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Data publikacji: 25 lipca 2024

Data aktualizacji: 26 lipca 2024

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1

Quan, Jihong. "A comparative research on Taoist concept between Jin ao xin hua and Jian Deng xin hua". Studies of Korean Literature 67 (31.07.2020): 95–117. http://dx.doi.org/10.20864/skl.2020.07.67.95.

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Nivison, David S., i Edward L. Shaughnessy. "The Jin Hou Su Bells Inscription and its Implications for the Chronology of Early China". Early China 25 (2000): 29–48. http://dx.doi.org/10.1017/s0362502800004260.

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Since the Jin Hou Su chime-bells from the cemetery of the Jin lords at Tianma-Qucun, Shanxi, became known to the scholarly world, the problem of the dates contained in its inscription has attracted the attention of scholars both in and outside of China. In this article we discuss two aspects of this problem. First, while the “thirty-third year” date of the inscription must certainly refer to King Xuan's reign, which is to say 795 B.C., the four full date notations of the inscription are incompatible with this year, but are instead compatible with the following year, 794 B.C. This article suggests two ways to reconcile this discrepancy. Second, while there can be no doubt that Jin Hou Su is Jin Xian Hou, the “Jin shijia” chapter of the Shi ji gives his dates of reign as 822 to 812 B.C., which is in turn incompatible with either 795 or 794 B.C. However, in the Shi ji's genealogy of Jin lords, the son of Xian Hou is Mu Hou and the grandson of Mu Hou is Zhao Hou, which contradicts the zhao-mu structure of the Zhou ancestral system. Therefore, we propose that the Shiji has reversed the order of Xian Hou and Mu Hou, such that Xian Hou's reign actually extended from King Xuan's thirty-third year through his forty-third year (795-785 B.C.). Not only does this simple change in the genealogy of the Jin lords resolve the problem of the dates in the Jin Hou Su bells inscription, but it also serves to explain an entire array of problems in the chronology of early China.

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3

KUROKAWA, Hisayuki, i Hiroyuki YAMATO. "Effects of Hub Terminal on Physical Distribution System". Journal of Japan Institute of Navigation 95 (1996): 343–50. http://dx.doi.org/10.9749/jin.95.343.

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FURUSHO, Masao, Yoshikazu FUJIOKA, Norikazu ONISHI i Susumu HASHIMOTO. "An Experimental Study on Apparent Hue of the Lightbuoy". Journal of Japan Institute of Navigation 81 (1989): 73–80. http://dx.doi.org/10.9749/jin.81.73.

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Tseng, Chu-Yao, Ching-Wen Huang, Hsin-Chia Huang i Wei-Chen Tseng. "Utilization Pattern of Traditional Chinese Medicine among Fracture Patients: A Taiwan Hospital-Based Cross-Sectional Study". Evidence-Based Complementary and Alternative Medicine 2018 (30.09.2018): 1–9. http://dx.doi.org/10.1155/2018/1706517.

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Traditional Chinese medicine (TCM) divides fracture treatment into three stages. Many TCM herbs and formulas have been used to treat fractures for thousands of years. However, research regarding the Chinese herbal products (CHPs) that should be used at different periods of treatment is still lacking. This study aims to identify the CHPs that should be used at different periods of treatment as well as confirm the TCM theory of fracture periods medicine. We used prescriptions of TCM outpatients with fracture diagnoses analyzed using the Chang Gung Research Database (CGRD) from 2000 to 2015. According to the number of days between the date of the fracture and the clinic visit date, all patients were assigned to one of three groups. Patients with a date gap of 0-13 days were assigned to the early period group; those with a date gap of 14-82 days were assigned to the middle period group; and those with a date gap of 83-182 days were assigned to the late period group. We observed the average number of herbal formulas prescribed by the TCM doctor at each visit was 2.78, and the average number of single herbs prescribed was 6.47. The top three prescriptions in the early fracture period were Zheng-gu-zi-jin-dang, Shu-jing-huo-xue-tang, and Wu-ling-san. In the middle fracture period, the top three formulas were Zheng-gu-zi-jin-dang, Shu-jing-huo-xue-tang, and Zhi-bai-di-huang-wan. In the late fracture period, the top three formulas were Shu-jing-huo-xue-tang, Gui-lu-er-xian-jiao, and Du-huo-ji-sheng-tang. The main single herbs used in the early fracture period were Yan-hu-suo, Gu-sui-bu, and Dan-shen. From the middle to the late period, the most prescribed single herbs were Xu-duan, Gu-sui-bu, and Yan-hu-suo. We concluded that the results showed that the CGRD utilization pattern roughly meets the TCM theory at different fracture periods.

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6

Lee, Rumi, Jiexi Li, Jun Li, Chang-Jiun Wu, Shan Jiang, Wen-Hao Hsu, Deepavali Chakravarti i in. "Abstract IA014: Synthetic essentiality identifies TDO2 as a key target in APC-deficient CRC". Cancer Research 82, nr 23_Supplement_1 (1.12.2022): IA014. http://dx.doi.org/10.1158/1538-7445.crc22-ia014.

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Abstract Loss of adenomatous polyposis coli (APC) is considered a critical initiating event in colorectal cancer (CRC), where it occurs in 90% of sporadic CRCs. APC deficiency results in activation of WNT; however, major hurdles persist to therapeutic intervention of this pathway. Here, the synthetic essentiality framework was used to discover other potential druggable vulnerabilities for APC-deficient cancers. Through this approach, tryptophan 2,3-dioxygenase 2 (TDO2) was identified as a synthetic essential effector of APC-deficient CRC. Upregulation of TDO2 activates the Kyn-AhR pathway, increasing glycolysis. Subsequent cancer cell growth and CXCL5 secretion leads to macrophage recruitment into the tumor microenvironment. APC-deficient CRC models were found to be susceptible to both TDO2 depletion and pharmacologic inhibition. Overall, this study identifies the TCF4-TDO2-AhR-CXCL5 axis as a critical pathway in the maintenance of APC-deficient CRC, informing potential genotype-specific therapeutic targets and the use of TDO2 inhibitors to combat this disease. Citation Format: Rumi Lee, Jiexi Li, Jun Li, Chang-Jiun Wu, Shan Jiang, Wen-Hao Hsu, Deepavali Chakravarti, Peiwen Chen, Kyle A. LaBella, Jing Li, Denise J. Spring, Di Zhao, Y. Alan Wang, Ronald A. DePinho. Synthetic essentiality identifies TDO2 as a key target in APC-deficient CRC [abstract]. In: Proceedings of the AACR Special Conference on Colorectal Cancer; 2022 Oct 1-4; Portland, OR. Philadelphia (PA): AACR; Cancer Res 2022;82(23 Suppl_1):Abstract nr IA014.

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7

Lee, Jun-Gab. "Fang Hao, The History of cultural intercourse between East and West(Translated and annotated by Son, Jun-Sik and Yoo, JIn-Hee Hakgobang, 2019~2021)". JOURNAL OF ASIAN HISTORICAL STUDIES 157 (31.12.2021): 579–91. http://dx.doi.org/10.17856/jahs.2021.12.157.579.

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8

Jin, Zhao. "Eingestauter ardor („Glut“, huo) – Differenzierung und Behandlung aus Sicht von Ärzten der Jin- und Yuan-Dynastie". Chinesische Medizin / Chinese Medicine 38, nr 2 (24.07.2023): 84–93. http://dx.doi.org/10.1007/s00052-023-00081-9.

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9

SHIMADA, Yoichi, Keiko TAKAHASHI i Shigeaki SHIOTANI. "Weather Routing between Japan and North America : International Hub Ports Focusing on Passage Time". Journal of Japan Institute of Navigation 123 (2010): 21–28. http://dx.doi.org/10.9749/jin.123.21.

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10

Li, Shang‐Jen. "Guihan Luo. Jin dai xi fang shi Hua sheng wu shi [History of Western Botanical and Zoological Studies in China]. (Zhongguo jin xian dai ke xue ji shu shi yan jiu cong shu.). 434 pp., illus., tables, bibl., index. Jinan: Shandong jiao yu chu ban she [Shandong Education Press], 2005. ¥46 (paper)." Isis 99, nr 2 (czerwiec 2008): 380–81. http://dx.doi.org/10.1086/591325.

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11

TAKEUCHI, Rei, i Hisayuki KUROKAWA. "A Study on Hub Port Strategy and Port Improvement in Japan Based on Characteristics of Container Transportation Network". Journal of Japan Institute of Navigation 129 (2013): 113–24. http://dx.doi.org/10.9749/jin.129.113.

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12

Fang, Li-Zhi. "Jiang Xiaoyuan ;, Wu Yan . Zijin shan tian wen tai shi gao: Zhongguo tian wen xue xian dai hua ge an. [History of Purplemountain Observatory.] (Zhongguo jin xian dai ke xue ji shu shi yan jiu cong shu.). 219 pp., tables, bibl., index. Jinan: Shandong jiao yu chu ban she [Shandong Education Press], 2004. 29 (paper)." Isis 99, nr 3 (wrzesień 2008): 645–46. http://dx.doi.org/10.1086/593267.

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13

Vicini, Stefano, Jian Feng Wang, Jin Hong Li, Wei Jian Zhu, Yue Hua Wang, Jian Hong Luo, Barry B. Wolfe i Dennis R. Grayson. "Functional and Pharmacological Differences Between RecombinantN-Methyl-d-Aspartate Receptors". Journal of Neurophysiology 79, nr 2 (1.02.1998): 555–66. http://dx.doi.org/10.1152/jn.1998.79.2.555.

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Vicini, Stefano, Jian Feng Wang, Jin Hong Li, Wei Jian Zhu, Yue Hua Wang, Jian Hong Luo, Barry B. Wolfe, and Dennis R. Grayson. Functional and pharmacological differences between recombinant N-methyl-d-aspartate receptors. J. Neurophysiol. 79: 555–566, 1998. N-methyl-d-aspartic acid (NMDA) receptors transiently transfected into mammalian HEK-293 cells were characterized with subunit-specific antibodies and electrophysiological recordings. Deactivation time course recorded in response to fastl-glutamate pulses were studied in isolated and lifted cells, as well as in outside-out membrane patches excised from cells expressing recombinant NR1 subunits in combination with the NR2A, NR2B, NR2C, or NR2D NMDA receptor subunits. Transfected cells were preidentified by the fluorescence emitted from the coexpressed Aequorea victoria jellyfish Green Lantern protein. Currents generated by NR1/NR2A channels displayed double exponential deactivation time course being faster than that in NR1/NR2B or NR1/NR2C channels. However, a large decay variability was observed within each cotransfection, suggesting that mechanisms additional to subunit composition may also regulate deactivation time course. NR1/NR2D channels displayed slowly deactivating currents. Channel deactivation was fast and comparable among receptors obtained by cotransfecting five distinct spliced variants of the NR1 subunit, each with the NR2A subunit. Additionally, recovery from desensitization was slower for NR1/NR2B than for NR1/NR2A channels. The average deactivation time course of responses to brief l-glutamate applications in cells where NR1/NR2A/NR2B cDNAs were cotransfected at variable ratio was intermediate between those of the NR1/NR2A and NR1/NR2B channels. Although immunocytochemical evidence indicates that the majority of cells are cotransfected by all plasmids in triple transfection, our experimental condition did not allow for a tight control of the expression of NMDA receptor subunits. This produced the result that many cells were characterized by deactivation time course and haloperidol sensitivities of separate NR1/NR2A and NR1/NR2B subunit heteromers. We also speculate on the possible formation of channels resulting from the coassembly in the same receptor of NR1/NR2A/NR2B subunits from a minority of cells that gave responses to brief application of l-glutamate characterized by slow deactivation time course and decreased haloperidol sensitivity.

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14

Lim, Myung Sun. "Traveling Speakers and the Intervening Local Public -Focusing on the yadam performance travelogues of Kim Jin-gu and Yoon Baek-nam-". Journal of Humanities 93 (31.05.2024): 151–81. http://dx.doi.org/10.31310/hum.093.05.

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15

Li, Huafang. "Jianxing Yu, Jun Zhou, and Hua Jiang, A Path for Chinese Civil Society: A Case Study on Industrial Associations in Wenzhou, China". Journal of Chinese Political Science 18, nr 4 (17.09.2013): 407–8. http://dx.doi.org/10.1007/s11366-013-9265-z.

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16

Liang, Yan, Jing Liu, Tao Luo, Jia Ge, Hao Tian, Guozhi Zhang, Linjun Fan i in. "Abstract P5-10-01: Phase 2 study of anlotinib combined with taxanes and lobaplatin in the neoadjuvant treatment of triple-negative breast cancer: efficacy, safety and biomarker analysis from the SWH-B006 (neoALTALL) trial". Cancer Research 83, nr 5_Supplement (1.03.2023): P5–10–01—P5–10–01. http://dx.doi.org/10.1158/1538-7445.sabcs22-p5-10-01.

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Abstract Background: Anlotinib, a novel multi-target tyrosine kinase inhibitor that effectively inhibits VEGFR, PDGFR, FGFR, c-KIT, c-MET, and RET, monotherapy has been proven effective in HER-2 negative metastatic breast cancer, but its efficacy in early-stage triple-negative breast cancer (TNBC) is unknown. This phase 2 study aims to evaluate the efficacy and safety of adding anlotinib to neoadjuvant chemotherapy in patients (pts) with primary TNBC. Methods: Pts with clinical stage II/III TNBC were to be treated with 5 cycles of anlotinib (12mg, d1-14, q3w) plus 6 cycles of taxanes (docetaxel 75 mg/m2 or nab-paclitaxel 125 mg/m2, d1 and d8, q3w) and lobaplatin (30 mg/m2, d1, q3w), followed by surgery. The primary endpoint was pathological complete response (pCR) in the breast and axilla (tpCR; ypT0/is ypN0) and the secondary endpoints include pCR in the breast (bpCR; ypT0/is), event-free survival (EFS), invasive disease-free survival (iDFS), overall survival (OS), and safety. Exploratory study included biomarker analysis and efficacy comparation based on FUSCC classification (IHC-based). Results: From Jan 2021 to Feb 2022, a total of 24 pts were enrolled. The median age was 50 years (range, 26-64), 54% were postmenopausal, 75% were nodal involved, 29% had stage III, and 79% were Ki-67 high (≥30%). At the data cut off time of 30th Jun 2022, all 24 pts received at least one dose of study treatment and underwent surgery. Overall, 21 pts received five courses of anlotinib. Two pts discontinued anlotinb for safety reason, and one pt discontinued anlotinb due to missed dose in cycle 4. After surgery, 14 out of 24 pts achieved a tpCR (58.3%; 95% CI, 36.6%–77.9%), and the bpCR rate was also 58.3% (14/24). Of the 18 pts with the node-positive disease at diagnosis, 15/18 (83.3%) became ypN0. Based on the FUSCC IHC-based subtypes, the tpCR rates were 66.7% (6/9) for BLIS subtype, 80% (4/5) for IM subtype and 0% (0/4) for LAR subtype, respectively. Next-generation sequencing revealed that the most commonly mutated genes in these pts were TP53 (19/21, 90.5%), MYC (7/21, 33.3%), BRCA1 (5/21, 23.8%), PIK3CA (4/21, 19.0%), BCL2L11 (4/21, 19.0%), and RB1 (3/21, 14.3%). Subgroup analysis showed that the tpCR were 71.4% (5/7) and 42.9% (6/14) in MYC-amplified and wild-type pts, respectively, and 80% (4/5) and 43.8% (7/16) in BRCA1-mutated and wild-type pts, respectively. All of 24 pts in the safety population showed at least one treatment emergent adverse events (TEAEs). Grade 3 or 4 TEAEs occurred in 14 pts (58.3%), and the most common events were leucopenia (29.2%; n=7), neutropenia (29.2%; n=7), thrombocytopenia (20.8%; n=5), anemia (16.7%; n=4), hypertension (12.5%; n=3), and oral mucositis (8.3%; n=2), respectively. No treatment-related deaths occurred. Conclusions: The addition of anlotinib to neoadjuvant chemotherapy showed manageable toxicity and promising antitumor activity for pts with early-stage TNBC. The study is still ongoing, and the enrollment has been completed. Clinical trial information: ChiCTR2100043027. Funding: Chia Tai Tianqing Pharmaceutical Group Co., Ltd. L. Corresponding author: Dr. Xiaowei Qi, qxw9908@foxmail.com. Department of Breast and Thyroid Surgery, Southwest Hospital, Army Medical University, Chongqing. Citation Format: Yan Liang, Jing Liu, Tao Luo, Jia Ge, Hao Tian, Guozhi Zhang, Linjun Fan, Lin Ren, Li Chen, Peng Tang, Kai Zhu, Xiuwu Bian, Jun Jiang, Yi Zhang, Xiaowei Qi, Peng Tang, Kai Zhu, Xiuwu Bian, Jun Jiang, Yi Zhang, Xiaowei Qi. Phase 2 study of anlotinib combined with taxanes and lobaplatin in the neoadjuvant treatment of triple-negative breast cancer: efficacy, safety and biomarker analysis from the SWH-B006 (neoALTALL) trial [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr P5-10-01.

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임경희 i Bak Gyung Yong. "Gender, Local and Oral Life History -The Case of Heo Gui-jin, born in 1923 year". Institute for Humanities and Social Sciences 16, nr 2 (maj 2015): 1–38. http://dx.doi.org/10.15818/ihss.2015.16.2.1.

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18

Yin, Yuxia. "Review of Hua & Jin (2012): Development of pragmatic and discourse skills in Chinese-speaking Children". International Journal of Chinese Linguistics 2, nr 1 (10.07.2015): 149–53. http://dx.doi.org/10.1075/ijchl.2.1.06yin.

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19

Kumar, Pradeep. "Jianxing Yu, Jun Zhou, and Hua Jiang: A Path for Chinese Civil Society: A Case Study on Industrial Associations in Wenzhou, China (2012)". VOLUNTAS: International Journal of Voluntary and Nonprofit Organizations 27, nr 5 (10.02.2015): 2536–38. http://dx.doi.org/10.1007/s11266-014-9455-0.

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Yeom, Jin Sup, i Jacob M. Buchowski. "Authors' Reply Re: “CT evaluation of occipitocervical joint violation by C1 lateral mass screw” by Jun-Song Yang, M.D; Hao Chen; Liang Yan, M.D; Peng Liu, M.D; Tuan-Jiang Liu, M.D; Da-Geng Huang, M.D; Ding-Jun Hao, M.D." Spine Journal 19, nr 11 (listopad 2019): 1903. http://dx.doi.org/10.1016/j.spinee.2019.07.007.

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21

Diyaljee, Vishnu. "Discussion of “New Model for Predicting Permanent Strain of Granular Materials in Embankment Subjected to Low Cyclic Loadings” by Wen-Bo Chen, Wei-Qiang Feng, Jian-Hua Yin, Jin-Miao Chen, Lalit Borana, and Ren-Peng Chen". Journal of Geotechnical and Geoenvironmental Engineering 147, nr 11 (listopad 2021): 07021026. http://dx.doi.org/10.1061/(asce)gt.1943-5606.0002656.

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Chen, Wen-Bo, Wei-Qiang Feng, Jian-Hua Yin, Jin-Miao Chen, Lalit Borana i Ren-Peng Chen. "Closure to “New Model for Predicting Permanent Strain of Granular Materials in Embankment Subjected to Low Cyclic Loadings” by Wen-Bo Chen, Wei-Qiang Feng, Jian-Hua Yin, Jin-Miao Chen, Lalit Borana, and Ren-Peng Chen". Journal of Geotechnical and Geoenvironmental Engineering 147, nr 11 (listopad 2021): 07021027. http://dx.doi.org/10.1061/(asce)gt.1943-5606.0002657.

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Jinyoung Kim. "A study of Wei-Jin mingshi and Buddhism in "Shishuoxinyu": With “Yin-hao” as the central figure". Journal of Chinese Cultural Studies ll, nr 15 (grudzień 2009): 289–303. http://dx.doi.org/10.18212/cccs.2009..15.017.

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정동매 i 김학철. "A Dilemma Choice between Slaughter and Redemption ― Comparative Analysis on Patriarchal Ideology of Yu Hua and Jin Yingxia". Journal of Chinese Language and Literature ll, nr 72 (grudzień 2015): 321–32. http://dx.doi.org/10.26586/chls.2015..72.013.

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Synthesis and Luminescence Property. "HUANG Jun,SHAO Zhi-meng,REN Yin-bao,ZHAO Qing-er,HONG Jia-dan,WANG Qian,DENG De-gang,YU Hua,XU Shi-qing". Chinese Journal of Luminescence 36, nr 10 (2015): 1126–31. http://dx.doi.org/10.3788/fgxb20153610.1126.

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Kim, HeyJung. "Pan-genre Approach to the Interpretation of the Rhythm of Bang, Jin-kwan Pansori and Heo, Heung-sik Changbon Shimchungga". Journal of Pansori 36 (31.10.2013): 7. http://dx.doi.org/10.18102/jp.2013.10.36.7.

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SHIBATA, Masatoshi, Masayoshi OTAKE, Seiko TSUCHIYA, Mikio CHIKYU, Atsushi HORIUCHI i Tatsuo KAWARASAKI. "Reproductive and Growth Performance in Jin Hua Pigs Cloned from Somatic Cell Nuclei and the Meat Quality of Their Offspring". Journal of Reproduction and Development 52, nr 5 (2006): 583–90. http://dx.doi.org/10.1262/jrd.18004.

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Duan, Feipeng, Yisheng Li, Meizhen Zhao, Tianyong Hu, Xinquan Pan, Yue Feng, Fang Ma, Shuqi Qiu i Yiqing Zheng. "Screening of Anti-Inflammatory Components of Qin Jin Hua Tan Tang by a Multivariate Statistical Analysis Approach for Spectrum-Effect Relationships". Journal of Analytical Methods in Chemistry 2021 (13.08.2021): 1–13. http://dx.doi.org/10.1155/2021/6348979.

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Qing Jin Hua Tan Tang (QJHTT) exerts therapeutic effects in patients with chronic obstructive pulmonary disease (COPD) by alleviating inflammation. However, the anti-inflammatory components of QJHTT have not yet been reported. Our study aimed to screen the active anti-inflammatory components of QJHTT using a multivariate statistical analysis approach for spectrum-effect relationships. Different polar fractions of QJHTT were prepared using ethanol, ethyl acetate, and n-butanol to analyze the phytochemical components. Phytochemical fingerprints were generated using ultrahigh-performance liquid chromatography. In total, 24 peaks were observed in ten batches of QJHTT extracts. The anti-inflammatory activity was evaluated using a xylene-induced ear-swelling mouse model. Additionally, the spectrum-effect relationship between the relative areas of the 24 peaks and pharmacological activity was investigated using multivariate statistical analysis. The potential anti-inflammatory ingredients obtained from the screening (multivariate statistical analysis) will be validated for their anti-inflammatory effects and mechanisms utilizing a lipopolysaccharide-induced macrophage inflammation model. QJHTT ethanol extract 1 exhibited good anti-inflammatory activity. Peaks 11, 12, 13, 14, and 16, which were closely correlated with anti-inflammatory activity, were identified as meranzin, baicalin, baicalein, chrysin-7-O-β-D-glucuronide, and wogonoside, respectively. The anti-inflammatory activities of meranzin, baicalin, baicalein, and wogonoside were verified in vitro. These four bioactive components significantly inhibited the secretion of inflammatory factors in the lipopolysaccharide-stimulated macrophage cell line. This research successfully screened the QJHTT anti-inflammatory active ingredient group. Meranzin, baicalin, baicalein, chrysin-7-O-β-D-glucuronide, and wogonoside were predicted to be the anti-inflammatory active ingredient groups of QJHTT.

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Ou, Chen. "Book review: Zhu Hua and Lixian Jin (Eds.), Development of pragmatic and discourse skills in Chinese-speaking children. Benjamins Current Topics, 60". First Language 35, nr 2 (31.03.2015): 184–86. http://dx.doi.org/10.1177/0142723715577462.

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Lu, Si, Yu Chen, Meiyu Fang, Zhengyun Zou, Di Wu, Zhiguo Luo, Jian Zhang i in. "Abstract CT208: Tebotelimab, a PD-1/LAG-3 bispecific antibody, in patients with untreated, unresectable, recurrent or metastatic, mucosal melanoma: An open-label, single-arm, Phase 1 study". Cancer Research 83, nr 8_Supplement (14.04.2023): CT208. http://dx.doi.org/10.1158/1538-7445.am2023-ct208.

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Abstract Background: Immune checkpoint inhibitors (CPIs) targeting PD-(L)1 have become a standard of care for untreated, advanced melanoma, but demonstrated limited efficacy in mucosal melanoma. Tebotelimab, also known as MGD013, is a PD-1/LAG-3 bispecific tetravalent DART® molecule with synergistic antitumor activity shown in preclinical studies. We conducted an open-label, single-arm, multi-cohort phase 1 study (NCT04653038) to assess the efficacy and safety of tebotelimab in melanoma patients (pts) including those with CPI-naïve mucosal melanoma. Methods: The CPI-naïve cohort of this study enrolled pts with unresectable, recurrent or metastatic, mucosal or acral melanoma who had received no systemic therapy. Tebotelimab 600 mg was administered intravenously once every two weeks. The primary endpoint was overall response rate (ORR) assessed by independent radiologic review committee (IRC) per RECIST v1.1 in the efficacy analysis set consisting of pts who received ≥1 dose of tebotelimab. A post-hoc sensitivity analysis was conducted in the IRC-response evaluable set consisting of pts with IRC-assessed target lesions in the efficacy analysis set who received ≥1 post-baseline tumor assessment by IRC or died within 13 weeks after first dose. Results are reported for mucosal melanoma. Results: At data cut-off (January 19, 2022), 25 pts with mucosal melanoma were enrolled (median age, 61 years; male, 40%; ECOG 1, 40%; TNM Stage IV, 92%; metastatic, 80%). LAG-3 expression level was ≥1% in seven (28%), <1% in 15 (60%), and unknown in three (12%). PD-L1 expression was positive (CPS≥1) in three (12%), negative (CPS<1) in 19 (76%), and unknown in three (12%). All pts received ≥1 dose of tebotelimab. In the efficacy analysis set (n=25), three, three, and four pts achieved complete response (CR), partial response (PR), and stable disease (SD), respectively, leading to a confirmed ORR of 24% (95% confidence interval [CI], 9-45), with median duration of response (DOR) not reached, and a disease control rate (DCR) of 40% (95% CI, 21-61). In the IRC-response evaluable set (n=20), three, three, and four pts achieved CR, PR, and SD, respectively, leading to a confirmed ORR of 30% (95% CI, 12-54), with median DOR not reached, and a DCR of 50% (95% CI, 27-73). Immune-related treatment-emergent adverse events occurred in 11 (44%) pts, most commonly, hypothyroidism (20%), hyperthyroidism (16%), and white blood cell count decreased (12%). Grade ≥3 and serious treatment-related adverse events (TRAEs) were reported in three (12%) and four (16%) pts, respectively. TRAEs led to treatment discontinuation and death each in one (4%). Conclusions: Tebotelimab demonstrated preliminary but promising antitumor activity and a tolerable safety profile in pts with untreated, unresectable, recurrent or metastatic, mucosal melanoma. Citation Format: Si Lu, Yu Chen, Meiyu Fang, Zhengyun Zou, Di Wu, Zhiguo Luo, Jian Zhang, Jing Chen, Gang Huang, Hongming Pan, Xiubao Ren, Ying Cheng, Haichuan Su, Yuan Xin, Qiong Hua, Jianmei Hou, Jun Guo. Tebotelimab, a PD-1/LAG-3 bispecific antibody, in patients with untreated, unresectable, recurrent or metastatic, mucosal melanoma: An open-label, single-arm, Phase 1 study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 2 (Clinical Trials and Late-Breaking Research); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(8_Suppl):Abstract nr CT208.

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Zheng, Yinan, Olugbenga Silas, Jonah Musa, Yishu Qu, Tao Gao, Kyeezu Kim, Brian Joyce i in. "Abstract 3021: Epigenetic signatures of virus-associated cervical cancer in women living with HIV". Cancer Research 83, nr 7_Supplement (4.04.2023): 3021. http://dx.doi.org/10.1158/1538-7445.am2023-3021.

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Abstract Background: Low- and middle-income countries are facing a high health burden of cervical cancer (CC). The situation is worsened by a high prevalence of human immunodeficiency virus (HIV). We aim to identify epigenetic signatures to help understand the virus-associated pathways underlying CC development, which is fundamental to developing effective CC screening tools or therapeutic approaches for women living with HIV. Methods: We recruited a total of 365 Nigerian women with mean age of 52 (239 HIV+ and 126 HIV-; 98 without CC, 106 with cervical lesions, and 161 with CC). DNA methylation profiling in cervical tissue samples was performed using Illumina EPIC array covering over 860K methylation sites. The epigenetic signatures were identified among HIV+ women through epigenome-wide association study comparing CC vs. CC-free (Bonferroni adjusted p <0.05), which were further validated by comparing: 1) pairs of tumor and adjacent normal samples; and 2) pairs of cervical lesions and adjacent normal samples. The comparisons were adjusted for age, BMI, education, employment, parity, study site, and technical batch variables. We then compared the identified signatures between HIV+ and HIV- among CC women to delineate the role of HIV. We constructed a methylation risk score (MRS) using the signatures, and we performed receiver operating characteristic (ROC) analysis to evaluate the performance of distinguishing across cancer statuses (CC, cervical lesions, CC-free). Results: We identified 46 differentially methylated markers (p-value ranging from 5.7e-8 to 2.4e-19) in HIV+ CC women. The effect sizes among the 46 markers in the paired tumor-normal analysis and the paired lesion-normal analysis were highly correlated with the CC vs. CC-free analysis (r=0.99 and r=0.95, respectively) with smaller magnitudes (1.8 and 4.3 times smaller, respectively). Gene ontology and Reactome pathway enrichment analysis revealed that these 46 markers were enriched in genes involving activation of PI3K/AKT/mTOR signaling network (e.g., RPTOR, HDAC3, MAPKAP1), which plays a crucial role in virus/host crosstalk and virus-induced carcinogenesis. The PI3K/AKT/mTOR signaling cascade suppressors, including gene PRDM8, were silenced by promoter hypermethylation among HIV+ CC women (p=4.3e-12). These epigenetic changes, however, were not observed in CC women without HIV. In an independent dataset, MRS was the lowest in women without CC (2.3±2.1), followed by women with cervical lesions (4.9±1.1), and the highest in CC women (9.6±3.9) (p-trend < 2e-16). The MRS achieved areas under the ROC curve = 0.93 and 0.88 in distinguishing CC and cervical lesions from CC-free among HIV+ women, respectively. Conclusion: HIV may communicate with cervical cells and promote CC through epigenetic activation of PI3K/AKT/mTOR signaling pathway. Our epigenetic signatures may serve as novel biomarkers for CC early detection and treatment for women living with HIV. Citation Format: Yinan Zheng, Olugbenga Silas, Jonah Musa, Yishu Qu, Tao Gao, Kyeezu Kim, Brian Joyce, Jun Wang, Demirkan Gursel, Abdulkareem Fatimah, Godwin Imade, Alani Akanmu, Jian-Jun Wei, Masha Kocherginsky, Kwang-Youn Kim, Firas Wehbe, Chad Achenbach, Rose Anorlu, Melissa Simon, Atiene Sagay, Folasade Ogunsola, Robert Murphy, Lifang Hou. Epigenetic signatures of virus-associated cervical cancer in women living with HIV [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3021.

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지준호. "A Study on the differentiation and development aspects of Zhu-zi xue - centering around the connection between Huang Gan and Jin-hua school in Yuan period". JOURNAL OF KOREAN PHILOSOPHICAL HISTORY ll, nr 23 (marzec 2008): 317–47. http://dx.doi.org/10.35504/kph.2008..23.011.

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TSYRENOV, Chinggis, i NYAMDAG Ganbat. "TO THE QUESTION OF JURCHEN POSTAL STATIONS DURING THE HOU JIN DYNASTY (BASED ON THE MATERIALS OF THE CHRONICLES «ANCHUN GURUN» AND «DAI QING TAIZU SHILU»)". Culture of Central Asia: written sources 11, nr 2 (17.12.2018): 161–69. http://dx.doi.org/10.30792/2304-1838-2018-2-161-169.

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Shieh, Shawn. "A Path for Chinese Civil Society: A Case Study on Industrial Associations in Wenzhou, China. By Jianxing Yu, Jun Zhou, and Hua Jiang. Lanham, Md.: Lexington Books, 2012. xi, 212 pp. $65.00 (cloth); $64.99 (ebook)." Journal of Asian Studies 72, nr 2 (maj 2013): 464–65. http://dx.doi.org/10.1017/s0021911813000259.

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Shi, Qiyun, Juncheng Xuhong, Hao Tian, Yi Zhang, Jun Jiang i Xiaowei Qi. "Abstract P5-02-52: Predictive and prognosis value of PIK3CA mutations in HER2-positive breast cancer treated with tyrosine kinase inhibitors (TKIs): a systemic review and meta-analysis". Cancer Research 83, nr 5_Supplement (1.03.2023): P5–02–52—P5–02–52. http://dx.doi.org/10.1158/1538-7445.sabcs22-p5-02-52.

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Abstract Background: PIK3CA mutations is one of the most frequent gene alterations in breast cancers, which was reported to be related to the treatment response of anti-HER2 regimens. However, the relationship between PIK3CA mutations and treatment response of a tyrosine kinase inhibitors (TKIs) is still unclear. We thus conducted a systemic review and meta-analysis to investigate the predictive and prognosis value of PIK3CA mutations in HER2-positive breast cancer treated with TKIs. Methods: The following databases were searched from inception to July 2022: Medline, Embase and the Cochrane Library. Abstracts from conferences were also reviewed for inclusion. The critical information was extracted from eligible studies. Results: A total of 16 reports including 17 studies were assessed for eligibility, enrolling 1706 patients. Ten studies including 902 patients were in the neoadjuvant setting, the pCR rate is significantly higher in PIK3CA wild-type (WT) patients than in mutated-type (MT) patients (OR = 0.45; 95% CI: 0.31-0.65; P< 0.001). Seven studies including 804 patients were in the metastatic setting, the pooled objective response rate (ORR) is significantly higher in PIK3CA WT patients than in MT patients (OR = 0.40; 95% CI: 0.23-0.70; P = 0.001), and similarly, the clinical benefit rate (CBR) in WT patients is also higher (OR = 0.43; 95% CI: 0.19-0.98; P=0.045). A total of 4 metastasis studies reported progression free survival (PFS), and 2 of them reported overall survival (OS), revealing a marginally significant relationship between PIK3CA mutation and worse PFS (HR = 0.82; 95% CI: 0.67-1.00; P=0.052) and OS (HR=0.63, 95%CI:0.39-1.02; P=0.062). No evidence of publication bias was found in both the neoadjuvant setting and metastatic setting. Conclusion: Our findings indicate that PIK3CA mutations is significantly associated with a lower rate of pCR when treated with TKI-containing regimens in neoadjuvant chemotherapy of early-stage HER2-positive breast cancer, and is significantly associated with lower ORR and CBR in metastatic HER2-positive breast cancer. Citation Format: Qiyun Shi, Juncheng Xuhong, Hao Tian, Yi Zhang, Jun Jiang, Xiaowei Qi. Predictive and prognosis value of PIK3CA mutations in HER2-positive breast cancer treated with tyrosine kinase inhibitors (TKIs): a systemic review and meta-analysis [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr P5-02-52.

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Li, Jun, Chengshan Niu, Zhongwei Guo, Huan Wang, Bailu Zheng, Yuge Dou, Apeng Liang i in. "Abstract 4488: TY-4028: a novel, targeted therapy for non small-cell lung cancer with EGFR exon 20 or HER2 exon 20 insertion mutations". Cancer Research 83, nr 7_Supplement (4.04.2023): 4488. http://dx.doi.org/10.1158/1538-7445.am2023-4488.

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Abstract Epidermal growth factor receptor (EGFR) activating mutations represent major drivers to the development of non-small cell lung cancer (NSCLC). Among the oncogenic EGFR mutations, a significant cohort, counting for approximately 4-10% of the EGFR mutation spectrum, bear EGFR exon 20ins mutations. Meanwhile, approximately 2% of NSCLC patients bear hotspot mutations in HER2. Strikingly, over 90% of the HER2 mutations occurred in NSCLC are identified as exon 20ins mutations. Despite the successful launch of 1st, 2nd, and 3rd generation of EGFR inhibitory agents in the clinic that inactivate oncogenic EGFR signaling through targeting specific EGFR mutations, de novo or acquired, none of these standard-of-care therapies is specific to EGFR exon 20ins or HER2 exon 20ins. In addition, trastuzumab and EGFR-TKIs have limited effectiveness for NSCLC patients with HER2 exon 20ins mutation. TAK-788 (mobocertinib) and JNJ6372 (amivantamab-vmjw) are the FDA approvals for NSCLC driven by EGFR exon 20ins mutations. Only T-Dxd is used as a second-line treatment for NSCLC patients with HER2 mutation. Considering the large population of lung cancer and the fact that many patients are missed in diagnosis due to the heterogeneous characteristics of EGFR and Her2 exon 20ins, there are probably more than ten thousand lung cancer patients suffering the EGFR or Her2 exon 20ins mutations. There are urgent unmet medical needs to develop target therapeutics for EGFR and Her2 exon 20ins mutations. We discovered and developed TY-4028, which is a novel, potent, and orally available inhibitor targeting EGFR and Her2 exon 20ins mutations and is currently in the IND enabling stage. In EGFR-related tumor cells and genetically engineered Ba/F3 cell lines, TY-4028 showed similar or better antitumor effects than TAK-788, and better antitumor effects than DZD9008. The B/P ratio (brain tissue AUC0-last/plasma AUC0-last) of SD rats was 1.63 and 1.04 respectively after oral administration of TY-4028 in male and female SD rats, which suggested that TY-4028 had good potential to cross Blood Brain Barrier (BBB). Preclinical studies showed a good PK profile and manageable toxicity with TY-4028. TY-4028 has remarkable efficacy in mouse models of EGFR exon 20ins and HER2 exon 20ins. The data showed that all doses of TY-4028 had significant effects, and the tumors nearly demonstrated complete regression in the PDX LU0387 model and PC9 CDX model. At the same dose, the efficacy of TY-4028 was similar to that of TAK-788, while the tolerance of TY-4028 was better than that of TAK-788. At the same dose, the efficacy of TY-4028 was better than that of DZD9008. Taken together, the data demonstrated TY-4028 has great potential to meet the unmet medical needs for NSCLC patients with EGFR exon 20ins mutation or HER2 exon 20ins mutation. #Jun Li and Chengshan Niu contributed equally to this work. *They are the correspondent authors. Citation Format: Jun Li, Chengshan Niu, Zhongwei Guo, Huan Wang, Bailu Zheng, Yuge Dou, Apeng Liang, Kaige Ji, Shengli Dong, Meihua Li, Yanchao Zhao, Yazhen Zhang, Aishen Gong, Hao Liu, Xinmiao Hu, Hui Su, Mingyu Jiang, Shaoqing Chen, Xiugui Chen, Yusheng Wu. TY-4028: a novel, targeted therapy for non small-cell lung cancer with EGFR exon 20 or HER2 exon 20 insertion mutations. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 4488.

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Kim, Kyeezu, Yinan Zheng, Claudia Hawkins, Edith Okeke, Olufunmilayo Lesi, Yishu Qu, Lewis R. Roberts i in. "Abstract 6013: DNA methylation-based inflammation score is associated with hepatocellular carcinoma among people living with HIV". Cancer Research 83, nr 7_Supplement (4.04.2023): 6013. http://dx.doi.org/10.1158/1538-7445.am2023-6013.

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Abstract Background: Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide. In countries with high human immunodeficiency virus (HIV) prevalence, such as Nigeria, HIV-associated HCC causes a great health burden due to its early onset, late diagnosis, and poorer prognosis. HIV infection is involved in inflammation of the liver, which may determine an increased risk of hepatocyte neoplastic transformation. Inflammation-related DNA methylation signatures obtained in liquid biopsy, such as circulating cell-free DNA (ccfDNA) extracted from serum/plasma are promising minimally-invasive biomarkers that may inform HCC among people living with HIV. Methods: A total of 289 Nigerian participants with information on ccfDNA and other covariates were included. Participants were classified into three groups by their HCC/HIV status: 1) HCC+/HIV+ (n=28); 2) HCC-/HIV+ (n=185); and 3) HCC+/HIV- (n=76). We constructed ccfDNA methylation inflammation scores using 49 CpGs previously linked to circulating C-reactive protein (CRP) concentrations, and higher scores represented elevated CRP concentrations with lower methylation levels. To compare the ccfDNA methylation inflammation score across the groups, we performed multivariable logistic regression analyses adjusting for age, sex, alcohol consumption, smoking status, body mass index, study sites, and technical variables. Results: Participants with HCC+/HIV+ presented the highest ccfDNA methylation inflammation scores (mean=-0.03, standard deviation [SD] =0.01). Participants with HCC-/HIV+ presented the lowest scores (mean=-0.05, SD=0.01). In the multivariable logistic regressions, one SD increase of inflammation score was associated with 2.5 times higher odds of having HCC among HIV-infected participants (HCC+/HIV+ vs. HCC+/HIV-; OR=2.56, 95% CI=1.39-4.73, P=0.002). No evidence was found for the association between the inflammation score and HIV status among HCC patients (HCC+/HIV+ vs. HCC+/HIV-; OR=1.00, 95% CI=0.59-1.70, P=0.991). In the secondary analysis comparing HCC+ vs. HCC- adjusting for HIV status, one SD increase of inflammation score was associated with 3.2 times higher odds of having HCC (OR=3.22, 95% CI=1.39-7.46, P=0.006). Conclusions: We observed that ccfDNA methylation inflammation score is associated with HCC status among people with HIV. Our findings suggest that ccfDNA methylation-based inflammatory profiles may serve as a potential biomarker for early detection and risk stratification of HCC in resource-constrained countries with a high prevalence of HIV. Citation Format: Kyeezu Kim, Yinan Zheng, Claudia Hawkins, Edith Okeke, Olufunmilayo Lesi, Yishu Qu, Lewis R. Roberts, Demirkan Gursel, Fatimah B. Abdulkareem, Alani Akanmu, Godwin Imade, Jian-Jun Wei, Masha Kocherginsky, Kwang-Youn Kim, Wasiu L. Adeyemo, Firas Wehbe, Chad J. Achenbach, Atiene Sagay, Folasade T. Ogunsola, Robert L. Murphy, Lifang Hou. DNA methylation-based inflammation score is associated with hepatocellular carcinoma among people living with HIV. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 6013.

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Wang, Lingna, i Yongqing Zhang. "Quality Analysis and High-Performance Liquid Chromatographic Fingerprint Analysis of New Cultivated Kind of <i>Lonicerae japonicae</i> Flos “Hua Jin 6” from Different Harvest Times". Chinese Medicine 08, nr 01 (2017): 18–32. http://dx.doi.org/10.4236/cm.2017.81003.

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Hou, Ruida, Ying Yu, Jun Yang i Jianxiong Jiang. "Abstract 4923: Prostaglandin E2 receptor EP2: A novel target for high-risk neuroblastoma". Cancer Research 83, nr 7_Supplement (4.04.2023): 4923. http://dx.doi.org/10.1158/1538-7445.am2023-4923.

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Abstract Neuroblastoma (NB) is the most common pediatric extracranial solid tumor. Based on tumor stage and histological features, 50% of NBs are classified as high-risk diseases, a subtype characterized by a quite unsatisfactory long-term survival even with the striking advances in NB management that have been achieved in the past decades. Cyclooxygenase-2/prostaglandin E2 (COX-2/PGE2) cascade has been reported to foster a proinflammatory tumor-nourishing microenvironment in NB. However, the specific downstream PGE2 receptor (EP) subtype which directly mediates this tumor promoting effect remains elusive. Therefore, in our research, we aim to 1) elucidate the culprit EP receptor that is directly involved in NB development; 2) evaluate the feasibility of inhibiting the PGE2 receptor subtype as a novel treatment strategy for high-risk NB. To start with, we analyzed the gene expression profiles of the COX2/PGE2/EP pathway from four major NB datasets (Versteeg, Kocak, SEQC, and NRC) on R2 platform. It indicates that the COX-2/PGE2/EP2 signaling axis is highly associated with the expression of high-risk NB markers, as well as an abysmal overall survival rate. Moreover, a time resolved fluorescence resonance energy transfer (TR-FRET) method was adopted to reveal that EP2 receptor is the key Gαs-coupled receptor that mediates PGE2-initiated cAMP signaling in high-risk NB cell lines. Genetic interference of EP2 receptor expression by CRISPR/Cas9-mediated genome editing and doxycycline induced conditional knockdown significantly inhibited high-risk NB development and progression both in neuro-sphere formation assay and in nude mice xenograft models. Finally, we tested the anti-NB efficacy of our recently developed selective and bioavailable small-molecule EP2 antagonists. With a consecutive treatment of three weeks, decreased tumor size and weight have been observed in both high-risk NB xenograft model and immunocompetent allograft model, simultaneously with decreased inflammation, angiogenesis, and enhanced apoptosis. Collectively, our results suggest that the PGE2/EP2 pathway contributes to the growth and malignant potential of high-risk NB; pharmacological inhibition on EP2 receptor by our drug-like compounds might provide a novel therapeutic strategy for this deadly pediatric cancer. Citation Format: Ruida Hou, Ying Yu, Jun Yang, Jianxiong Jiang. Prostaglandin E2 receptor EP2: A novel target for high-risk neuroblastoma. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 4923.

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Zhou, Jun, Li Hua, Jian Feng, Ning Bao, Dan Zhang, Jingjing Wang, Marrit Putker i Ludovic Bourre. "Abstract 1942: Characterization of a panel of CRISPR/Cas9 engineered KRAS G12C inhibitor-resistant tumor models". Cancer Research 84, nr 6_Supplement (22.03.2024): 1942. http://dx.doi.org/10.1158/1538-7445.am2024-1942.

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Abstract Introduction: KRAS is one of the most frequent mutated oncogenes and has been recognized as undruggable for many years. AMG510, the first therapy to directly target KRAS, was approved by the FDA to treat non-small cell lung cancer (NSCLC) bearing KRAS G12C mutation. However, the emergence of resistance in patients remains a challenge and limits its clinical benefits, which calls for next-generation targeted therapy or combination strategies to overcome the resistance to KRAS G12C inhibitors. A variety of secondary mutations in KRAS attributing to the resistance have been identified, which requires robust in vitro and in vivo preclinical models to validate potential therapeutics targeting these mutations. Therefore, we generated a panel of KRAS G12C inhibitor-resistant tumor models to facilitate the development of possible strategies to overcome such resistance. Methods: First, a secondary KRAS mutation, including H95D, H95Q, H95R, Q61H and R68S, was introduced by using CRISPR/Cas9 technology in MIA PaCa cell line, which harbors a homozygous KRAS G12C mutation in addition to Y96D, Y96C and Y96S previously published by us. Point mutation knock-in was validated by sanger sequencing, and cell identity was confirmed by SNP assay. In vitro, the parental and mutated cells were treated with either AMG510 and MRTX849 and cell viability was measured by CellTiter-Glo. In vivo efficacy of KRAS G12C inhibitors, AMG510 and MRTX849, SOS1 inhibitor, BI-3406 and MEK inhibitor, Trametinib were evaluated in the Y96D mutated MIA PaCa subcutaneous xenograft. Results: Homozygous secondary point mutation knock-in in MIA PaCa cells was confirmed by sanger sequencing. Similar growth rate and morphology was observed in selected clones compared to the parental line. Similar to Y96D mutation previously published, R68S mutation was highly resistant to both KRAS G12C inhibitors, with IC50 increased more than 100 fold for both MRTX849 and AMG510, whereas H95D, H95Q and H95R mutation was more resistant to MRTX849, while Q61H had a minimal effect on either one of the inhibitors. In addition, cells expressing KRAS G12C/Y96D were also resistant to AMG510 and MRTX849 in in vivo study, whereas combination of BI-3406 (single treatment: TGI of 27%) and Trametinib (single treatment: TGI of 76%) suppressed tumor growth significantly with TGI of 93% on day 17 after randomization compared to control group (p<0.001). Also, the combination showed significant improvement compared to BI-3406 single treatment (p<0.001) whereas no significant improvement was observed compared to Trametinib single treatment (p>0.05). Conclusion: CRISPR/Cas9 engineered second site KRAS mutations in cells harboring KRAS G12C mutation displayed a differentially resistant profile to KRAS G12C inhibitors. Thus, H95D/Q/R, R68S and Y96D can be used as preclinical inhibitor-resistant models to evaluate clinical strategies to overcome resistance to KRAS-targeted therapies. Citation Format: Jun Zhou, Li Hua, Jian Feng, Ning Bao, Dan Zhang, Jingjing Wang, Marrit Putker, Ludovic Bourre. Characterization of a panel of CRISPR/Cas9 engineered KRAS G12C inhibitor-resistant tumor models [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 1942.

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Zhu, Xiu-Zhi, Yi-Fan Zhou, Yun-Yi Wang, Xiao-Hong Ding, Xi Jin, Zhi-Ming Shao, Yi-Zhou Jiang i Zhong-Hua Wang. "Abstract PO1-15-08: Genomic characterization of triple-negative breast cancer metastases reveals PKD1 as a novel biomarker for immunotherapy". Cancer Research 84, nr 9_Supplement (2.05.2024): PO1–15–08—PO1–15–08. http://dx.doi.org/10.1158/1538-7445.sabcs23-po1-15-08.

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Abstract Background: While primary triple-negative breast cancer (TNBC) garners significant research attention, the genomic alterations that occur in metastasis remain insufficiently understood, especially within Asian populations. Furthermore, the genomic information obtained from the primary tumor inadequately guides metastatic cancer treatment, highlighting the critical need for in-depth investigations into metastatic TNBC. Methods: We constructed the largest cohort of TNBC metastases (n = 296) among advanced TNBC patients treated at Fudan University Shanghai Cancer Center (FUSCC) between October 2018 and December 2020. Comprehensive DNA sequencing was conducted on the collected metastatic samples to analyze genomic alterations associated with treatment response. The underlying mechanisms of specific biomarkers were also explored. Results: We presented the genomic landscape of 296 TNBC metastases, encompassing mutant genes, mutation sites and copy number variations. Through multidimensional analysis, significant disparities in TNBC were observed between Western and Asian populations, primary and metastatic tumors, as well as different metastatic sites. Notably, our findings underscore the importance of sequencing TNBC metastases to guide precision therapy, which was associated with longer progression-free survival compared to physician-chosen treatments, shedding light on the pivotal clinical value of genomic studies in metastatic settings. Furthermore, efficacy analysis suggested that PKD1 mutations enriched in metastases mediated resistance to immunotherapy. These findings were further validated through three clinical trials (NCT03805399, NCT04129996, and NCT04395989). Mechanistic studies unveiled the involvement of PKD1 in TNBC immune evasion by upregulating CCL2, thereby facilitating the recruitment of M2-type tumor-associated macrophages. Conclusion: Our study emphasizes the critical significance and necessity of genomic profiling of metastases in guiding precision therapy for TNBC. Moreover, our findings reveal PKD1 as a novel and promising biomarker for immunotherapy. Citation Format: Xiu-Zhi Zhu, Yi-Fan Zhou, Yun-Yi Wang, Xiao-Hong Ding, Xi Jin, Zhi-Ming Shao, Yi-Zhou Jiang, Zhong-Hua Wang. Genomic characterization of triple-negative breast cancer metastases reveals PKD1 as a novel biomarker for immunotherapy [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO1-15-08.

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SUWANNAPOOM, CHATMONGKON, ZHI-YONG YUAN, JIN-MIN CHEN, MIAN HOU, HAI-PENG ZHAO, LI-JUN WANG, TRUONG SON NGUYEN i in. "Erratum: CHATMONGKON SUWANNAPOOM, ZHI-YONG YUAN, JIN-MIN CHEN, MIAN HOU, HAI-PENG ZHAO, LI-JUN WANG, TRUONG SON NGUYEN, TRUONG Q. NGUYEN, ROBERT W. MURPHY, JAQUELINE SULLIVAN, DAVID S. MCLEOD & JING CHE (2016) Taxonomic revision of the Chinese Limnonectes (Anura, Dicroglossidae) with the description of a new species from China and Myanmar. Zootaxa, 4093: 181–200." Zootaxa 4137, nr 4 (13.07.2016): 599. http://dx.doi.org/10.11646/zootaxa.4137.4.13.

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Li, Zhiping, Xuanmao Jiao, Gordon Robertson, Gabriele Di Sante, Anthony W. Ashton, Agnese DiRocco, Min Wang i in. "Abstract 2598: The DACH1 gene is frequently deleted in prostate cancer, restrains prostatic intraepithelial neoplasia, augments DNA damage repair and predicts therapy responses". Cancer Research 83, nr 7_Supplement (4.04.2023): 2598. http://dx.doi.org/10.1158/1538-7445.am2023-2598.

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Abstract Background: Prostate cancer (PCa), the second leading cause of death in American men, includes distinct genetic subtypes with distinct therapeutic vulnerabilities. The DACH1 gene encodes a winged helix/Forkhead DNA-binding protein that competes for binding to FOXM1 sites. Methods: Analysis of DACH1 gene deletion and gene expression was conducted from public data bases and human prostate cancer samples. Transgenic mice were generated in which the Dach1 gene was deleted in the prostate of prostate Oncomice. Cells derived from Dach1 gene deletion mice and human prostate cancer cell lines with Dach1 knockdown were analyzed for DNA damage repair responses. Results: DACH1 gene deletion within the 13q21.31-q21.33 region, occurred in up to 18% of human PCa, and was associated with increased AR activity, and poor prognosis. DACH1 homozygous deletions more frequent in the metastatic site than in the primary tumors (Mich: 10% vs. 18%, N=59; FHCRC: 4% vs.11%, N= 54, SU2C: not profiled vs. 3.3, N=150). The prevalence of DACH1 heterozygous deletions was higher in the metastatic lesions than in primary tumors within a given cohort for three of six cohorts (Mich: 27.3% vs. 36%, N=59; FHCRC: 15% vs. 59%, N=54; SU2C: 0% vs. 26%, N=150, respectively). The patients with homozygous DACH1 deletions had reduced overall survival (medians of 84 vs. 120 months, N=667, log rank test P=9.3x10-3). Low DACH1 gene expression (expressed as a z-score with a z-score threshold of -1.25) was significantly correlated with earlier biochemical recurrence (BCR, log rank p value = 4.7x10-4, n=79). In prostate OncoMice, prostate-specific deletion of the Dach1 gene enhanced prostatic intraepithelial neoplasia (PIN) and was associated with increased DNA damage. Reduced Dach1 increased DNA damage in responses to genotoxic stresses. DACH1 was recruited to sites of DNA damage, augmenting recruitment of Ku70/Ku80. Reduced Dach1 expression was associated with resistance to TGFβ kinase and PARP inhibitors. Conclusions: Reduced Dach1 expression may define a subclass of PCa that warrants specific therapies. Citation Format: Zhiping Li, Xuanmao Jiao, Gordon Robertson, Gabriele Di Sante, Anthony W. Ashton, Agnese DiRocco, Min Wang, Jun Zhao, Sankar Addya, Chenguang Wang, Peter A. McCue, Andrew P. South, Carlos Cordon-Cardo, Runzhi Liu, Kishan Patel, Rasha Hamid, Jorim Parmar, James B. DuHadaway, Nikolaus Schultz, Andrew Kossenkov, Lai Yee Phoon, Hao Chen, Li Lan, Yunguang Sun, Kenneth A. Iczkowski, Hallgeir Rui, Richard G. Pestell. The DACH1 gene is frequently deleted in prostate cancer, restrains prostatic intraepithelial neoplasia, augments DNA damage repair and predicts therapy responses [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2598.

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Zhong, Siyu, Peter Holtappels i Roland Dittmeyer. "Simultaneous Operability of Thermocatalytic and Electrocatalytic CO2 Reduction Reactions". ECS Meeting Abstracts MA2023-01, nr 49 (28.08.2023): 2559. http://dx.doi.org/10.1149/ma2023-01492559mtgabs.

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The direct electrochemical reduction reaction of carbon dioxide (eCO2RR) captured from the ambient air into base chemicals and fuels holds great potential for an elegant implementation of a net-zero emission carbon cycle. This assumes that the energy used to drive the capturing and conversion process is largely free of carbon dioxide emissions, i.e., from renewables such as wind and photovoltaics. Moreover, high Faradaic efficiency for the desired products at sufficiently high current density in eCO2RR has to be demonstrated to compete with more conventional multi-step Power-to-X conversion schemes both in terms of overall energy efficiency and cost.[1] eCO2RR is known for its wide variety of products.[2] However, hydrogen evolution reaction (HER), which is more thermodynamically reactive, inevitably seizes protons and electrons in the cathode. In addition, the reaction pathway of C2+ products is more complex than that of C1 products because it is strongly dependent on the catalyst surface and electrocatalytic operating conditions. For example, the formation of C-C bonds is interfered with the formation of C-H and C-O bonds on the catalyst surface, resulting in the direct generation of multi-carbon products technically challenging.[3] Due to these kinetic barriers, the C2+ products show much lower the energy efficiency, Faraday efficiency, and partial reduction current density of than those of the C1 products. The mechanistic aspects of the reaction pathways for the various C2+ products have not been fully deciphered, which ultimately limits the commercial application of eCO2RR conversion to C2+ products.[4] Noting that industrial thermocatalytic processes produce and supply long-chain hydrocarbons in a long-term stable manner, we propose the production of C2+ products by combining simultaneous thermocatalysis and electrocatalysis. In the ongoing work, hydrogen from the water electrolysis is further converted to syngas via a reverse water-gas shift reaction (rWGS), followed by an established conversion route to fuels and chemicals such as Fischer-Tropsch or methanol synthesis and methanol to olefins, gasoline or jet fuel.[5] Here, a reactor and test bench capable of operating at 20 bar and 200 degrees Celsius have been fabricated to enable simultaneous thermocatalytic and electrocatalytic production of C2+ products. Furthermore, different catalysts can be employed to explore the catalytic processes on the catalyst surface. References [1] H. Shin, K.U. Hansen, F. Jiao, Techno-economic assessment of low-temperature carbon dioxide electrolysis, Nature Sustainability 4 (2021) 911-919. [2] J. Chen, T. Wang, Z. Li, B. Yang, Q. Zhang, L. Lei, P. Feng, Y. Hou, Recent progress and perspective of electrochemical CO2 reduction towards C2-C5 products over non-precious metal heterogeneous electrocatalysts, Nano Research 14 (2021) 3188-3207. [3] K.D. Yang, C.W. Lee, K. Jin, S.W. Im, K.T. Nam, Current status and bioinspired perspective of electrochemical conversion of co2 to a long-chain hydrocarbon, J Phys Chem Lett 8 (2017) 538-545. [4] Y. Zheng, A. Vasileff, X. Zhou, Y. Jiao, M. Jaroniec, S.Z. Qiao, Understanding the roadmap for electrochemical reduction of co2 to multi-carbon oxygenates and hydrocarbons on copper-based catalysts, J Am Chem Soc 141 (2019) 7646-7659. [5] H. Kirsch, U. Sommer, P. Pfeifer, R. Dittmeyer, Power-to-fuel conversion based on reverse water-gas-shift, Fischer-Tropsch Synthesis and Hydrocracking: Mathematical modeling and simulation in Matlab/Simulink, Chemical Engineering Science 227 (2020) 115930.

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Xia, Qi-Dong, Yao-Bing Chen, Jian-Xuan Sun, Chen-Qian Liu, Jin-Zhou Xu, Zhi-Peng Yao, Ye An i in. "Abstract 2127: TERT C228T and KDM6A alterations are potential predictive biomarkers in non-muscle-invasive bladder cancer treated with intravesical Bacillus Calmette-Guérin instillation". Cancer Research 83, nr 7_Supplement (4.04.2023): 2127. http://dx.doi.org/10.1158/1538-7445.am2023-2127.

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Abstract Introduction: Bacillus Calmette-Guérin (BCG) is the standard of care for high-risk non-muscle-invasive bladder cancer (NMIBC) following transurethral resection. However, patients often have heterogeneous responses. Even among those who initially respond well to BCG, 10-20% relapse. Identification of reliable biomarkers predicting the efficacy of BCG remains an unmet need. En bloc resection is a novel technique representing a substantial advancement in the surgical management of NMIBC. We sought to investigate genomic and tumor microenvironmental (TME) profiles in NMIBC and explore potential predictive markers for BCG treatment following en-block resection. Methods: A total of 40 patients with high-risk NMIBC (cTis-T1N0M0) were retrospectively enrolled who underwent en bloc resection followed by BCG instillation. Surgical samples were subjected to NGS sequencing using a 520-gene panel (Burning Rock Biotech, Guangzhou) and multiplex immunofluorescence (mIF) assay. Results: The cohort had a median age of 63 years, and 80% were male. After a median follow-up of 21.8 months, 19/40 patients relapsed with a one-year relapse-free survival (RFS) rate of 57.5%. All tumors were microsatellite stable and showed a median TMB of 7.98muts/Mb. Genomic profiling revealed a high prevalence of alterations in TERT (55%), KDM6A (32.5%), KMT2D (32.5%), FGFR3(30%), PIK3CA (30%), TP53(27.5%), KMT2C (25%), and ARID1A (20%). TME analysis showed higher proportions of M1 macrophages and CD56 dim NK cells in the tumoral compartment and more intense infiltration of CD8+ T cells, exhausted CD8+T, CD56 bright NK cells, and M2 macrophages in the stromal compartment. Multivariate analysis identified TERT C228T mutation (HR=3.28 [95%CI:1.225-8.79], p=0.0181) and alteration in KDM6A (HR=2.94 [95%CI:1.040-8.29], p=0.042) as two independent factors associated with inferior RFS. Patients with concomitant TERT C228T and KDM6A alteration had the shortest RFS (median RFS:5.83months) compared with those who were free of (median RFS: NR) or harbored either one of the two alterations (median RFS:9.13months) (p=0.0022). We also found that tumoral infiltration of CD8+T cells was positively associated with RFS (HR=0.29 [95%CI:0.097-0.885], p=0.0208). Conclusion: The study comprehensively depicted the genomic and TME profiles in NMIBC and identified potential predictive biomarkers for BCG treatment. Our findings may facilitate the stratification of patients and better guide the clinical decision-making on the management of NMIBC. Citation Format: Qi-Dong Xia, Yao-Bing Chen, Jian-Xuan Sun, Chen-Qian Liu, Jin-Zhou Xu, Zhi-Peng Yao, Ye An, Meng-Yao Xu, Si-Han Zhang, Xing-Yu Zhong, Na Zeng, Si-Yang Ma, Hao-Dong He, Heng-Long Hu, Jia Hu, Yi Lu, Lin Shao, Si-Qi Li, Zheng Liu, Shao-Gang Wang. TERT C228T and KDM6A alterations are potential predictive biomarkers in non-muscle-invasive bladder cancer treated with intravesical Bacillus Calmette-Guérin instillation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2127.

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Du, Kun, Rong-yi Ding, Zhi-hao Wang, Zhi-gang Song, Bing-feng Xu, Ming Zhou, Yun Bai i Jin Zhang. "Erratum for “Direct Inversion Algorithm for Pipe Resistance Coefficient Calibration of Water Distribution Systems” by Kun Du, Rong-yi Ding, Zhi-hao Wang, Zhi-gang Song, Bing-feng Xu, Ming Zhou, Yun Bai, and Jin Zhang". Journal of Water Resources Planning and Management 144, nr 10 (październik 2018): 08218001. http://dx.doi.org/10.1061/(asce)wr.1943-5452.0000989.

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Zhu, Xiu-Zhi, Xi Jin, Hu-Yun-Long Zhang, Xiyu Liu, Yi-Fan Zhou, Yi-Yu Chen, Tong Fu i in. "Abstract PO1-15-07: Subtyping-directed precision treatment refines traditional one-size-fits-all therapy in HR+/HER2- breast cancer: a sub-study of the MULAN umbrella trial". Cancer Research 84, nr 9_Supplement (2.05.2024): PO1–15–07—PO1–15–07. http://dx.doi.org/10.1158/1538-7445.sabcs23-po1-15-07.

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Abstract Background: The standard approach of using one-size-fits-all endocrine therapy for hormone receptor-positive and HER2-negative (HR+/HER2-) breast cancers has faced significant challenges due to variations in treatment response among individuals. Consequently, there is still an urgent need to understand the molecular biology of HR+/HER2- breast cancer and explore precision treatment strategy. Methods: We established a multiomics cohort (n = 351), multicenter real-world clinical cohorts (n = 643), a prospective clinical cohort (MULAN trial), and a drug-testing platform containing patient-derived organoids (n = 126) and patient-derived tumor fragments (n = 49) of HR+/HER2- breast cancers. Integrating "bench" and “bedside” data, we conducted comprehensive preclinical and clinical translational research on precision strategies in HR+/HER2- breast cancer. Results: We implemented a comprehensive classification system for HR+/HER2- breast cancer, comprising four distinct subtypes. We further demonstrated the efficacy and mechanisms of subtyping-directed precision treatment strategies through clinical cohort studies, omics analysis and functional assays: endocrine therapy alone for the canonical luminal subtype; the addition of CDK4/6 inhibitor and PARP inhibitor for the proliferative subtype; the immunotherapy for the immunogenic subtype; and tyrosine kinase inhibitors for the receptor tyrosine kinase-driven subtype. Using clinically applicable subtyping methods, we validated that matched precision treatment strategies outperformed unmatched approaches in a real-world cohort, almost doubling the median progression-free survival time for patients with refractory advanced HR+/HER2- breast cancer (9.83 months [95% CI, 5.74-13.93] vs 4.77 months [95% CI, 3.35-6.18]; hazard ratio 0.64 [95% CI, 0.41-0.99]). Importantly, the first-stage analysis of the MULAN phase II umbrella clinical trial (NCT04355858) verified the higher objective response rate (88.9%, 95%CI: 51.7%-99.7%) of the subtyping-directed precision treatment. Conclusion: Our study emphasizes the superiority of subtyping-directed precision treatment strategies for HR+/HER2- breast cancer, refines traditional “one-size-fits-all” therapy, and facilitates the translation of precision treatment strategies from bench to bedside. Overall study design Part 1 Subtype Molecular Characteristics: Molecular features of the four subtypes of HR+/HER2- breast cancer. Part 2 Multidimensional Efficacy Validation: Integrating data from a multiomics cohort, real-world study, drug testing platform and prospective clinical research to validate the subtyping-directed precision treatment strategy in HR+/HER2- breast cancer. Part 3 Subtyping-directed Precision Treatment Strategy: Integrating clinical cohort studies, omics analysis and functional assays revealed the heterogeneity of treatment response in HR+/HER2- breast cancer, and proposed a subtyping-directed precision treatment strategy. CIN, chromosomal instability; RTK, receptor tyrosine kinase; CNA, copy-number alteration; ER, estrogen receptor; HR, hormone receptor; HER2, human epidermal growth factor receptor 2. Citation Format: Xiu-Zhi Zhu, Xi Jin, Hu-Yun-Long Zhang, Xiyu Liu, Yi-Fan Zhou, Yi-Yu Chen, Tong Fu, Ming-Liang Jin, Ya-Xin Zhao, Yi-Fan Xie, Ruo-Xi Wang, Zhong-Hua Wang, Lei Fan, Yi-Zhou Jiang, Zhi-Ming Shao. Subtyping-directed precision treatment refines traditional one-size-fits-all therapy in HR+/HER2- breast cancer: a sub-study of the MULAN umbrella trial [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO1-15-07.

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Jiang, Tingting, Indira Wu, Yvonne Kim, Nageswara Alla, Giao Tran, Dustin Ma, Forum Shah i in. "Abstract 6601: Analytical validation of a robust integrated genomic and epigenomic liquid biopsy for biomarker discovery, therapy selection, and response monitoring". Cancer Research 83, nr 7_Supplement (4.04.2023): 6601. http://dx.doi.org/10.1158/1538-7445.am2023-6601.

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Abstract Background: Despite its revolutionary impact, cancer genomics alone provides little information on tumor phenotype or functional state, which are governed by epigenetic mechanisms, notably methylation of regulatory regions. Tumor and host epigenetic methylation signatures reflect not only tumor phenotype, such as histology, prognosis, protein expression, and functional sub-type, but also that of the tumor microenvironment and the patient, including immune status, therapy-related adverse events, comorbidities, and disease location. Epigenetic markers also provide more sensitive and precise measures of tumor burden, opening up applications for longitudinal therapy response and monitoring. Here we report the initial validation of GuardantINFINITY, a liquid biopsy assay combining genomic information from >800 genes with characterization of the blood-quiet regulatory methylome, both at single-molecule sensitivity from a single tube of peripheral blood. Methods: Analytical performance was assessed using 594 cancer patient cfDNA, cell line, and cancer-free donor samples at 5-30ng cfDNA input. Results: Reportable ranges established for SNVs were ≥0.04% variant allele fraction (VAF), ≥0.04% for indels, ≥0.06% for fusions, ≥2.12 copies for amplifications (CNAs), <1.7 copies for copy loss. Observed 95% limits of detection (LoD) were 0.282% for SNVs across all genes (0.2% for oncogenic hotspots), 0.397% for non-homopolymeric indels, 0.05% for fusions, 2.5 copies for CNAs, 16.3% VAF or 1.84 copies for gene deletions, 7.3 copies for viral (HPV, EBV) detection, and 0.06% for MSI-H. For promoter and sample-level methylation, LoDs were 0.06% and 0.05% tumor fraction, respectively. cfDNA cancer samples demonstrated 100% accuracy for SNVs and Indels above 0.5% VAF and 100% for CNAs and fusions across the reportable range. The analytical false positive rate per base was 6.84e-6 for SNVs, 3.42e-6 for indels, and 0 for CNAs and fusions, with positive predictive values of 97.5% for SNVs, 98% for indels, and 100% for CNAs above 2.5 copies and all tested fusions. Conclusions: GuardantINFINITY is a patient-care-ready liquid biopsy capable of integrated genomic and epigenomic analysis of all solid tumors at single-molecule sensitivity. In addition to traditional genotyping compatible with Guardant360 for more content, the technology’s demonstrated LoD showed the potential for ultra-sensitive ctDNA detection for MRD and recurrence surveillance, tumor fraction quantitation for therapy monitoring, oncogenic virus detection, immunogenotyping, epigenotyping, and tumor phenotype characterization, representing a new standard in biomarker discovery. Citation Format: Tingting Jiang, Indira Wu, Yvonne Kim, Nageswara Alla, Giao Tran, Dustin Ma, Forum Shah, Jun Zhao, Sai Chen, Sante Gnerre, Melis Hazar, Hao Wang, Catalin Barbacioru, Karen Ryall, Ankit Jambusaria, Anupam Chakravarthy, Anthony Zunino, Theresa Pham, Farsheed Ghadiri, Evan Diehl, Benjamin Morck, Arancha Sanchez, Rochelle Dayan, XianXian Liu, Jeffrey Werbin, Jill Lai, Brett Kennedy, Ross Eppler, Justin Odegaard, Han-Yu Chuang, Helmy Eltoukhy. Analytical validation of a robust integrated genomic and epigenomic liquid biopsy for biomarker discovery, therapy selection, and response monitoring [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 6601.

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HU, CHUN-LIN, i JIN-HUA DING. "CHUN-LIN HU & JIN-HUA DING (2014) A new species of Neobelocera Ding & Yang (Hemiptera: Delphacidae: Delphacinae: Tropidocephalini) from China, with a key to species of the genus. Zootaxa, 3784(2): 196–199." Zootaxa 3790, nr 3 (22.04.2014): 500. http://dx.doi.org/10.11646/zootaxa.3790.3.9.

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Shao, Zhi-Ming, Zhong-Hua Wang, Yi-Zhou Jiang, Yin Liu, Xiu-Zhi Zhu, Yi Xiao, Song-Yang Wu i in. "Abstract OT3-27-01: Subtyping-based platform guides precision medicine for heavily pretreated metastatic triple-negative breast cancer: a multicenter, phase 2, umbrella, FUTURE trial". Cancer Research 83, nr 5_Supplement (1.03.2023): OT3–27–01—OT3–27–01. http://dx.doi.org/10.1158/1538-7445.sabcs22-ot3-27-01.

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Abstract Background: Triple-negative breast cancer (TNBC) is a heterogeneous disease and lacks effective treatment. Our previous study classified TNBCs into four subtypes (luminal androgen receptor [LAR], immunomodulatory [IM], basal-like immune-suppressed [BLIS], mesenchymal-like [MES]) with distinct molecular features. We aimed to assess the efficacy and safety of molecular subtype-derived precision treatment in patients with heavily pretreated metastatic TNBC. Methods: This open-label, phase 2, umbrella trial included patients from four centers in China. Participants were women (aged ≥18 years) with histologically confirmed metastatic TNBC with disease progression after multiple lines of standard chemotherapy. Patients were enrolled into seven parallel arms according to their molecular subtypes: LAR with or without ERBB2 somatic mutation/amplification assigned to arm A (pyrotinib with capecitabine) and arm B (androgen inhibitor included therapy); IM assigned to arm C (anti-PD-1 antibody with nab-paclitaxel); BLIS with or without BRCA1/2 germline mutation assigned to arms D (PARP inhibitor included therapy) and E (anti-VEGFR included therapy); MES without or with PI3K-AKT mutation assigned to arms F (anti-VEGFR included therapy) and G (everolimus with nab-paclitaxel). Bayesian predictive probability was adopted to monitor each arm, which can be terminated independently according to a prespecified futility or efficacy boundary. This trial is registered with ClinicalTrials.gov, NCT03805399. Findings: Between October 18, 2018, and February 11, 2022, we enrolled 141 patients. All patients were heavily pretreated and resistant to six categories of the most common chemotherapeutic agents used in breast cancer treatment, with a median of 3 previous lines of therapies in the metastatic setting (Table 1 and 2). The median follow-up was 18.3 months (IQR 11.7-27.7). A confirmed objective response was achieved in 42 (29.8%, 95% CI 22.4-38.1) of the 141 patients. The median PFS was 3.4 months (95% CI 2.7-4.2), and the median OS was 10.7 months (95% CI 9.0-12.3) (Table 3). Arms A, C, E and G achieved efficacy boundaries, with 3 (75.0%) out of 4 patients in arm A, 20 (43.5%) out of 46 patients in arm C, 13 (28.3%) out of 46 patients in arm E, and 3 (33.3%) out of 9 patients in arm G achieving objective responses. Potential predictive biomarkers of efficacy in each arm were explored. Safety data were consistent with the known safety profiles of relevant drugs. Interpretation: We demonstrate the feasibility and clinical utility of a subtyping-based, genomic sequencing-guided strategy which allows the majority of heavily pretreated metastatic TNBCs to benefit from precision treatment. Most arms exhibit promising efficacy and manageable toxicities, providing subtyping schema to optimize personalized treatment. Table 1. The FUTURE trial schema. Patients are stratified into seven arms using the FUSCC 484-gene NGS panel testing and IHC subtyping. Abbreviations: mTNBC, metastatic triple-negative breast cancer; NGS, next-generation sequencing; IHC, immunohistochemistry; FUSCC, Fudan University Shanghai Cancer Center; LAR, luminal androgen receptor; IM, immunomodulatory; BLIS, basal-like immune-suppressed; MES, mesenchymal-like; n, number; AR, androgen receptor; PD-1, programmed cell death-1; PARPi, poly ADP-ribose polymerase inhibitor; VEGF, vascular endothelial growth factor; mTORi, mammalian target of rapamycin inhibitors. Table 2. Patient characteristics in the FUTURE trial. Table 3. Summary of treatment efficacy of TNBC in the FUTURE trial Citation Format: Zhi-Ming Shao, Zhong-Hua Wang, Yi-Zhou Jiang, Yin Liu, Xiu-Zhi Zhu, Yi Xiao, Song-Yang Wu, Wen-Jia Zuo, Qiang Yu, A-Yong Cao, Jun-Jie Li, Ke-Da Yu, Guang-Yu Liu, Jiong Wu, Tao Sun, Jiuwei Cui, Zheng Lv, Hui-Ping Li, Xiao-Yu Zhu. Subtyping-based platform guides precision medicine for heavily pretreated metastatic triple-negative breast cancer: a multicenter, phase 2, umbrella, FUTURE trial [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr OT3-27-01.

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