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Journal articles on the topic "Xiu geng tang"
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Cheng, Wen-Yu, Shih-Lu Wu, Chien-Yun Hsiang, Chia-Cheng Li, Tung-Yuan Lai, Hsin-Yi Lo, Wei-Shuen Shen, et al. "Relationship Between San-Huang-Xie-Xin-Tang and Its Herbal Components on the Gene Expression Profiles in HepG2 Cells." American Journal of Chinese Medicine 36, no. 04 (January 2008): 783–97. http://dx.doi.org/10.1142/s0192415x08006235.
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Traditional Chinese medicine (TCM) has been used for thousands of years. Most Chinese herbal formulae consist of several herbal components and have been used to treat various diseases. However, the mechanisms of most formulae and the relationship between formulae and their components remain to be elucidated. Here we analyzed the putative mechanism of San-Huang-Xie-Xin-Tang (SHXXT) and defined the relationship between SHXXT and its herbal components by microarray technique. HepG2 cells were treated with SHXXT or its components and the gene expression profiles were analyzed by DNA microarray. Gene set enrichment analysis indicated that SHXXT and its components displayed a unique anti-proliferation pattern via p53 signaling, p53 activated, and DNA damage signaling pathways in HepG2 cells. Network analysis showed that most genes were regulated by one molecule, p53. In addition, hierarchical clustering analysis showed that Rhizoma Coptis shared a similar gene expression profile with SHXXT. These findings may explain why Rhizoma Coptis is the principle herb that exerts the major effect in the herbal formula, SHXXT. Moreover, this is the first report to reveal the relationship between formulae and their herbal components in TCM by microarray and bioinformatics tools.
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Friedemann, Thomas, Udo Schumacher, Yi Tao, Alexander Kai-Man Leung, and Sven Schröder. "Neuroprotective Activity of Coptisine fromCoptis chinensis(Franch)." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/827308.
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Coptis chinensisrhizomes (CR) are one important ingredient of traditional Chinese herbal formulas such as San-Huang-Xie-Xin-Tang which is used for treatment of cardiovascular and neurodegenerative diseases. Recent studies suggest that the extract of CR might be a potential therapeutic agent for amelioration of neurological disorders associated with oxidative stress. In the present study we aimed at revealing the main active compound(s) of the CR extract and at investigating the mechanism of action. Four main alkaloids of the CR extract (berberine, coptisine, jatrorrhizine, and palmatine) were selected for this study. Results showed that out of those alkaloids only pretreatment with coptisine significantly attenuated tert-butylhydroperoxide induced reduction of cell viability, increased rate of apoptosis, and declined mitochondrial membrane potential. Elisa assay and quantitative real-time PCR analyses revealed that thioredoxin-interacting protein (TXNIP) gene expression was downregulated by coptisine, which could explain the neuroprotective effect, hypothetically, by strengthening the thioredoxin defense system against oxidative stress and attenuation of apoptosis signal-regulating kinase (Ask1) mediated apoptotic signaling. A comparison between coptisine and CR extract identified coptisine as the main single component responsible for the neuroprotective effect. Based on the results the CR extract and coptisine are promising candidate agents for prevention or improvement of diabetic neuropathy and neurodegenerative disorders.
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Tang, Haoran, Feng Xie, Yue Zhang, and Shidong Jia. "Abstract 1049: Liquid biopsy-based comprehensive genomic profiling reveal mutational landscape in advanced breast cancer." Cancer Research 83, no. 7_Supplement (April 4, 2023): 1049. http://dx.doi.org/10.1158/1538-7445.am2023-1049.
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Abstract Introduction: Breast cancer is the most common malignancy worldwide in females, with more than 2.26 million new cases and 680 thousand of deaths in 2020. Advanced breast cancer is characterized by complicated genomic landscape and requires comprehensive genomic profiling. However, tissue biopsy is hard to get in patients with recurrent metastasis. Meanwhile, limited studies have been reported to use liquid biopsy and were not capable of reporting gene copy number loss. Here we reported a comprehensive genomic profiling study in advanced breast cancer patients using liquid biopsy. Methods: The prospective study is part of the Predicine’s Phoenix Program, a global molecular biomarkers screening program in multiple solid tumors. Currently, the study enrolled 220 advanced breast cancer patients from 8 centers in China, who were naïve to the 1st line treatment. 10ml of blood was collected from each patient and delivered to a central lab for ctDNA analysis. The study applied PredicineCARE, an NGS-based liquid biopsy assay, to profile somatic mutations, copy number variations, and gene fusions among these patients. Results: The study identified 793 somatic mutations and 283 copy number variants among blood samples from 220 patients. The most common altered genes were TP53(101/220, 46%), PIK3CA(77/220, 35%), BRCA2(37/352, 17%), PTEN(26/220, 12%), and ATM(24/220, 11%). Gene copy number gain incidents were identified on MYC(n=28), AKT3(n=23), FGFR1(n=18), and PIK3CA(n=16), etc. The study also reported gene copy number loss incidents through liquid biopsy, such as CDKN2A(n=17), BRCA1(n=12), TP53(n=11), RB1(n=11), BRCA2(n=10), PTEN(n=9), and ATM(n=8). Conclusions: This study revealed the comprehensive mutational landscape of advanced breast cancer patients through liquid biopsy, providing novel biomarkers for clinical diagnosis and targeted therapy mechanism studies. Citation Format: Haoran Tang, Feng Xie, Yue Zhang, Shidong Jia. Liquid biopsy-based comprehensive genomic profiling reveal mutational landscape in advanced breast cancer [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 1049.
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Tang, Haoran, Feng Xie, Yue Zhang, and Shidong Jia. "Abstract 5582: Liquid biopsy-based comprehensive genomic profiling reveal mutational landscape in real-world patients with unresectable NSCLC." Cancer Research 83, no. 7_Supplement (April 4, 2023): 5582. http://dx.doi.org/10.1158/1538-7445.am2023-5582.
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Abstract Introduction: NSCLC accounts for more than 80% of all lung cancer, and has been shown for clinical benefits from targeted therapies, according to tests of multiple genes, such as EGFR, KRAS, ALK, ERBB2. Previous studies revealed molecular characteristics and responses of targeted therapies in NSCLC. However, most studies used tissue biopsies. There is increasing interest to characterize the molecular profile of NSCLC through liquid biopsy. Hence, here we report a comprehensive genomic profiling study in unresectable NSCLC patients using liquid biopsy. Methods: The prospective study is part of the Predicine’s Phoenix Program, a global molecular biomarkers screening program in multiple solid tumors. Currently, the study enrolled 352 unresectable advanced NSCLC patients from 24 centers in China, who were naïve to the 1st line treatment or recurrent after 1st line targeted therapies. 10ml of blood was collected from each patient and delivered to a central lab for ctDNA analysis. The study applied PredicineCARE, an NGS-based liquid biopsy assay, to profile somatic mutations, copy number variations, and gene fusions among these patients. Results: The study identified 1614 somatic mutations and 202 copy number variants among blood samples from 352 patients. The most common altered genes were TP53(176/352, 50%), EGFR(144/352, 41%), PIK3CA(35/352, 10%), CDNK2A(35/352, 10%), KRAS(28/352, 8%), and RB1(28/352, 8%). Gene copy number gain incidents were identified on MYC(n=22), PIK3CA(n=16), EGFR(n=15), and MET(n=7), etc. Notably, the study also reported gene copy number loss incidents through liquid biopsy, such as CDKN2A(n=16), PTEN(n=11), and RB1(n=10). The study identified 12 gene fusion incidents, including 7 EML4-ALK fusions, 2 RET fusions(KIF5B-RET and NCOA4-RET), 2 NTRK fusions(ETV6-NTRK3 and NOS1AP-NTRK1), and 1 rare CD74-NRG1 fusion. Conclusions: This study revealed the comprehensive mutational landscape of advanced NSCLC through liquid biopsy, providing novel biomarkers for clinical diagnosis and targeted therapy mechanism studies. Citation Format: Haoran Tang, Feng Xie, Yue Zhang, Shidong Jia. Liquid biopsy-based comprehensive genomic profiling reveal mutational landscape in real-world patients with unresectable NSCLC. [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 5582.
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Du, Jun, Wanbo Tang, Xin Jiao, Limin Zhao, Pengfei Du, Yuqi Zhang, Jian Bao, Han Chen, Chaoshe Guo, and W. Frank An. "Abstract 6717: Targeting mutant KRAS proteins with novel TCR-mimic fully human antibodies." Cancer Research 84, no. 6_Supplement (March 22, 2024): 6717. http://dx.doi.org/10.1158/1538-7445.am2024-6717.
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Abstract Mutated KRAS proteins are ideal cancer targets, as they are expressed frequently and specifically in certain solid tumors. A large proportion of human colorectal cancer and pancreatic ductal adenocarcinoma express the tumor driver KRAS gene mutations G12V/G12D, but drugs targeting G12V/G12D are not available, revealing a huge unmet clinical need. While small molecules often fail to target the KRAS mutation G12V/G12D, T cell receptor-mimic (TCR-mimic) antibodies can specifically recognize KRAS mutations presented by human leukocyte antigen (HLA), opening up possibilities for targeting such intracellular antigens. Here, we discovered novel antibodies highly specific to G12V/HLA and G12D/HLA complexes by immunizing our proprietary RenTCR-mimicTM mice and using high-throughput Beacon-based screening. These TCR-mimic antibodies have higher affinities compared to endogenous TCRs, which may effectively reduce the possibility of tumor escape. Germline distribution analysis indicated their high sequence diversity, which suggests diverse epitope targeting. Although pancreatic cancer is extremely difficult to treat and has an extremely low KRAS mutant peptide-HLA complex density on the cell surface, our TCR-mimic antibodies exhibited potent in vitro tumor lysis activity when assembled into CD3 T cell engagers. Furthermore, these antibodies demonstrated convincing off-target safety. Together, our results indicate promising therapeutic potential of these KRAS mutation-targeted TCR-mimic antibodies for the treatment of solid tumors. Citation Format: Jun Du, Wanbo Tang, Xin Jiao, Limin Zhao, Pengfei Du, Yuqi Zhang, Jian Bao, Han Chen, Chaoshe Guo, W. Frank An. Targeting mutant KRAS proteins with novel TCR-mimic fully human antibodies [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 6717.
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Tang, Haoran, Cancan Jia, Feng Xie, Yue Zhang, Xiaoxi Dong, Yong Huang, and Shading Jia. "Abstract 2410: Comparative genomic profiling of unresectable NSCLC patients in the U.S. and China using a globally harmonized liquid biopsy assay platform." Cancer Research 84, no. 6_Supplement (March 22, 2024): 2410. http://dx.doi.org/10.1158/1538-7445.am2024-2410.
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Abstract Background: Non-Small Cell Lung Cancer (NSCLC), accounting for over 80% of all lung cancers, benefits from targeted therapies based on genetic tests like EGFR, KRAS, ALK, and ERBB2. While prior studies focused on molecular characteristics through tissue biopsies, limited research has explored NSCLC molecular profiles via liquid biopsy, especially across different human races. This study presents a comprehensive genomic profiling analysis of unresectable NSCLC patients in the U.S. and China, using a globally harmonized liquid biopsy assay. Methods: As part of Predicine's Phoenix Program, a global molecular biomarkers screening initiative, 61 patients in the U.S. and 352 patients in China with unresectable advanced NSCLC were enrolled. All were treatment-naïve or recurred after 1st-line targeted therapies. Blood samples (10ml) were tested using PredicineCARE, an NGS-based liquid biopsy assay, to profile somatic mutations, copy number variations, and gene fusions. Results: The assay, validated in both regions using the same reference materials, achieved a Limit of Detection (LOD) of 0.25% mutation allele frequency, with a positive predictive value exceeding 99%. Profiling NSCLC patients in the U.S. and China revealed common genes like TP53, CDKN2A, EGFR, KRAS, RB1, and PIK3CA. TP53 and PIK3CA variations showed equivalent prevalence. However, EGFR variations were significantly higher in China (p<0.05), while CDKN2A (p<0.001), KRAS (p<0.01), and RB1 (p<0.01) variations were notably higher in the U.S. Conclusions: This study unveils the mutational landscape of advanced NSCLC through liquid biopsy. Unique prevalence patterns between U.S. and China cohorts suggest novel biomarkers for clinical diagnosis and provide insights for targeted therapy mechanism studies. Citation Format: Haoran Tang, Cancan Jia, Feng Xie, Yue Zhang, Xiaoxi Dong, Yong Huang, Shading Jia. Comparative genomic profiling of unresectable NSCLC patients in the U.S. and China using a globally harmonized liquid biopsy assay platform [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 2410.
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Xie, Lu, Zhenyu Cai, Xiaodong Tang, Wei Guo, Fanfei Meng, Xin Zhang, Xiaoliang Shi, and Fei Pang. "Abstract 5669: Distinct genetic features between osteosarcomas firstly metastasizing to bone and to lung." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5669. http://dx.doi.org/10.1158/1538-7445.am2022-5669.
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Abstract Background Osteosarcoma (OS) is a highly aggressive malignant tumor of mesenchymal origin and prone to early hematogenous metastases. The 5-year overall survival of metastatic OS is only approximately 20% to 30%. Therefore, it is still clinical dilemma in the treatment of OS. Thus,understanding the molecular features of metastatic osteosarcoma become increasingly important. Methods Formalin-fixed, paraffin-embedded or fresh tissues and matched blood samples were collected from OS patients for whole exome sequencing using next-generation sequencing at OrigiMed (Shanghai, China), a College of American Pathologists accredited and Clinical Laboratory Improvement Amendments certified laboratory. Genomic alterations including single nucleotide variations (SNVs), short and long insertions/deletions (INDELs), copy number variations (CNVs), and gene rearrangements were assessed. Tumor mutational burden (TMB) and the number of tumor neoantigens (NEO) were also measured. Results In total, 38 patients including 29 males and 9 females were recruited with a median age of 19.5 years. Among them, 12 patients had first metastases to bone (group B). The metastatic sites included femur, fibula, pelvis, ribs, sacrum, and spine. The median age of group B was 19.5 years. Twenty-six (26) patients had first metastases to lung (group L). The median age of group L was 14 years.The most frequently mutated genes in OS was TP53 (55.3%), followed by MYC (36.8%), MUC16 (26.3%), PTK2 (21.1%), RAD21 (21.1%), and CDK4 (18.4%). However, genetic features between Groups B and Group L patients were different. In group B patients, the median percentage of SNVs and short INDELs was 94.7% of the overall mutations, and the median percentage of CNVs was 4.3%. In contrast, the median percentage of SNVs and short INDELs in group L was 58.8%, and the median percentage of CNVs was 36.7%. The mutations patterns were clearly different between Group B and Group L with a predominant SNV & INDEL in Group B and a mixture feature of SNV & INDEL and CNV in Group L. Inaddition the median TMB in group B was significantly higher than that in group L (4.85 muts/Mb vs 2.4 muts/Mb, P<0.05). Also, the median number of tumor NEO in group B was nearly 6 times higher than that in group L (743 vs 128.5, P=0.0016). Conclusion Our study identified different molecular features of patients with OS firstly metastasizing to lung and to bone. OS with first bone metastases had a predominant SNV and short INDEL, high TMB level, and high NEO counts, while OS with first lung metastasis had an increased CNV, low TMB, and low NEO counts. Our results suggest that metastatic OS that firstly spread to bone and to lung may be two distinct subgroups and may adopt different treatment strategies. Citation Format: Lu Xie, Zhenyu Cai, Xiaodong Tang, Wei Guo, Fanfei Meng, Xin Zhang, Xiaoliang Shi, Fei Pang. Distinct genetic features between osteosarcomas firstly metastasizing to bone and to lung [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5669.
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Belmontes, Brian, Katherine Slemmons, Siyuan Liu, Antonia Policheni, Jodi Moriguchi, Hong Tan, Fang Xie, et al. "Abstract B177: The discovery and preclinical characterization of AMG 193, a first-in-class MTA-cooperative PRMT5 inhibitor with broad activity against MTAP-null cancers." Molecular Cancer Therapeutics 22, no. 12_Supplement (December 1, 2023): B177. http://dx.doi.org/10.1158/1535-7163.targ-23-b177.
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Abstract Homozygous deletion of the methylthioadenosine phosphorylase (MTAP) gene occurs in approximately 15% of all cancers due to its proximity to the commonly deleted tumor suppressor gene CDKN2A. Elevated methylthioadenosine (MTA) levels, driven by loss of MTAP, compete with the methyl donor S-adenosylmethionine (SAM) for binding to protein arginine N-methyltransferase 5 (PRMT5), placing the methyltransferase in a hypomorphic state, and vulnerable to further PRMT5 inhibition. The screening of a DNA-encoded library, designed to identify small molecules that preferentially bind to PRMT5 in the presence of MTA, resulted in the identification of AM-9934 as a promising hit. Using structure-based drug design, potency and cooperativity were enhanced to deliver AM-9747, an MTA-cooperative PRMT5 inhibitor suitable for in vivo proof-of-concept studies. Further optimization led to AMG 193, an orally bioavailable and MTA-cooperative PRMT5 inhibitor with potent biochemical and cellular activity, and an improved pharmacokinetic profile. Insights into the binding mode of AMG 193 were elucidated by the crystal structure of AMG 193 bound to the MTA-PRMT5 complex. AMG 193 activity is enriched in MTAP-null cells in vitro, as illustrated in the HCT116 isogenic pair; AMG 193 is ~40X selective for MTAP-null cells (IC50 = 0.1 mM) over MTAP WT cells (IC50 > 4 mM) in viability assays and >100X selective in an assay evaluating symmetric dimethylarginine (SDMA) levels. AMG 193 was profiled in a panel of >850 cancer cell lines, and response demonstrated preferential sensitivity in MTAP-null cells compared to WT across multiple cancer lineages, including pancreatic, lung, biliary tract, and lymphoma. Response strongly correlated with both MTAP and CDKN2A copy number loss, and cell lines that were dependent on PRMT5, as shown by RNAi and CRISPR knockdown, were most sensitive to AMG 193 treatment. In vitro mechanism-of-action studies demonstrated that PRMT5 inhibition induced DNA damage, cell cycle arrest in G2/M, and an increase in alternative mRNA splicing in MTAP-null cells. In mice oral, once-daily administration of AMG 193 selectively inhibited SDMA in tumor versus normal tissue and was well tolerated with no hematologic perturbations. Importantly, AMG 193 demonstrated robust anti-tumor activity across a broad range of MTAP-null CDX and PDX tumor models derived from NSCLC, pancreatic, and esophageal cancers. In vitro synergy was observed with the combination of AMG 193 and several chemotherapeutic agents, including carboplatin and paclitaxel, or the KRASG12C inhibitor, sotorasib. In vivo, these combinations led to enhanced anti-tumor activity relative to single agent in MTAP-null NSCLC tumor models. In February 2022, AMG 193 became the first MTA-cooperative PRMT5 inhibitor to enter clinical development and is currently being evaluated in subjects with advanced MTAP-null solid tumors in the ongoing FIH study (NCT05094336). Citation Format: Brian Belmontes, Katherine Slemmons, Siyuan Liu, Antonia Policheni, Jodi Moriguchi, Hong Tan, Fang Xie, Famke Aeffner, Matthew G Rees, Melissa M Ronan, Jennifer A Roth, Mikkel Vestergaard, Sanne Cowland, Jan Andersson, Ian Sarvary, Patricia Lopez, Nuria Tamayo, Liping H Pettus, Susmith Mukund, Jennifer R Allen, Sanne Glad, Matthew P Bourbeau. The discovery and preclinical characterization of AMG 193, a first-in-class MTA-cooperative PRMT5 inhibitor with broad activity against MTAP-null cancers [abstract]. In: Proceedings of the AACR-NCI-EORTC Virtual International Conference on Molecular Targets and Cancer Therapeutics; 2023 Oct 11-15; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2023;22(12 Suppl):Abstract nr B177.
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Weng, JingRong, JinXin Lin, YuMo Xie, GuanNan Tang, LiangLiang Bai, JinHua Chen, ZengHong Huang, et al. "Abstract 6006: RNA m6A methylation relay the oncogenic flow from DNA methylationto gene expression of ANKRD13B." Cancer Research 83, no. 7_Supplement (April 4, 2023): 6006. http://dx.doi.org/10.1158/1538-7445.am2023-6006.
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Abstract Background: Colorectal cancer (CRC) is one of the most common causes of cancer-related death in the world. More comprehensive studies of key molecular alterations in CRC progression were urgent. DNA methylation promotes tumor progression. However, the mechanism of the ANKRD13 gene methylation that drives colorectal cancer evolution remains largely unknown. This was the first study focused on the role of ANKRD13 and the hypermethylated mechanisms in colorectal cancer. Methods: Chi-Square tests were utilized to the comparison of the baseline characteristics of patients with hypomethylation ANKRD13B and hypermethylated ANKRD13B. Kaplan-Meier analysis were used to estimate the difference of overall survival between the two groups patients. The methylation level of ANKRD13B was quantified by qMSP in colorectal cancer, normal colon epitheliums and colorectal adenoma tissues. CRISPR/dCas9-DNMT3A and CRISPR/dCas9-TET1-CD methylation editing tools were applied to enable targeted and specific CpG methylation at the CpG loci near stop codon of ANKRD13B. Transwell-migrated assay, wound scratch assay and colony formation assay were preformed to ascertain the abilities of viability, migration and invasion in the editing CRC cell lines. The methylated RNA immunoprecipitation (MeRIP) assays, chromatin immunoprecipitation (ChIP) assays and 5-AZA treatment assays were performed combined with qPCR to quantify the m6A levels of ANKRD13B mRNA following hypermethylated-editing. Results: Here, we identified a novel oncogenic gene, ANKRD13B, encoding ankyrin repeat domain 13B. This gene was frequently hypermethylated in CpG islands surrounding the stop codon region of colorectal cancer. This hypermethylation was associated with poor clinical outcomes in patients diagnosed with colorectal cancer. Compared with normal tissue (4.2%), this type of epigenetic alteration upregulated ANKRD13B expression in both adenoma (73.0%) and adenoma cancer tissues (83.3%) (P< 0.0001), and it also promoted colorectal cancer cell growth, invasion, and migration. Demethylation treatment can reduce the ANKRD13B expression and the growth, migration, and invasion of the cancer cell. Moreover, we found that the aberrant ANKRD13B methylated surrounding the stop codon, and it can promote RNA N6-methyladenosine methylation modification, suggesting that aberrant DNA 5mC methylation promotes ANKRD13B expression and tumor progression in an RNA m6A-dependent manner. Conclusions: In summary, our findings illustrated that ANKRD13B is an oncogenic gene of colorectal cancer that is commonly methylated and overexpressed in colorectal cancer whose function in the pathogenesis of colorectal cancer depends on RNA m6A-dependent manner. Aberrant DNA 5mC methylation promotes ANKRD13B expression and tumor progression in an RNA m6A-dependent Manner. Key words: ANKRD13B, DNA methylation, Epigenetic regulation, Colorectal cancer Citation Format: JingRong Weng, JinXin Lin, YuMo Xie, GuanNan Tang, LiangLiang Bai, JinHua Chen, ZengHong Huang, ZhuoKai Zhuang, ShaoYong Peng, Heng Wang, GaoPo Xu, Yu Zhang, XiaoXia Liu, MeiJin Huang, YanXin Luo, XiaoLin Wang, Huichuan Yu. RNA m6A methylation relay the oncogenic flow from DNA methylationto gene expression of ANKRD13B [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 6006.
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Liu, Xiaoran, Yaxin Liu, Cancan Jia, Yue Zhang, Feng Xie, Haoran Tang, Shidong Jia, and Huiping Li. "Abstract 1752: Comprehensive genomic profiling of advanced breast cancer subtypes: Insights from liquid biopsy analysis and implications for personalized therapies." Cancer Research 84, no. 6_Supplement (March 22, 2024): 1752. http://dx.doi.org/10.1158/1538-7445.am2024-1752.
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Abstract Background: Breast cancer stands as the most prevalent malignancy affecting women’s health. The disease consists of three subtypes, including hormone receptor (HR) positive, HER2-positive, and triple-negative breast cancer (TNBC). In recent years, the advent of targeted therapies such as PI3K inhibitors has significantly improved the prognosis of breast cancer patients. However, the detection of relevant molecular markers, such as PIK3CA mutations, relies on tissue samples, which imposes limitations on the clinical application of these therapies. Consequently, this study presents a comprehensive analysis of genomic profiling that compares breast cancer patients across distinct pathological classifications, utilizing a liquid biopsy approach. Methods: In this retrospective study, 214 patients with advanced breast cancer were recruited. Plasma samples collected prior to first line treatment were analyzed using PredicineCARE, a targeted next-generation sequencing (NGS) liquid biopsy assay, to detect somatic alterations in ctDNA of blood, including single nucleotide variations (SNVs), gene fusions, and copy number variations (CNVs). Results: Based on the IHC classifications of tumor tissue, this cohort comprised 119 HR-positive, 61 HER2-positive, and 34 TNBC patients. The assay identified a total of 1456 mutations and 2357 gene copy number variants in plasma samples. Among these, the most frequently mutated genes and those with copy number variations (top 5) in HR-positive patients were TP53 (40%), PIK3CA (39%), ATM (22%), ERBB2 (19%), and FGFR1 (19%). In HER2-positive patients, they were TP53 (39%), PIK3CA (31%), ERBB2 (30%), NTRK1 (20%), and RAD50 (20%). For TNBC patients, the top genes were TP53 (59%), ERBB2 (44%), PIK3CA (35%), NTRK1 (35%), and BRCA2 (26%). Regarding the PIK3CA gene, the most prevalent mutation site was H1047, occurring in 12.61% of HR-positive patients, 14.75% of HER2-positive patients, and 11.76% of TNBC patients. Similarly, both E542 (4.20% in HR-positive, 3.28% in HER2-positive, and 2.94% in TNBC patients) and E545 (3.36% in HR-positive, 3.28% in HER2-positive, and 2.94% in TNBC patients) showed equivalent prevalence across the three classifications. These findings suggest the potential efficacy of PI3K inhibitors in various pathological types of breast cancer. Conclusions: This study offers insights into the genomic landscape of advanced breast cancer subtypes through liquid biopsy. The observed prevalence of PIK3CA mutations supports the potential efficacy of PI3K inhibitors across these diverse types of breast cancer, laying the groundwork for personalized therapeutic strategies and biomarker identification for prognosis and targeted therapies. Citation Format: Xiaoran Liu, Yaxin Liu, Cancan Jia, Yue Zhang, Feng Xie, Haoran Tang, Shidong Jia, Huiping Li. Comprehensive genomic profiling of advanced breast cancer subtypes: Insights from liquid biopsy analysis and implications for personalized therapies [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 1752.
Books on the topic "Xiu geng tang"
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Shi, Guoqi. Li geng tang cong shuo: Yi juan ; Ji bei ju xia chang : yi juan ; Shi lun wu da : yi juan. Shanghai: Shanghai gu ji chu ban she, 2010.
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Kiyoshi, Suganuma, Sumi Hiroyuki, Zhang Weiqiao, and Torefuru Kurabu Tōgō Iryō Kenkyūjo., eds. Na dou qing shu zhi zhi hao xin ji geng sai, nao zhong feng, tang niao bing, chi dai zheng. Taibei Xian Xindian Shi: Shi mao chu ban she, 2005.
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translator, Lin Fangyu, ed. Wo de tian ran tian dian quan shu: 70 dao shao tang geng mei wei gao bing, ta pai, dian xin, guo jiang, shan yong xin xian hao shi cai, hong bei man man da zi ran feng wei. Xinbei Shi: Qi guang chu ban, 2016.
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Yi tong li, Yi tong shi ; Xun gu wei ; Geng jia za ji ; Xu xin fang yan ; Liang Han di fang zi zhi zhi du kao ; Zu pu xue gai yao ; Lun yu zheng yao ; Xin sheng huo jie zheng ; Rui shao tang xie zhu ; Wu ye ren sheng huo ; Shuo wen yan jiu fa. Nanjing Shi: Feng huang chu ban she, 2015.
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