RAD18 is a crucial mismatch repair gene associated with the post-replication repair, and genetic variations in RAD18 gene are closely related to tumorigenesis. We selected 6 RAD18 SNP and performed mismatch amplification PCR on 650 cases of CIN III, 580 cervical squamous cell carcinoma (CSCC), and 1320 healthy controls. The RAD18 rs250403 GG and G allele (AG + GG) genotype risk in CIN III and CSCC were significantly increased. The results showed a significant correlation between the GG genotype of rs615967 and the risk of CIN III and CSCC. Carriers of the G allele (AG + GG) at RAD18 rs615967 also had an increased risk. More noteworthy was that the RAD18 rs250403 (A/G) and rs615967 (A/G) haplotypes associated with high risk of CIN III and CSCC were AG-GG, GG-AA, GG-AG, and GG-GG. Clinical data analysis further showed that the polymorphisms of RAD18 rs250403 and rs615967 were significantly correlated with prognostic indicators such as family history of tumor, differentiation grade, lymph node metastasis, and vascular involvement. RAD18 protein expression was significantly decreased in CSCCs with the rs615967-AG and rs615967-GG genotype. In summary, the 2 genetic polymorphisms of the RAD18 were associated with susceptibility and prognosis in CIN III and CSCC, and specific high-risk haplotypes of these 2 SNPs could serve as genetic predictive biomarkers.

This study investigated the differential metabolites after rheumatoid arthritis (RA) rats were treated with Jinteng Qingbi granules. Collagen-induced arthritis rats were divided into three groups, namely normal group, model group, and Jinteng Qingbi granules group. Serum compounds were identified, annotated, and classified using metabolomics to explain the physicochemical properties and biological functions. The metabolites were screened using univariate and multivariate statistical analyses. There were differences in serum metabolites between RA and normal rats; Jinteng Qingbi granules improved RA and recovered the metabolite levels to normal. Compared to the normal group, 51 differential ions were screened, and 108 ions were changed in the Jinteng Qingbi granules group compared to the RA model. Eight metabolites were upregulated in the RA model group compared to the normal group, whereas 10 metabolites were downregulated. Treatment with Jinteng Qingbi granules increased the levels of 12 metabolites such as cinnamate and decreased the levels of 16 metabolites such as allamandin in the RA model. Differential ion enrichment was mainly related to the histidine metabolic pathway in amino acid metabolism. Jinteng Qingbi granules resulted in improvements in the RA model, which were mainly associated with lipids and lipid-like molecules, organic acids, and derivatives, providing a new possibility and basis for screening biomarkers for the diagnosis and treatment of RA.

The risk of endometriosis (EM), which is a common complex gynaecological disease, is related to genetic predisposition. However, it is unclear how genetic variants confer the risk of EM. Here, via Sherlock integrative analysis, we combined large-scale genome-wide association studies (GWAS) summary statistics on EM (N = 245,494) with a blood-based eQTL dataset (N = 1490) to identify EM risk-related genes. For validation, we leveraged two independent eQTL datasets (N = 769) for integration with the GWAS data. Thus, we prioritised 14 genes, including GIMAP4, TOP3A, and NMNAT3, which showed significant association with susceptibility to EM. We also utilised two independent methods, Multi-marker Analysis of GenoMic Annotation and S-PrediXcan, to further validate the EM risk-associated genes. Moreover, protein-protein interaction network analysis showed the 14 genes were functionally connected. Functional enrichment analyses further demonstrated that these genes were significantly enriched in metabolic and immunerelated pathways. Differential gene expression analysis showed that in peripheral blood samples from patients with ovarian EM, TOP3A, MKNK1, SIPA1L2, and NUCB1 were significantly upregulated, while HOXB2, GIMAP5, and MGMT were significantly downregulated compared with their expression levels in samples from the controls. Immunohistochemistry further confirmed the increased expression levels of MKNK1 and TOP3A in the ectopic and eutopic endometrium compared to normal endometrium, while HOBX2 was downregulated in the endometrium of women with ovarian EM. Finally, in ex vivo functional experiments, MKNK1 knockdown inhibited ectopic endometrial stromal cells (EESCs) migration and invasion. TOP3A knockdown inhibited EESCs proliferation, migration, and invasion, while promoting their apoptosis. Convergent lines of evidence suggested that MKNK1 and TOP3A are novel EM risk-related genes. (c) 2023 The Author(s). Published by Elsevier B.V. on behalf of Research Network of Computational and Structural Biotechnology. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

目的:基于数据挖掘技术探讨房定亚教授治疗急性痛风性关节炎的临床用药规律.方法:收集 2014 年 10 月至 2019 年 12 月在中国中医科学院西苑医院房定亚教授特需门诊就诊的 78 例急性痛风性关节炎患者的中药处方,应用中医传承辅助平台(V2.5)临床采集系统,录入数据,采用复杂系统熵聚类、关联规则算法等数据挖掘的方法,分析房定亚教授治疗急性痛风性关节炎的组方特点和用药规律.结果:共纳入中药处方78首,辨证以湿热阻络为主,涉及药物93味,使用频次 ﹥30次的药物有葛根、土茯苓、车前草、马齿苋、玄参等 9 味,获得置信度为 1 的药物组合 24 个,提取核心药物组合 8 个,挖掘潜在治疗新处方 4 首.结论:房定亚教授治疗急性痛风性关节炎以清热利湿为主,佐以活血通络,体现其辨病与辨证相结合,专病专方治疗疾病的思想.

Abstract Background Low-grade serous ovarian cancer is a rare subtype of ovarian cancer and lack of large-scale systematic studies worldwide.This study is aimed to select the target gene and figure out the expression and clinical significance of it in low-grade serous ovarian cancer. Methods and Results The mRNA data was downloaded from the Gene Expression Omnibus (GEO), then the differentially expressed genes (DEGs) between cancer and normal tissue were screened out by R software. Under comprehensive consideration, C1orf106 was chosen as our target gene based on the significant |logFC|, known molecular function and research innovation. Immunohistochemistry and qRT-PCR both showed that C1orf106 was highly expressed in tumor tissue. Contacted with clinical information, high-expression of C1orf106 was associated with lower Body Mass Index (< 25kg/m 2 ) and no residual lesion. Kaplan-Meier analysis showed that high-expression of C1orf106 was associated with better overall survival, but may not be correlated with progression-free survival. COX regression model indicated that C1orf106 was one of the prognostic factor for low-grade serous ovarian cancer, but not independently. Conclusion C1orf106 was highly expressed in low-grade serous ovarian cancer. High expression of C1orf106 indicated a better overall survival. Therefore, C1orf106 may be one of the biomarkers with diagnostic and prognostic value in low-grade serous ovarian cancer, but the precise mechanism still needs further research.

目的 研究金藤清痹颗粒通过调节免疫微环境对类风湿关节炎大鼠的干预作用及其机制.方法 通过注射牛Ⅱ型胶原和弗氏不完全佐剂建立胶原诱导型关节炎(CIA)大鼠模型,造模成功后随机分为模型组、甲氨蝶呤组、雷公藤多苷组及金藤清痹颗粒低、中、高剂量组,每组10只,另以10只正常大鼠作为正常组,给药组灌胃给予相应剂量药物,模型组和正常组灌胃给予等体积0.9％氯化钠注射液.每7 d进行1次足底厚度检测和关节指数评分,HE染色观察膝关节滑膜病理改变,免疫组化检测滑膜CD68、CD86、CD206表达,流式细胞术检测外周血中辅助性T细胞17(Th17)和调节性T细胞(Treg)比例,Western blot法检测TLR4/NF-κB信号通路蛋白表达,RT-qPCR法检测TLR4、IKKβmRNA表达.结果 金藤清痹颗粒与甲氨蝶呤、 雷公藤多苷均能减轻CIA大鼠四肢关节肿胀(P<0.05),降低M1/M2型巨噬细胞比例、Th17/Treg细胞比例、TLR4 mRNA及TLR4、p-IκBα、细胞核p65蛋白表达(P<0.05,P<0.01),升高IKKβ、 胞质p65蛋白及IKKβmRNA表达(P<0.05,P<0.01),并呈剂量依赖性.结论 金藤清痹颗粒能够通过影响M1/M2型巨噬细胞极化,调节Th17/Treg细胞平衡,调控TLR4/NF-κB信号通路表达,改善免疫微环境,从而缓解类风湿关节炎大鼠关节肿胀症状.

PD-1/PD-L1 inhibitor treatments are relatively inefficacious in advanced cervical cancer patients. The presence of myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment may be one significant barrier to efficacy. It has been shown that all-trans retinoic acid (ATRA) can differentiate MDSCs into mature myeloid cells. However, whether ATRA suppression of MDSCs function could enhance PD-L1 blockade-mediated tumor immunotherapy remains unknown. Here, the frequency of tumor-infiltrating MDSCs in cervical cancer patients was measured. ATRA was used to target MDSCs both in vitro and in tumor-bearing mice. The impact of ATRA on the human cell line HeLa was also investigated. The frequency of MDSCs and T cells was determined by flow cytometry. The expression of immunosuppressive genes was measured with quantitative real time-PCR and infiltration of immune cells was assessed by immunohistochemical examination. We found that tumor-infiltrating PD-L1 + MDSCs were more prevalent in cervical cancer patients. Blockade of PD-L1 expression in MDSCs with anti-PD-L1 antibody cannot relieve the suppressive activity of MDSCs induced by HeLa cells, while ATRA efficiently abrogated the suppressive activity of MDSCs. Furthermore, ATRA had no effect on PD-L1 expression in HeLa cells in vitro. In in vivo treatment, ATRA decreased MDSCs accumulation and increased the frequency of CD8 + T cells in BALB/C mice with U14 cervical tumors. Importantly, a combination treatment of ATRA and anti-PD-L1 antibody further delayed U14 tumor growth and increased the proportion of CD62L − CD8 + T cells, CD62L − CD4 + T cells, CD107a + CD8 + T cells as well as IFN-γ and TNF-α levels in tumors. Our results provide a rationale for the use of ATRA to suppress MDSCs and enhance anti-PD-L1 cancer immunotherapy in cervical cancer.

类风湿关节炎(rheumatoid arthritis,RA)是一种以侵蚀性关节炎症为主要临床表现的全身性自身免疫性疾病,可以发生于任何年龄[1,2].RA的发病机制目前尚不明确,其基本病理表现为"滑膜炎",并逐渐出现关节软骨和骨破坏,最终导致关节畸形和功能丧失,可并发肺部疾病、心血管疾病、恶性肿瘤、抑郁症等.流行病学显示,我国RA的患病率为0.42％,患者总数约500万[3],男女比约为1∶4[4,5].现代医学并无根治RA的方法,临床多采用非甾体抗炎药、激素、免疫抑制剂等[6].中医药对缓解RA关节及关节外症状、提高临床疗效、改善生活质量等方面具有独特优势[7,8].

BACKGROUND:Enhanced glycolysis occurs in most human cancer cells and is related to chemoresistance. However, detailed mechanisms remain vague.METHODS:Using proteinomics analysis, we found that the glycolytic enzyme Phosphoglycerate mutase 1 (PGAM1) was highly expressed in the paclitaxel-resistant ovarian cancer cell line SKOV3-TR30, as compared to its parental cell line SKOV3. Cell Counting Kit-8 proliferation experiment, plasmids and siRNA transfection, pyruvic acid and lactic acid production detection, immunofluorescence staining of functional mitochondria and oxygen consumption rate and extracellular acidification rate measurement were uesd to assess the glycolytic metabolism and paclitaxel resistance in ovarian cancer cells. The expression and prognostic effect of PGAM1 in 180 ovarian cancer patients were analyzed.RESULTS:SKOV3-TR30 cells display higher glycolytic flux and lower mitochondrial function than SKOV3 cells. Down-regulation of PGAM1 in SKOV3-TR30 cells resulted in decreased paclitaxel resistance. Up-regulation of PGAM1 in SKOV3 cells led to enhanced paclitaxel resistance. Analysis of the glycolytic flux revealed that PGAM1-mediated pyruvic acid or lactic acid production could modulate the capabilities of ovarian cancer cell resistance to paclitaxel. Our data also show high expression of PGAM1 as significantly correlated with reduced overall survival and reduced progression free survival in ovarian cancer patients.CONCLUSIONS:PGAM1 acts to promote paclitaxel resistance via pyruvic acid and/or lactate production in ovarian cancer cells. Inhibiting PGAM1 may provide a new approach to favorably alter paclitaxel resistance in ovarian cancer.

风湿病是以侵犯关节、骨骼、血管、肌肉及周围软组织(滑囊、肌腱、筋膜等)或结缔组织为特点的一组异质性疾病的统称,其中大多数为自身免疫性疾病.地黄饮子阴阳并补、滋阴涵阳、水火相济、培本固元.房定亚教授力倡辨病与辨证相结合,擅以专方专药治疗专病,在临床中经常运用地黄饮子治疗风湿病,他认为地黄饮子可以改善体质、调节激素水平和免疫功能,能够治疗元气不足、肾精匮乏而导致的形神衰退性疾病,对于久病体虚的风湿病患者尤为适宜.结合类风湿关节炎合并干燥综合征、多发性肌炎、脊髓型颈椎病3个验案对房教授运用地黄饮子治疗风湿病的经验进行介绍.

大柴胡汤首载于《伤寒论》和《金匮要略》，是治疗少阳、阳明合病的经典方剂。房定亚教授善用大柴胡汤治疗符合少阳、阳明合病的各类疑难杂症，尤以肝胆疾病、胃肠疾病、肺系疾病、皮肤疾病为主。本文列举四则医案，体现房教授运用大柴胡汤的要点，并介绍本方与其他方剂合用的经验。

Mutations of the thyroid hormone receptor interactor 11 gene (TRIP11, OMIM: 604505) at 14q32.12 have been associated with the autosomal recessive achondrogenesis type IA (ACG1A, OMIM: 200600) or osteochondrodysplasia (ODCD, OMIM: 184260). In this clinical report of a Chinese family, the mother had two consecutive pregnancies with similar aberrant phenotypes in the fetuses showing severe limb shortening. Whole exome sequencing (WES) of DNA from the second fetus identified a heterozygous frameshift mutation (NM_004239: c.3852delT) of TRIP11. Although this was consistent with the fetal clinical phenotypes, initial review of the WES results implied another novel mutation. To test this, we used high-precision clinical exome sequencing (HPCES) and found a mutation in Intron 18 of TRIP11 (c.5457+77T>G). Moreover, the sequencing depth of this mutation was only 3× that of WES compared with 161× that by HPCES. To ascertain the pathogenesis of the mutation (c.5457+77T>G), RT-PCR conducted using the parents' blood samples showed a 77-bp intronic sequence in the transcripts, which might have encoded for a shortened protein because of early termination due to code shifting. Our study furthers current understanding of deep intron function and provides a novel diagnostic method of deep intragenic mutations in families having two or more consecutive pregnancies with similar aberrant fetal phenotypes.

Recent studies have shown that the expression of ENPP1 is related to differentiation, death, dissemination and chemosensitivity of tumor cells. So far, there is no research in ovarian carcinoma. This study aimed at exploring the role of ENPP1 gene in ovarian carcinoma, the relationship with prognostic indicators and chemotherapy resistance, and investigates the possibility of molecular targeted therapy. The expression of ENPP1 in 41 normal ovarian epithelial tissues, 97 ovarian serous cystadenoma and 103 HGSOC tissues was detected by IHC. In ovarian cancer tissues and ovarian cancer cell lines, mRNA and protein expression of ENPP1 was determined by qRT-PCR and Western blot. The ENPP1 expression was knockdowned by siRNA. Cell proliferation was measured with the BrdU Cell Proliferation ELISA. Cell migration and invasion were detected by Wound-Healing, Transwell migration and Matrigel invasion assay. Caspase 3 activity was determined by the CaspACE. The expression of EMT markers such as E-cadherin, N-cadherin, and Vimentin was measured, and the expression of PCNA and MMP9 was also be detected. The results showed that the expression of ENPP1 was significantly increased in high-grade ovarian serous carcinoma, the number of strong expression was 85.4% (22.3%+63.1%) and only 1.03% (1.03%+0.0%) in serous cystadenoma, but no in normal ovarian epithelium (P< 0.05). And the stronger the expression of ENPP1, the later the FIGO stage and the poorer differentiation of cells (P = 0.001 or <0.001, respectively). However, no correlation was found between the expression of ENPP1 and chemosensitivity. ENPP1 was also highly expressed in ovarian cancer tissues and in epithelial ovarian cancer cell lines (A2780, CaoV3, OVCAR3, SKOV3 and 3ao). After down-regulation of ENPP1 expression by RNA interference, the cell proliferation, migration and invasion of ovarian cancer cell decreased significantly, the expression of apoptosis related gene caspase 3 increased significantly, while the expression of PCNA and MMP9 was significantly down regulated. In addition, EMT biological characteristics of A2780 and SKOV3 cells were also inhibited. In summary, the increased expression of ENPP1 may be related to the occurrence of HGSOC, and indicate that the disease progresses rapidly and the prognosis is poor. ENPP1 may be considered as a potential molecular therapeutic target.

银屑病关节炎属于自身免疫性疾病,其病程迁延,易复发,晚期可发生关节畸形.本病病位在关节、络脉,涉及肝脾肾,病机关键为湿热毒蕴、络脉痹阻,发作期以湿热毒蕴络脉为主,缓解期以脾虚湿滞络脉为要.发作期治疗重在清热解毒、凉血通络,选用四妙勇安汤加减;缓解期注重健脾益气、祛湿通络,选用参苓白术散加减.久病入络,湿热毒邪痹阻络脉,气血运行不畅,瘀血内生;脾虚湿阻,气血化生无源,推动无力,瘀血内生.因此,临床治疗应注重调和气血、化瘀通络.

儿童进行性骨化性肌炎是一种先天性遗传性结缔组织病，临床较罕见，尚缺乏有效治疗手段。房定亚教授治疗本病在初期应用活血化痰、软坚散结兼顾补肾，后期患儿病情稳定，则从疾病病理出发，运用中药调节免疫，取得较好效果。附验案进行分析。

白塞病是一种以血管炎为基本病理改变的慢性全身性炎症疾病,病变可累及多系统,病情复杂,缠绵难愈.周彩云教授主张中西医结合治疗白塞病,提出了分期辨治的治疗原则,认为"湿热毒邪内蕴、热毒伤络"为本病病机关键,急性活动期关键病机为"湿热毒邪内蕴、热毒伤络",治疗应以清热解毒、凉血护络为大法,可兼以清热利湿;间歇期病机特点为"脾气亏虚、湿热毒余邪内蕴、络脉受损",治疗应益气健脾,兼清热解毒利湿、凉血护络.

Traditional Chinese medicine (TCM) has been used successfully to treat rheumatoid arthritis (RA). Qingre Huoxue treatment (Qingre Huoxue decoction (QRHXD)/Qingre Huoxue external preparation (QRHXEP)) is a therapeutic scheme of TCM for RA. To date, there have been few studies comparing the efficacy and safety of QRHXD and conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) for the treatment of active RA. This was investigated in a multicenter, double-blind, randomized controlled trial involving 468 Chinese patients with active RA [disease activity score (DAS)-28 > 3.2] treated with QRHXD/QRHXEP (TCM group), methotrexate plus hydroxychloroquine [Western medicine (WM) group], or both [integrative medicine (IM) group]. Patients were followed up for 24 weeks. The primary outcome measure was the change in DAS-28 from baseline to 24 weeks. The secondary outcome measures were treatment response rate according to American College of Rheumatology 20, 50, and 70% improvement criteria (ACR-20/50/70) and the rate of treatment-related adverse events (TRAEs). The trial was registered at (NCT02551575). DAS-28 decreased in all three groups after treatment (p < 0.0001); the score was lowest in the TCM group (p < 0.05), while no difference was observed between the WM and IM groups (p > 0.05). At week 24, ACR-20 response was 73.04% with TCM, 80.17% with WM, and 73.95% with IM (based on the full analysis set [FAS], p > 0.05); ACR-50 responses were 40.87, 47.93, and 51.26%, respectively, (FAS, p > 0.05); and ACR-70 responses were 20.87, 22.31, and 25.21%, respectively, (FAS, p > 0.05). Thus, treatment efficacy was similar across groups based on ACR criteria. On the other hand, the rate of TRAEs was significantly lower in the TCM group compared to the other groups (p < 0.05). Thus, QRHXD/QRHXEP was effective in alleviating the symptoms of active RA-albeit to a lesser degree than csDMARDs-with fewer side effects. Importantly, combination with QRHXD enhanced the efficacy of csDMARDs. These results provide evidence that QRHXD can be used as an adjunct to csDMARDs for the management of RA, especially in patients who experience TRAEs with standard drugs.

目的:观察不同中医证型活动期类风湿关节炎(RA)患者血液高凝状态的差异,探讨RA凝血/纤溶异常与中医学"热、湿、瘀、肾虚"等病邪的关系.方法:选取2013年8月至2015年1月中国中医科学院西苑医院风湿病科收治的活动期RA患者209例作为研究对象,检测D-二聚体(DD)、纤维蛋白原(Fbg)、血小板计数(PLT),并进行中医证型分类,最后将采集的数据进行统计分析.结果:活动期RA患者DD、Fbg、PLT水平明显高于健康对照组;与肝肾阴虚、肾气虚寒2组"虚"性证候比较,湿热痹阻、寒湿痹阻、瘀血痹阻证、湿热夹瘀等"实"性证候的DD、Fbg、PLT水平的升高更为显著.RA患者DD、Fbg水平与病情活动均显著正相关,PLT与类风湿关节炎患者病情评分亦呈正相关,但相关性较DD、Fbg低.结论:DD、Fbg、PLT等凝血/纤溶指标在RA湿热夹瘀、瘀血痹阻等实性证型中的含量显著高于肾气虚寒型等虚性证型.DD、Fbg可能成为新的RA病情活动度监测指标.

干燥综合征是一种常见的主要累及人体外分泌腺的免疫病,除口干、眼干等腺体损害相关表现外还可出现呼吸、循环等多系统的损害,严重影响患者的身心健康及生存质量.现代医学对于本病尚无特效治疗,目前临床采用中医治疗本病已屡见不鲜,且取得了较好的疗效反馈.干燥综合征属于中医学"燥痹"范畴,其病机复杂,病情缠绵难愈.周彩云教授根据多年临证经验,提出本病发生发展的重要环节为热气怫郁、玄府闭塞,因此当以"达郁散热、宣通气液"为治疗大法.此外,根据"燥者濡之""脾胃为气血生化之源"提出"养阴生津、运化脾胃"为治疗干燥综合征的第二大法,且在治疗过程中应重视"身心同调",在临证中取得了较为满意的效果.本文拟从"热气怫郁"理论阐述其对于干燥综合征的治疗经验,以期为本病的临床治疗开拓思路.

Background: Paclitaxel, as an anti-microtubule drug, has been recommended to be the first-line chemotherapy agent for ovarian cancer for about two decades. However, most patients with advanced stage relapse within two years and ultimately die of relapsed cancer displaying increased chemoresistance. The mechanisms underlying paclitaxel resistance remain ncompletely understood.Methods: The paclitaxel-resistant ovarian cancer cell line SKOV3-TR30 and its parental cell line SKOV3 were analyzed by proteinomics. The glycolytic enzyme PGAM1-modulated glycolytic flux including pyruvic acid production and lactic acid production, and mitochondrial function was investigated using the assays kit. The correlations between PGAM1 expression, overall survival and progression free survival were evaluated for ovarian cancer patients. To elucidate the underlying mechanisms involved in paclitaxel resistance, PGAM1 gene knockout, gene overexpression and/or manipulation of glycolytic products were employed, followed by Western blot, immunostaining, and cell viability assay.Results: PGAM1 was highly expressed in the paclitaxel resistant ovarian cancer cell line SKOV3-TR30, as compared to its parental cell line SKOV3. A high expression of PGAM1 was ignificantly correlated with a reduced overall survival and progression free survival in ovarian cancer patients. Under paclitaxel exposure, SKOV3 cells showed a stronger mitochondrial function than SKOV3-TR30 cells, suggesting that under the stress, SKOV3-TR30 cells had responded with enhanced glycolysis rather than undergoing oxidative phosphorylation. Down-regulation of PGAM1 in SKOV3 TR30 cells resulted in decreased paclitaxel resistance. Up-regulation of PGAM1 in SKOV3 cells led to enhanced paclitaxel resistance. Analysis of the lycolytic flux revealed that PGAM1-mediated pyruvic acid or lactic acid production could control the capabilities of ovarian cancer cell resistance to paclitaxel.Conclusions: Our study demonstrated that PGAM1 could act as a modulator linked to paclitaxel sensitivity in ovarian cancer cells. Blocking PGAM1 may provide a new approach to reverse paclitaxel resistance in ovarian cancer patients.