the transcribed strand, rather than the untranscribed strand, of mRNAs, which further increased the likelihood of TP53 R248Q induction. Further, experimental thiopurine treatment was able to directly induce TP53 R248Q variants in MMR-deficient cultured cells, including Nalm6 and MCF10A MSH2-/-, by activating the thio-dMMR mutational signature, while MMR-proficient MCF10A cells did not experience R248Q induction. The sequential acquisition of MMR deficiency mutations, followed by TP53 mutations, during post-diagnosis ALL evolution was supported by clonal evolution analysis of serial patient samples. p53 R248Q promoted resistance to multiple ALL chemotherapeutic agents, and was associated with on-treatment relapse and poor relapse-treatment response. Our findings indicate that the enrichment of TP53 R248Q in relapsed ALL is due to synergistic mutagenesis from thiopurine treatment and MMR deficiency, followed by selection for TP53 R248Q9s chemoresistance phenotype. This suggests that cancer drug resistance mutations may not always pre-exist subclonally at diagnosis, but may be therapy-induced in some patients. Additionally, the qualitative and quantitative mutational signature output of a mutagen (e.g., thiopurines) can vary based on the genetic background. Finally, our findings suggest potential therapeutic strategies, including avoiding thiopurine treatment in MMR-deficient relapses, and therapeutic p53 mutant reactivation, to deal with this genetically-unstable, chemoresistant disease. Citation Format: Fan Yang, Samuel W. Brady, Huiying Sun, Chao Tang, Lijuan Du, Malwine Barz, Xiaotu Ma, Yao Chen,","PeriodicalId":10518,"journal":{"name":"Clinical Research (Excluding Clinical Trials)","volume":"32 4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90608470","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}

{"title":"Abstract 644: Tumor circadian dysfunction is associated with improved survival in breast cancer patients on neoadjuvant chemotherapy (NAC)","authors":"S. Giacchetti, D. Vlachou, G. Bjarnason, David A. Rand, Francis Lévi","doi":"10.1158/1538-7445.AM2021-644","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-644","url":null,"abstract":"","PeriodicalId":10518,"journal":{"name":"Clinical Research (Excluding Clinical Trials)","volume":"87 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85982641","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}

{"title":"Abstract 497: Human CD73 knock-in mice facilitate evaluation ofin vivoefficacy of anti-human CD73 cancer immunotherapies","authors":"Chengzhang Shang, Huilin Li, Jing Zhang, E. Lin, L. Yu, Yuelei Shen","doi":"10.1158/1538-7445.AM2021-497","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-497","url":null,"abstract":"","PeriodicalId":10518,"journal":{"name":"Clinical Research (Excluding Clinical Trials)","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86001673","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}

{"title":"Abstract 515: Heterogeneity of PD-1hiCD8 T cells associates with response to PD-1 blockade in hepatocellular carcinoma","authors":"Assaf Magen, Pauline Hamon, Étienne Humblin, Alessandra S. Schanoski, Joel Kim, J. Berichel, E. Kenigsberg, M. Schwartz, T. Marron, A. Kamphorst, M. Merad","doi":"10.1158/1538-7445.AM2021-515","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-515","url":null,"abstract":"","PeriodicalId":10518,"journal":{"name":"Clinical Research (Excluding Clinical Trials)","volume":"14 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86050074","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}

{"title":"Abstract LB071: Tuning the tumor myeloid microenvironment (TME) by targeting TREM2+tumor-associated macrophages to overcome resistance to immune checkpoint inhibitors","authors":"N. Jahchan, M. Binnewies, Joshua L. Pollack, R. Mehta, S. Dash, Christina Tun, Erick Lu, Xiaoyan Du, K. Baker, L. Reyno, V. Sriram","doi":"10.1158/1538-7445.AM2021-LB071","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-LB071","url":null,"abstract":"The tumor microenvironment (TME) often contains high levels of suppressive myeloid cells that may contribute to innate checkpoint inhibitor (CPI) resistance. Pionyr9s Myeloid Tuning approach involves altering the composition and/or the function of myeloid cells in the TME. To this end, therapeutic targeting of tumor-associated macrophages (TAMs) is a promising strategy to increase CPI response rates in solid tumor indications, as well as to overcome resistance to CPI therapies. Pionyr and others identified the transmembrane protein triggering receptor expressed on myeloid cells-2 (TREM2) as a highly enriched TAMs target. Furthermore, TREM2 mRNA expression negatively correlates with patient survival in a variety of tumor types, supporting the involvement of TAMs in tumor progression. Pionyr developed a lead anti-TREM2 monoclonal antibody (mAb), termed PY314, as well as a murinized version of PY314, termed PY314m. PY314m demonstrated significant anti-tumor activity either as single agent in CPI-sensitive syngeneic tumor models or in combination with anti-PD-1 in CPI-resistant syngeneic tumor models. Mechanistically, PY314m reduced the pro-tumorigenic MHC class II-low, M2-like TAMs, induced pro-inflammatory cytokine production, significant increased CD8+ T cell infiltration into the TME. These findings suggest that PY314 therapy could be used to overcome CPI resistance in humans. To select patients most likely to benefit from PY314 therapy, Pionyr developed a qualitative IHC assay that detects TREM2 expression levels in formalin-fixed, paraffin-embedded human tumor tissues. Screening for TREM2 expression in tumor tissues demonstrated that TREM2+ TAMs were present in multiple solid tumor indications and their number increased with disease grade in a selected set of indications. Ongoing efforts are aimed at better understanding localization of TREM2+ TAMs within the TME, and spatial relationship of the TREM2+ TAMs to other immune cells present in the TME. The TREM2 IHC assay will be used to test our hypothesis that patients with tumors with high level of TREM2+ TAMs are most likely to benefit from PY314 treatment. Citation Format: Nadine S. Jahchan, Mikhail Binnewies, Joshua L. Pollack, Ranna Mehta, Subhadra Dash, Christine Tun, Erick Lu, Xiaoyan Du, Kevin P. Baker, Len Reyno, Venkataraman Sriram. Tuning the tumor myeloid microenvironment (TME) by targeting TREM2+ tumor-associated macrophages to overcome resistance to immune checkpoint inhibitors [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr LB071.","PeriodicalId":10518,"journal":{"name":"Clinical Research (Excluding Clinical Trials)","volume":"54 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90934408","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}

{"title":"Abstract 380: WNT signal pathway activation correlates with innate resistant to immune checkpoint therapies in NSCLC","authors":"D. Ren, Bo Zhang, Renwang Liu, Fuyu Gong, Yue-zong Bai, W. Xie, Huandong Huo, Hao Zhang, Zuoqing Song","doi":"10.1158/1538-7445.AM2021-380","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-380","url":null,"abstract":"Background: Immune checkpoint inhibitors targeting the programmed cell death-1 receptor (PD-1) improve survival in a subset of patients with NSCLC. There are still lots of patients could not reach the clinical benefit, even though with the positive expression of the programmed cell death 1 ligand 1 (PD-L1). Here, we aimed to research the immune resistance mechanism in NSCLC. Methods: The genomic data and clinical data of the discovery cohort was obtained from The Cancer Genome Atlas (TCGA). The clinical data of validation cohort in NSCLC treated by immunotherapy was retrospective collected. And tissue from patients with NSCLC were performed to whole exome sequencing in a College of American Pathologists-certified and Clinical Laboratory Improvement Amendments-accredited lab. Results: Activation of WNT signaling was inferred that somatic mutations or somatic copy number alterations in WNT signaling elements including APC, WNT16, AXIN2, WNT4, AXIN1, CTNNB1, BCL9L and SMAD4. Two cohort have been enrolled in this study, the discovery cohort from TCGA, and the validation cohort from the Chinese patients with NSCLC. The frequency of WNT pathway alterations from the TCGA cohort was 16%, and which was represented mutually exclusive molecular subsets. In TCGA cohort, activating alteration WNT signaling were associated with shorter median PFS (18.8 vs 3.9 months, p=0.036, HR=0.24 (0.09-0.68)). Conclusions: Mutations predicted to activate the WNT pathway were associated with innate resistance to immune checkpoint blockade in NSCLC Citation Format: Dian Ren, Bo Zhang, Renwang Liu, Fuyu Gong, Yuezong Bai, Wenzhuan Xie, Huandong Huo, Hao Zhang, Zuoqing Song. WNT signal pathway activation correlates with innate resistant to immune checkpoint therapies in NSCLC [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 380.","PeriodicalId":10518,"journal":{"name":"Clinical Research (Excluding Clinical Trials)","volume":"38 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91100015","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}

{"title":"Abstract 376: Prognostic significance of Glasgow prognostic score in NSCLC patients treated with immunotherapy after platinum-based cytotoxic chemotherapy","authors":"H. Kang, I. Kim, Jin Woo Kim","doi":"10.1158/1538-7445.AM2021-376","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-376","url":null,"abstract":"Introduction: The Glasgow prognostic score (GPS) reflects the host systemic inflammatory response and is validated prognostic factor in lung cancer. However, little is known about the prognostic role in non-small cell lung cancer (NSCLC) patients treated with immunotherapy after platinum-based cytotoxic chemotherapy. Patient and Methods: This study used a lung cancer cohort of the Catholic Medical Center of Korea between January 2018 and June 2020. We included the patients who were diagnosed with unresectable advanced stage NSCLC or recurrent disease after pulmonary resection and had received at least one regimen of platinum-based chemotherapy before being administered immunotherapy. The patients with NSCLC treated with anti-PD1 or anti-PD-L1 (pembrolizumab, nivolumab, or atezolizumab) and assessed the prognostic value of the GPS. The GPS was calculated using C-reactive protein and albumin concentrations within 1 week before starting anti-PD1 or anti-PD-L1 treatment. Results: A total of 78 patients with NSCLC treated with immunotherapy as 2nd or 3rd line therapy after platinum-based chemotherapy. Kaplan-Meier analyses revealed that higher GPS was significant predictors of shorter progression free survival (PFS) (Log rank Conclusion: Higher GPS were identified as one of poor prognostic factor for OS and PFS in NSCLC patients received immunotherapy as 2nd or 3rd line therapy after platinum-based chemotherapy. Citation Format: Hye Seon Kang, In Kyoung Kim, Jin Woo Kim. Prognostic significance of Glasgow prognostic score in NSCLC patients treated with immunotherapy after platinum-based cytotoxic chemotherapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 376.","PeriodicalId":10518,"journal":{"name":"Clinical Research (Excluding Clinical Trials)","volume":"36 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91189799","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}