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Safety and antitumour activity of cadonilimab, an anti-PD-1/CTLA-4 bispecific antibody, for patients with advanced solid tumours (COMPASSION-03): a multicentre, open-label, phase 1b/2 trial

Ë«ÌØÒìÐÔ¿¹PD-1/CTLA-4¿¹Ì忨¶ÈÄáÀûµ¥¿¹£¨cadonilimab£©ÓÃÓÚÍíÆÚʵÌåÁö»¼ÕߵݲȫÐԺͿ¹Ö×Áö»îÐÔÑо¿£¨COMPASSION-03ÊÔÑ飩£ºÒ»Ïî¶àÖÐÐÄ¡¢¿ª·Å±êÇ©µÄ1b/2ÆÚÁÙ´²ÊÔÑé

Issue LANCET ONCOLOGY 2023, Volume 24 Issue 10 1134-1146

ÆÚ¿¯£º¡¶ÁøÒ¶µ¶?Ö×Áöѧ¡·£¨LANCET ONCOLOGY£©£¬2023Ä꣬µÚ24¾íµÚ10ÆÚ£¬1134-1146Ò³

Author Gao Xiangyu / Xu Nong / Li Ziyu / Shen Lin / Ji Ke / Zheng Zhong / Liu Dan / Lou Hanmei / Bai Li / Liu Tianshu / Li Yunxia / Li Yuzhi / Fan Qingxia / Feng Mei / Zhong Haijun / Huang Yi / Lou Ge / Wang Jing / Lin Xiaoyan / Chen Ye / An Ruifang / Li Changzheng / Zhou Qi / Huang Xin / Guo Zengqing / Wang Shubin / Li Guiling / Fei Junwei / Zhu Lijing / Zhu Hong / Li Xiumin / Li Fenghu / Liao Sihai / Min Qinghua / Tang Lei / Shan Fei / Gong Jifang / Gao Yunong / Zhou Jun / Lu Zhihao / Li Xiaofan / Li Jianjie / Ren Hui / Liu Xiaohong / Yang Hongxia / Li Wenting / Song Weifeng / Wang Zhongmin Maxwell / Li Baiyong / Xia Michelle / Wu Xiaohua / Ji Jiafu

Abstract

Background Immune checkpoint inhibitors targeting PD-1 or CTLA-4 individually have shown substantial clinical benefits in the treatment of malignancies. We aimed to assess the safety and antitumour activity of cadonilimab monotherapy, a bispecific PD-1/CTLA-4 antibody, in patients with advanced solid tumours.Methods This multicentre, open-label, phase 1b/2 trial was conducted across 30 hospitals in China. Patients aged 18 years or older with histologically or cytologically confirmed, unresectable advanced solid tumours, unsuccessful completion of at least one previous systemic therapy, and an Eastern Cooperative Oncology Group performance status of 0 or 1 were eligible for inclusion. Patients who had previously received anti-PD-1, anti-PD-L1, or anti-CTLA-4 treatment were not eligible for inclusion. In the dose escalation phase of phase 1b, patients received intravenous cadonilimab at 6 mg/kg and 10 mg/kg every 2 weeks. In the dose expansion phase of phase 1b, cadonilimab at 6 mg/kg and a fixed dose of 450 mg were given intravenously every 2 weeks. In phase 2, cadonilimab at 6 mg/kg was administered intravenously every 2 weeks in three cohorts: patients with cervical cancer, oesophageal squamous cell carcinoma, and hepatocellular carcinoma. The primary endpoints were the safety of cadonilimab in phase 1b and objective response rate in phase 2, based on the Response Evaluation Criteria in Solid Tumors (RECIST), version 1.1. The safety analysis was done in all patients who received at least one dose of cadonilimab. Antitumour activity was assessed in the full analysis set for the cervical cancer cohort, and in all patients with measurable disease at baseline and who received at least one dose of cadonilimab in the oesophageal squamous cell carcinoma and hepatocellular carcinoma cohorts. The study is registered on ClinicalTrial.gov, NCT03852251, and closed to new participants; follow-up has been completed. Findings Between Jan 18, 2019, and Jan 8, 2021, 240 patients (83 [43 male and 40 female] in phase 1b and 157 in phase 2) were enrolled. Phase 2 enrolled 111 female patients with cervical cancer, 22 patients with oesophageal squamous cell carcinoma (15 male and seven female), and 24 patients with hepatocellular carcinoma (17 male and seven female). During dose escalation, no dose-limiting toxicities occurred. Grade 3-4 treatment-related adverse events occurred in 67 (28%) of 240 patients; the most frequent grade 3 or worse treatment-related adverse events were anaemia (seven [3%]), increased lipase (four [2%]), decreased bodyweight (three [1%]), decreased appetite (four [2%]), decreased neutrophil count (three [1%]), and infusion-related reaction (two [1%]). 17 (7%) patients discontinued treatment due to treatment-related adverse events. 54 (23%) of 240 patients reported serious treatment-related adverse events, including five patients who died (one due to myocardial infarction; cause unknown for four). In phase 2, in the cervical cancer cohort, with a median follow-up of 14 center dot 6 months (IQR 13 center dot 1-17 center dot 5), the objective response rate was 32 center dot 3% (32 of 99; 95% CI 23 center dot 3-42 center dot 5). In the oesophageal squamous cell carcinoma cohort, with a median follow-up of 17 center dot 9 months (IQR 4 center dot 0-15 center dot 1), the objective response rate was 18 center dot 2% (four of 22; 95% CI 5 center dot 2-40 center dot 3). In the hepatocellular carcinoma cohort, with a median follow-up of 19 center dot 6 months (IQR 8 center dot 7-19 center dot 8), the objective response rate was 16 center dot 7% (four of 24; 95% CI 4 center dot 7-37 center dot 4). Interpretation Cadonilimab showed an encouraging tumour response rate, with a manageable safety profile, suggesting the potential of cadonilimab for the treatment of advanced solid tumours.Copyright (c) 2023 Elsevier Ltd. All rights reserved.

Cite this article as: [1]Gao Xiangyu, Xu Nong, Li Ziyu, et al.Safety and antitumour activity of cadonilimab, an anti-PD-1/CTLA-4 bispecific antibody, for patients with advanced solid tumours (COMPASSION-03): a multicentre, open-label, phase 1b/2 trial[J].LANCET ONCOLOGY,2023,24(10):1134-1146.

New insights into molecules and pathways of cancer metabolism and therapeutic implications

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Issue CANCER COMMUNICATIONS 2020, Volume 41 Issue 1 16-36

ÆÚ¿¯£º¡¶°©Ö¢Í¨Ñ¶¡·£¨CANCER COMMUNICATIONS£©£¬2020Ä꣬µÚ41¾íµÚ1ÆÚ£¬16-36Ò³

Author Tang Zhenye / Xu Zhenhua / Zhu Xiao / Zhang Jinfang

Keywords cancer metabolism / metabolic pathway / metabolomic profiling / therapeutic implication

Abstract

Cancer cells are abnormal cells that can reproduce and regenerate rapidly. They are characterized by unlimited proliferation, transformation and migration, and can destroy normal cells. To meet the needs for cell proliferation and migration, tumor cells acquire molecular materials and energy through unusual metabolic pathways as their metabolism is more vigorous than that of normal cells. Multiple carcinogenic signaling pathways eventually converge to regulate three major metabolic pathways in tumor cells, including glucose, lipid, and amino acid metabolism. The distinct metabolic signatures of cancer cells reflect that metabolic changes are indispensable for the genesis and development of tumor cells. In this review, we report the unique metabolic alterations in tumor cells which occur through various signaling axes, and present various modalities available for cancer diagnosis and clinical therapy. We further provide suggestions for the development of anti-tumor therapeutic drugs.

Cite this article as: [1]Tang Zhenye, Xu Zhenhua, Zhu Xiao, et al.New insights into molecules and pathways of cancer metabolism and therapeutic implications[J].CANCER COMMUNICATIONS,2020,41(1):16-36.

Downregulation of the circadian rhythm regulator HLF promotes multiple-organ distant metastases in non-small cell lung cancer through PPAR/NF-¦Êb signaling

ÖçÒ¹½ÚÂɵ÷½ÚÒò×ÓHLFϵ÷ͨ¹ýPPAR/NF-¦ÊBÐźÅͨ·´Ù½ø·ÇСϸ°û·Î°©¶àÆ÷¹ÙÔ¶´¦×ªÒÆ

Issue CANCER LETTERS 2020, Volume 482 56-71

ÆÚ¿¯£º¡¶°©Ö¢¿ì±¨¡·£¨CANCER LETTERS£©£¬2020Ä꣬µÚ482¾í£¬56-71Ò³

Author Chen Jiarong / Liu Aibin / Lin Zhichao / Wang Bin / Chai Xingxing / Chen Shasha / Lu Wenjie / Zheng Mingzhu / Cao Ting / Zhong Meigong / Li Ronggang / Wu Minyan / Lu Zhuming / Pang Wenguang / Huang Wenhai / Xiao Lin / Lin Daren / Wang Zhihui / Lei Fangyong / Chen Xiangmeng / Long Wansheng / Zheng Yan / Chen Qiong / Zeng Jincheng / Ren Dong / Li Jun / Zhang Xin / Huang Yanming

Keywords NSCLC / Distant metastasis / Circadian rhythms regulator / Hepatic leukemia factor (HLF) / PPAR alpha / PPARr gamma / NF-kappa B pathway

Abstract

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related death due to its early recurrence and widespread metastatic potential. Accumulating studies have reported that dysregulation of circadian rhythmsassociated regulators is implicated in the recurrence and metastasis of NSCLC. Therefore, identification of metastasis-associated circadian rhythm genes is clinically necessary. Here we report that the circadian gene hepatic leukemia factor (HLF), which was dramatically reduced in early-relapsed NSCLC tissues, was significantly correlated with early progression and distant metastasis in NSCLC patients. Upregulating HLF inhibited, while silencing HLF promoted lung colonization, as well as metastasis of NSCLC cells to bone, liver and brain in vivo. Importantly, downexpression of HLF promoted anaerobic metabolism to support anchorage-independent growth of NSCLC cells under low nutritional condition by activating NF-kappa B/p65 signaling through disrupting translocation of PPAR alpha and PPAR gamma. Further investigations revealed that both genetic deletion and methylation contribute to downexpression of HLF in NSCLC tissues. In conclusion, our results shed light on a plausible mechanism by which HLF inhibits distant metastasis in NSCLC, suggesting that HLF may serve as a novel target for clinical intervention in NSCLC.

Cite this article as: [1]Chen Jiarong, Liu Aibin, Lin Zhichao, et al.Downregulation of the circadian rhythm regulator HLF promotes multiple-organ distant metastases in non-small cell lung cancer through PPAR/NF-¦Êb signaling[J].CANCER LETTERS,2020,482:56-71.

PD-L1 expression and Tumor mutation burden as Pathological response biomarkers of Neoadjuvant immunotherapy for Early-stage Non-small cell lung cancer: A systematic review and meta-analysis

PD-L1±í´ïÓëÖ×ÁöÍ»±ä¸ººÉ×÷ΪÔçÆÚ·ÇСϸ°û·Î°©Ð¸¨ÖúÃâÒßÖÎÁƲ¡Àí·´Ó¦ÉúÎï±êÖ¾ÎïµÄϵͳ×ÛÊöÓëÜöÝÍ·ÖÎö

Issue CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY 2022, Volume 170

ÆÚ¿¯£º¡¶Ö×ÁöѧÓëѪҺѧÆÀÂÛ¡·£¨CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY£©£¬2022Ä꣬µÚ170¾í

Author Deng Hongsheng / Zhao Yi / Cai Xiuyu / Chen Hualin / Cheng Bo / Zhong Ran / Li Feng / Xiong Shan / Li Jianfu / Liu Jun / He Jianxing / Liang Wenhua

Keywords Non-small cell lung cancer / PD-L1 expression / Tumor mutation burden / Neoadjuvant immunotherapy / Pathologic response

Abstract

To date, there is no approved biomarker for predicting pathological response in neoadjuvant programmed cell death (ligand) 1 (PD-(L)1) blockades treated early-stage non-small cell lung cancer (NSCLC). Databases including PubMed, Embase, ClinicalTrials.gov, and Conference abstracts were searched for clinical trials of neoadjuvant PD-1/PD-L1 blockades for resectable NSCLC. Data regarding major pathological response (MPR), pathological complete response (pCR) in patients with high/low pretreatment PD-L1 expression, and tumor mutation burden (TMB) were synthesized using fixed-model meta-analysis and evaluated by odds ratio with 95 % confidence interval. This analysis included 10 studies involving 461 NSCLC patients. Compared with PD-L1 expression <1%, PD-L1 expression >= 1% is associated with a higher rate of MPR and pCR. High-TMB associated with MPR and pCR. Similar findings were observed in subgroup analyses despite mono-PD-1/PD-L1 blockade or their combination with chemotherapy. Notably, 50 % as the cutoff value for PD-L1 expression demonstrated better prediction efficacy for MPR than that of 1%.

Cite this article as: [1]Deng Hongsheng, Zhao Yi, Cai Xiuyu, et al.PD-L1 expression and Tumor mutation burden as Pathological response biomarkers of Neoadjuvant immunotherapy for Early-stage Non-small cell lung cancer: A systematic review and meta-analysis[J].CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY,2022,170.

COVID-19 in persons with chronic myeloid leukaemia

ÂýÐÔËèϵ°×Ѫ²¡»¼ÕßÖеÄÐÂÐ͹Ú×´²¡¶¾·ÎÑ×£¨COVID-19£©Çé¿ö

Issue LEUKEMIA 2020, Volume 34 Issue 7 1799-1804

ÆÚ¿¯£º¡¶°×Ѫ²¡¡·£¨LEUKEMIA£©£¬2020Ä꣬µÚ34¾íµÚ7ÆÚ£¬1799-1804Ò³

Author Li Weiming / Wang Danyu / Guo Jingming / Yuan Guolin / Yang Zhuangzhi / Gale Robert Peter / You Yong / Chen Zhichao / Chen Shiming / Wan Chucheng / Zhu Xiaojian / Chang Wei / Sheng Lingshuang / Cheng Hui / Zhang Youshan / Meng Li / Jiang Qian / Li Qing / Qin Jun

Abstract

We studied by questionnaire 530 subjects with chronic myeloid leukaemia (CML) in Hubei Province during the recent SARS-CoV-2 epidemic. Five developed confirmed (N = 4) or probable COVID-19 (N = 1). Prevalence of COVID-19 in our subjects, 0.9% (95% Confidence Interval, 0.1, 1.8%) was ninefold higher than 0.1% (0, 0.12%) reported in normals but lower than 10% (6, 17%) reported in hospitalised persons with other haematological cancers or normal health-care providers, 7% (4, 12%). Co-variates associated with an increased risk of developing COVID-19 amongst persons with CML were exposure to someone infected with SARS-CoV-2 (P = 0.037), no complete haematologic response (P = 0.003) and co-morbidity(ies) (P = 0.024). There was also an increased risk of developing COVID-19 in subjects in advanced phase CML (P = 0.004) even when they achieved a complete cytogenetic response or major molecular response at the time of exposure to SARS-CoV-2. 1 of 21 subjects receiving 3rd generation tyrosine kinase-inhibitor (TKI) developed COVID-19 versus 3 of 346 subjects receiving imatinib versus 0 of 162 subjects receiving 2nd generation TKIs (P = 0.096). Other co-variates such as age and TKI-therapy duration were not significantly associated with an increased risk of developing COVID-19. Persons with these risk factors may benefit from increased surveillance of SARS-CoV-2 infection and possible protective isolation.

Cite this article as: [1]Li Weiming, Wang Danyu, Guo Jingming, et al.COVID-19 in persons with chronic myeloid leukaemia[J].LEUKEMIA,2020,34(7):1799-1804.

The RNA m<SUP>6</SUP>A Reader YTHDF1 Is Required for Acute Myeloid Leukemia Progression

RNA m?AÔĶÁÆ÷ YTHDF1ÊǼ±ÐÔËèϵ°×Ѫ²¡½øÕ¹Ëù±ØÐèµÄÒò×Ó

Issue CANCER RESEARCH 2023, Volume 83 Issue 6 845-860

ÆÚ¿¯£º¡¶°©Ö¢Ñо¿¡·£¨CANCER RESEARCH£©£¬2023Ä꣬µÚ83¾íµÚ6ÆÚ£¬845-860Ò³

Author Hong Yun-Guang / Yang Zhigang / Chen Yan / Liu Tian / Zheng Yuyuan / Zhou Chun / Wu Guo-Cai / Chen Yinhui / Xia Juan / Wen Ruiting / Liu Wenxin / Zhao Yi / Chen Jin / Gao Xiangwei / Chen Zhanghui

Abstract

N-6-methyladenosine (m(6)A), the most abundant modification in mRNAs, has been defined as a crucial modulator in the progression of acute myelogenous leukemia (AML). Identification of the key regulators of m(6)A modifications in AML could provide further insights into AML biology and uncover more effective therapeutic strategies for patients with AML. Here, we report overexpression of YTHDF1, an m(6)A reader protein, in human AML samples at the protein level with enrichment in leukemia stem cells (LSC). Where-as YTHDF1 was dispensable for normal hematopoiesis in mice, depletion of YTHDF1 attenuated self-renewal, proliferation, and leukemic capacity of primary human and mouse AML cells in vitro and in vivo. Mechanistically, YTHDF1 promoted the translation of cyclin E2 in an m(6)A-dependent manner. Structure-based virtual screening of FDA-approved drugs identified tegaserod as a potential YTHDF1 inhibitor. Tegaserod blocked the direct binding of YTHDF1 with m(6)A-modified mRNAs and inhibited YTHDF1-regulated cyclin E2 translation. Moreover, tegaserod reduced the viability of patient-derived AML cells in vitro and prolonged survival in patient-derived xenograft models. Together, our study defines YTHDF1 as an integral regulator of AML progression by regulating the expression of m(6)A-modified mRNAs, which might serve as a potential therapeutic target for AML. Significance: The m(6)A reader YTHDF1 is required for progres-sion of acute myelogenous leukemia and can be targeted with the FDA-approved drug tegaserod to suppress leukemia growth.

Cite this article as: [1]Hong Yun-Guang, Yang Zhigang, Chen Yan, et al.The RNA m<SUP>6</SUP>A Reader YTHDF1 Is Required for Acute Myeloid Leukemia Progression[J].CANCER RESEARCH,2023,83(6):845-860.

Nanoparticles advanced from preclinical studies to clinical trials for lung cancer therapy

ÄÉÃ׿ÅÁ£´ÓÁÙ´²Ç°Ñо¿ÂõÏò·Î°©ÖÎÁÆÁÙ´²ÊÔÑé

Issue CANCER NANOTECHNOLOGY 2023, Volume 14 Issue 1

ÆÚ¿¯£º¡¶°©Ö¢ÄÉÃ×¼¼Êõ¡·£¨CANCER NANOTECHNOLOGY£©£¬2023Ä꣬µÚ14 ¾íµÚ1ÆÚ

Author Liu Yifan / Cheng Wenxu / Xin HongYi / Liu Ran / Wang Qinqi / Cai Wenqi / Peng Xiaochun / Yang Fuyuan / Xin HongWu

Keywords Lung cancer / Nanoparticle / Immune targeted therapy / Nanotherapy

Abstract

Lung cancer is the leading cause of cancer mortality. As a heterogeneous disease, it has different subtypes and various treatment modalities. In addition to conventional surgery, radiotherapy and chemotherapy, targeted therapy and immunotherapy have also been applied in the clinics. However, drug resistance and systemic toxicity still cannot be avoided. Based on the unique properties of nanoparticles, it provides a new idea for lung cancer therapy, especially for targeted immunotherapy. When nanoparticles are used as carriers of drugs with special physical properties, the nanodrug delivery system ensures the accuracy of targeting and the stability of drugs while increasing the permeability and the aggregation of drugs in tumor tissues, showing good anti-tumor effects. This review introduces the properties of various nanoparticles including polymer nanoparticles, liposome nanoparticles, quantum dots, dendrimers, and gold nanoparticles and their applications in tumor tissues. In addition, the specific application of nanoparticle-based drug delivery for lung cancer therapy in preclinical studies and clinical trials is discussed.

Cite this article as: [1]Liu Yifan, Cheng Wenxu, Xin HongYi, et al.Nanoparticles advanced from preclinical studies to clinical trials for lung cancer therapy[J].CANCER NANOTECHNOLOGY,2023,14(1).

The application of Aptamer in biomarker discovery

ÊÊÅäÌåÔÚÉúÎï±êÖ¾Îï·¢ÏÖÖеÄÓ¦ÓÃ

Issue BIOMARKER RESEARCH 2023, Volume 11 Issue 1

ÆÚ¿¯£º¡¶ÉúÎï±êÖ¾ÎïÑо¿¡·£¨BIOMARKER RESEARCH£©£¬2023 Ä꣬µÚ11¾íµÚ1ÆÚ

Author Li Yongshu / Tam Winnie Wailing / Yu Yuanyuan / Zhuo Zhenjian / Xue Zhichao / Tsang Chiman / Qiao Xiaoting / Wang Xiaokang / Wang Weijing / Li Yongyi / Tu Yanyang / Gao Yunhua

Keywords Aptamer / Biomarker discovery / SELEX / SOMAScan / Cardiovascular diseases / cancer / Neurodegeneration-related diseases

Abstract

Biomarkers are detectable molecules that can reflect specific physiological states of cells, organs, and organisms and therefore be regarded as indicators for specific diseases. And the discovery of biomarkers plays an essential role in cancer management from the initial diagnosis to the final treatment regime. Practically, reliable clinical biomarkers are still limited, restricted by the suboptimal methods in biomarker discovery. Nucleic acid aptamers nowadays could be used as a powerful tool in the discovery of protein biomarkers. Nucleic acid aptamers are single-strand oligonucleotides that can specifically bind to various targets with high affinity. As artificial ssDNA or RNA, aptamers possess unique advantages compared to conventional antibodies. They can be flexible in design, low immunogenicity, relative chemical/thermos stability, as well as modifying convenience. Several SELEX (Systematic Evolution of Ligands by Exponential Enrichment) based methods have been generated recently to construct aptamers for discovering new biomarkers in different cell locations. Secretome SELEX-based aptamers selection can facilitate the identification of secreted protein biomarkers. The aptamers developed by cell-SELEX can be used to unveil those biomarkers presented on the cell surface. The aptamers from tissue-SELEX could target intracellular biomarkers. And as a multiplexed protein biomarker detection technology, aptamer-based SOMAScan can analyze thousands of proteins in a single run. In this review, we will introduce the principle and workflow of variations of SELEX-based methods, including secretome SELEX, ADAPT, Cell-SELEX and tissue SELEX. Another powerful proteome analyzing tool, SOMAScan, will also be covered. In the second half of this review, how these methods accelerate biomarker discovery in various diseases, including cardiovascular diseases, cancer and neurodegenerative diseases, will be discussed.

Cite this article as: [1]Li Yongshu, Tam Winnie Wailing, Yu Yuanyuan, et al.The application of Aptamer in biomarker discovery[J].BIOMARKER RESEARCH,2023,11(1).