Transcriptomics Reveals the Mechanism of Purpureocillium lilacinum GZAC18-2JMP in Degrading Keratin Material.

Microbial degradation of keratin is characterized by its inherent safety, remarkable efficiency, and the production of copious degradation products. All these attributes contribute to the effective management of waste materials at high value-added and in a sustainable manner. Microbial degradation of keratin materials remains unclear, however, with variations observed in the degradation genes and pathways among different microorganisms. In this study, we sequenced the transcriptome of Purpureocillium lilacinum GZAC18-2JMP mycelia on control medium and the medium containing 1% feather powder, analyzed the differentially expressed genes, and revealed the degradation mechanism of chicken feathers by P. lilacinum GZAC18-2JMP. The results showed that the chicken feather degradation rate of P. lilacinum GZAC18-2JMP reached 64% after 216 h of incubation in the fermentation medium, reaching a peak value of 148.9 µg·mL-1 at 192 h, and the keratinase enzyme activity reached a peak value of 211 U·mL-1 at 168 h, which revealed that P. lilacinum GZAC18-2JMP had a better keratin degradation effect. A total of 1001 differentially expressed genes (DEGs) were identified from the transcriptome database, including 475 upregulated genes and 577 downregulated genes. Kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis of the DEGs revealed that the metabolic pathways related to keratin degradation were mainly sulfur metabolism, ABC transporters, and amino acid metabolism. Therefore, the results of this study provide an opportunity to gain further insight into keratin degradation and promote the biotransformation of feather wastes.

Allulose mitigates chronic enteritis by reducing mitochondria dysfunction via regulating cathepsin B production.

Metabolic changes have been linked to the development of inflammatory bowel disease (IBD), which includes colitis. Allulose, an endogenous bioactive monosaccharide, is vital to the synthesis of numerous compounds and metabolic processes within living organisms. Nevertheless, the precise biochemical mechanism by which allulose inhibits colitis remains unknown. Allulose is an essential and intrinsic protector of the intestinal mucosal barrier, as it maintains the integrity of tight junctions in the intestines, according to the current research. It is also important to know that there is a link between the severity of inflammatory bowel disease (IBD) and colorectal cancer (CRC), chemically-induced colitis in rodents, and lower levels of allulose in the blood. Mice with colitis, either caused by dextran sodium sulphate (DSS) or naturally occurring colitis in IL-10-/- mice, had less damage to their intestinal mucosa after being given allulose. Giving allulose to a colitis model starts a chain of reactions because it stops cathepsin B from ejecting and helps lysosomes stick together. This system effectively stops the activity of myosin light chain kinase (MLCK) when intestinal epithelial damage happens. This stops the breakdown of tight junction integrity and the start of mitochondrial dysfunction. To summarise, the study's findings have presented data that supports the advantageous impact of allulose in reducing the advancement of colitis. Its ability to stop the disruption of the intestinal barrier enables this. Therefore, allulose has potential as a medicinal supplement for treating colitis.

Arabinose confers protection against intestinal injury by improving integrity of intestinal mucosal barrier.

There is a growing amount of research that highlights the significant involvement of metabolic imbalance and the inflammatory response in the advancement of colitis. Arabinose is a naturally occurring bioactive monosaccharide that plays a crucial role in the metabolic processes and synthesis of many compounds in living organisms. However, the more detailed molecular mechanism by which the administration of arabinose alleviates the progression of colitis and its associated carcinogenesis is still not fully understood. In the present study, arabinose is recognized as a significant and inherent protector of the intestinal mucosal barrier through its role in preserving the integrity of tight junctions within the intestines. Also, it is important to note that there is a positive correlation between the severity of inflammatory bowel disease (IBD) and colorectal cancer (CRC), as well as chemically-induced colitis in mice, and lower levels of arabinose in the bloodstream. In two mouse models of colitis, caused by dextran sodium sulfate (DSS) or by spontaneous colitis in IL-10-/- mice, damage to the intestinal mucosa was reduced by giving the mice arabinose. When arabinose is administrated to model with colitis, it sets off a chain of events that help keep the lysosomes together and stop cathepsin B from being released. During the progression of intestinal epithelial injury, this process blocks myosin light chain kinase (MLCK) from damaging tight junctions and causing mitochondrial dysfunction. In summary, the results of the study have provided evidence supporting the beneficial effects of arabinose in mitigating the progression of colitis. This is achieved through its ability to avoid dysregulation of the intestinal barrier. Consequently, arabinose may hold promise as a therapeutic supplementation for the management of colitis.

Corrigendum to "Basal cell carcinoma arising from the scrotum: An understated entity" [Urol Case Rep 33 (2020) 101332].

[This corrects the article DOI: 10.1016/j.eucr.2020.101332.].

A modified single-endobutton technique combined with nice knot for treatment of Rockwood type III or V acromioclavicular joint dislocation.

PURPOSE: Double-endobutton technique, as a widely accepted strategy for the treatment of acromioclavicular joint dislocation, is undergoing constant improvement. This study aims to assess the clinical effect of a modified single-endobutton combined with the nice knot in the fixation of Rockwood type III or V acromioclavicular joint dislocation. METHODS: From January 2016 to June 2019, 16 adult patients (13 males and 3 females) with Rockwood type III or V acromioclavicular joint dislocation were treated with a modified single-endobutton technique combined with the nice knot in our department. The age ranged from 18 to 64 years old with an average of 32.8 years old. Operative time, intraoperative blood loss, post-operative clinical outcomes and radiographic results were recorded and analyzed. Preoperative and last follow-up scores in the Constant-Murley Scale, Neer score, Rating Scale of the American Shoulder and Elbow Surgeons and VAS scale and complications such as infection, re-dislocation, implant loosening, medical origin fracture and hardware pain were recorded and evaluated. RESULTS: Sixteen patients were followed up for 6 to 18 months with an average of 10.3 months. The operative time was 50-90 min with an average of (62.5 ± 3.10) min. The intraoperative blood loss was 30-100 ml, with an average of (55.0 ± 4.28) ml. The complications, such as wound infection, internal fixation failure and fractures, were not found in these cases. According to Karlsson criteria, there were excellent in 14 cases, good in 2 cases at the final follow-up. The mean VAS score of the patients was 5.88 ± 0.26 preoperatively, compared with 0.19 ± 0.14 at the final follow-up evaluation. The difference was statistically significant (P < 0.05). The mean Constant score was 45.5 ± 2.0 preoperatively, compared to 94.0 ± 0.73 at the final follow-up evaluation. The difference was statistically significant (P < 0.05). Patients had statistically significant preoperative and postoperative AC (acromioclavicular distance) and CC (coracoclavicular distance) distances (P < 0.05); 6 months postoperatively the AC(P = 0.412) and CC(P = 0.324) distances were not statistically significant compared to the healthy side. CONCLUSION: Nice knot provides a reliable fixation for the single-endobutton technique in the treatment of acromioclavicular dislocations. The modified single-endobutton technique combined with the nice knot can achieve good clinical outcomes in the treatment of Rockwood type III or V acromioclavicular joint dislocation.

Upregulation of circRNA hsa_circ_0008726 in Pre-eclampsia Inhibits Trophoblast Migration, Invasion, and EMT by Regulating miR-345-3p/RYBP Axis.

Accumulating evidence shows that impaired spiral artery remodeling, placental dysfunction, and insufficient trophoblast infiltration contribute to the etiology and pathogenesis of pre-eclampsia (PE). circRNAs are a class of endogenous non-coding RNAs implicated in the pathogenesis of many diseases, including PE. This study aims to investigate the role of circRNA hsa_circ_0008726 in regulating the migration and invasion of extravillous trophoblast cells. RNase R assay was performed to confirm that circ_0008726 was a circular transcript. The expression of circ_0008726, RYBP, and miR-345-3p was examined by qRT-PCR. The functional interaction between miR-345-3p and circ_0008726 or RYBP was confirmed using dual-luciferase reporter assay and RNA immunoprecipitation (RIP). Cell migration and invasion ability was analyzed by Transwell assays. Western blot was used for the quantification of RYBP protein level. Circ_0008726 expression was significantly increased in PE placenta tissues as compared with normal placenta tissues. Circ_0008726 was resistant to RNase R digestion and was predominately located in the cytoplasm of HTR-8/SVneo cells. Silencing circ_0008726 promoted cell migration and EMT (epithelial-mesenchymal transition), while circ_0008726 overexpression suppressed these processes. Mechanistically, circ_0008726 sponged miR-345-3p to negatively regulate its expression, and miR-345-3p negatively modulated the expression of RYBP. In PE samples, the expression level of circ_0008726 was negatively correlated with miR-345-3p level, but was positively correlated with RYBP expression. Transfection of miR-345-3p mimic or RYBP knockdown counteracted the effects of circ_0008726 overexpression on cell migration and EMT. Our data demonstrate the upregulation of circ_0008726 in PE placenta, which inhibits the migration, invasion, and EMT of HTR-8/SVneo cells by targeting miR-345-3p/RYBP axis. These data suggest that circ_0008726 could be a potential biomarker and therapeutic target for PE.

The Clinical Application and Prospect of Smart Prenatal Care and Postpartum Recovery.

Scientific and technological advancement has increased the requirement for modern medical systems, leading to smartphone-based intelligent prenatal care and postpartum recovery. This kind of prenatal care and postpartum recovery including a remote monitoring system for fetal heart monitoring, blood glucose, and weight overcomes the restrictions of time and space and provides all-round, convenient, rapid, and accurate services to the medical systems, doctors, and pregnant women. This paper reviews the current research on intelligent medical services for pregnant women, particularly for prenatal care and postpartum recovery.

The abnormal expression of Tim-3 is involved in the regulation of myeloid-derived suppressor cells and its correlation with preeclampsia.

INTRODUCTION: Maternal immune system tolerance to the semi-allogeneic fetus is critical to a successful pregnancy. We previously reported that myeloid-derived suppressor cells (MDSC) was associated with maternal immune imbalance. T cell immunoglobulin and mucin-containing protein 3 (Tim-3)/Galectin-9 (Gal-9) pathway modulates function of various immune cells in maternal-fetal interface. However, the regulatory effects of Tim-3/Gal-9 signaling on MDSCs and its role in preeclampsia (PE) remain unclear. METHODS: In the current study we investigated the expression of Tim-3 on MDSC in preeclampsia (PE) patients to further explore the pathogenesis of PE. RESULTS: The proportion of Tim-3+ M-MDSC (monocytic MDSC) cells was higher in PE patients than in healthy control. Meanwhile, the protein expression of Gal-9, as the ligand of Tim-3, was increased in placenta of PE patients. M-MDSC also expressed a higher level of interferon-γ (IFN-γ) and a lower level of transforming growth factor-ß (TGF-ß) in PE. Furthermore, our study suggested that blocking Tim-3 could attenuate the inhibitory function of MDSC. DISCUSSION: The abnormal expression of Tim-3 on MDSC might be involved in the pathogenesis of PE, and could be a marker to evaluate the immune function in PE.

[Retracted] Long non­coding RNA MCM3AP­AS1 drives ovarian cancer progression via the microRNA­143­3p/TAK1 axis.

Following the publication of this article, the authors' attention was drawn to the fact that Table I and Fig. 6 contained some errors: The former contained some incorrect data, whereas the latter contained some inappropriately selected tumor images. Following a further investigation in the Editorial Office, it has come to light that there were other possible anomalies associated with the presentation of the tumor images, and also that parts of the figure may have been published previously. Taking everything into consideration, the Editor has decided that the article should be retracted from the publication due to a lack of confidence in the data presented in this article. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not received any reply. The Editor regrets any inconvenience that the retraction of the paper will cause. [the original article was published in Oncology Reports 44: 1375­1384, 2020; DOI: 10.3892/or.2020.7694].

Estrogen and Preeclampsia: Potential of Estrogens as Therapeutic Agents in Preeclampsia.

There is a significant decline in the estrogen levels in preeclampsia, and exogenous administration of estradiol normalizes blood pressure and other associated symptoms of preeclampsia. The decrease in estrogen levels may be due to changes in enzyme activities of hydroxysteroid (17-ß) dehydrogenase 1, aromatase, and COMT. There is also a decrease in the novel, estrogenic G-protein-coupled receptor 30 (GPR30) in the placental trophoblast cells in preeclampsia. The activation of GPR30 protects the placenta from hypoxia-reoxygenation injury, decreases apoptosis and increases proliferation through eNOS and PI3K-Akt signaling pathways. Estrogens may also increase Ca2+-activated K+ channel function, decrease the release of inflammatory cytokines, and oxidative stress to improve placental perfusion. Both preclinical and clinical studies show the decrease in the 2-methoxyestradiol levels in preeclampsia, which may be due to a decrease in estradiol itself along with a decrease in the enzymatic actions of the COMT enzyme. 2-Methoxyestradiol activates HIF1α and vascular endothelial growth factor receptors (VEGFR-2) to maintain placental perfusion by increasing angiogenesis. The present review discusses the preclinical and clinical studies describing the role of estrogen in preeclampsia along with possible mechanisms.

Integrin ß1 regulates proliferation, apoptosis, and migration of trophoblasts through activation of phosphoinositide 3 kinase/protein kinase B signaling.

AIMS: Abnormal trophoblast invasion is one of the onsets of preeclampsia (PE). Studies found that integrin ß1 (ITGB1) is closely related to PE, but the role of ITGB1 in the progression of trophoblast remained unclear. Therefore, we studied the functional role of ITGB1 in PE and its effects on trophoblast. METHODS: ITGB1 expression in placenta tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR). The effects of transfection on HTR-8/SVneo cells were analyzed by qRT-PCR and western blotting. After cell transfection, colony formation assay, flow cytometry, wound healing assay, and transwell assay were performed to detect cell proliferation, apoptosis, migration, and invasion. Western blotting assay was used for determining phosphoinositide 3 kinase (PI3K) and protein kinase B (Akt) signaling pathway. After inhibiting PI3K/Akt pathway, apoptosis-regulated proteins were detected by western blotting, and the effects of inhibitor on the migration and invasion changes were examined. RESULTS: ITGB1 was downregulated in placenta tissues from PE patients, as compared with normal. ITGB1 overexpression in HTR-8/SVneo cells enhanced cell proliferation, migration, and invasion, reduced cell apoptosis, and improved phosphorylation of PI3K and Akt. However, ITGB1 depletion resulted in an opposite effect to its overexpression. Inhibition of PI3K/Akt pathway completely blocked the effect of ITGB1 overexpression on cells, because we observed that apoptosis-regulated proteins were highly upregulated, and that cell migration and invasion were reduced. CONCLUSION: ITGB1 regulated HTR-8/SVneo cell progression by activation of the PI3K/Akt pathway.

Application and Prospects of Molecular Imaging in Immunotherapy.

Recently, immunotherapies that target the interactions of programmed cell death 1 (PD-1) with its major ligands, programmed death ligand 1 (PD-L1) and programmed death ligand 2 (PD-L2), have achieved significant success. To date, several immune checkpoint inhibitors targeting the PD-1/PD-L1 pathway have been developed to treat melanoma, non-small cell lung cancer, head and neck cancer, renal cell carcinoma, and urothelial carcinoma. Despite promising outcomes with immunotherapy, there are many limitations to several current immune biomarkers for predicting immune benefits and to traditional imaging for evaluating the efficacy and prognosis of immunotherapy and monitoring adverse reactions. In this review, we recommend a novel imaging method, molecular imaging. This paper reviews the application and prospects of molecular imaging in the context of current immunotherapies in regard to the following aspects: 1) detecting the expression of PD-1/PD-L1; 2) evaluating the efficacy of immunotherapy; 3) assessing patient prognosis with immunotherapy; 4) monitoring the toxicity of immunotherapy; and 5) other targets imaging.

Basal cell carcinoma arising from the scrotum: An understated entity.

Basal cell carcinoma (BCC) is the most commonly occurring carcinoma among humans. Reports of this lesion on nonexposed areas, such as the scrotum, soles, vulva, groin, pubic region, and axilla, are relatively uncommon. We present the case of a male patient with BCC located in the scrotum with a duration of 12 years who was successfully treated by local excision. Histopathology revealed infiltration by BCC. Our objective of this report is to remind specialists like urologists of the possibility of scrotal BCC when encountering scrotal lesions of unknown origin or not responding to topical treatments in a reasonable time frame.

Long non­coding RNA MCM3AP­AS1 drives ovarian cancer progression via the microRNA­143­3p/TAK1 axis.

The long non­coding RNA (lncRNA) MCM3AP antisense 1 (MCM3AP­AS1) has previously been shown to be a key regulator of multiple types of cancer; however whether it is important in the context of ovarian cancer (OC) is uncertain. The present study determined that MCM3AP­AS1 expression in samples from patients with OC was significantly increased, and was associated with tumor stage, presence of lymph node metastases and poorer overall survival. The role of this lncRNA was investigated in vitro, and it was observed that knockdown of MCM3AP­AS1 impaired OC cell proliferation, migration and colony formation. Similarly, it disrupted tumor growth in vivo. The present study further determined that MCM3AP­AS1 was able to directly interact with microRNA (miRNA or miR)­143­3p as a competing endogenous (ce)RNA for this miRNA, thereby regulating the expression of transforming growth factor­ß­activated kinase 1 (TAK1), a known target of miR­143­3p in OC. Consistent with this, inhibition of miR­143­3p was sufficient to partially reverse the effects of MCM3AP­AS1­knockdown, which inhibited the proliferation, migration and invasion of OC cells. Together, these results indicate that MCM3AP­AS1 serves as an oncogenic lncRNA in OC by binding to miR­143­3p and thereby promoting TAK1 expression, and suggest that this lncRNA may be a possible target for therapy in OC.

circ_KIAA1429 accelerates hepatocellular carcinoma advancement through the mechanism of m6A-YTHDF3-Zeb1.

AIMS: Hepatocellular carcinoma (HCC), one of the most common cancer, causes the fourth cancer-related deaths around the world. N6-methyladenosine (m6A) has been reported to mediate circRNA translation in cancer biology. However, the mechanisms by which m6A and circRNA in post-transcriptional in HCC progression remain poorly understood. This study aimed to explore the mechanisms by which m6A and circRNA in post-transcriptional in HCC progression. MAIN METHODS: circ_KIAA1429 (hsa_circ_0084922) expression profiles in matched normal and HCC tissues were detected using microarray analysis. The biological roles of circ_KIAA1429 in progression of HCCC were measured both in vitro and in vivo. KEY FINDINGS: In this study, we found hsa_circ_0084922, which came from KIAA1429, named circ_KIAA1429, was upregulated in HCC cells and tumor tissues. Overexpression of circ_KIAA1429 can facilitate HCC migration, invasion, and EMT process. However, knockdown of circ_KIAA1429 lead to the opposite results. Furthermore, it was demonstrated that Zeb1 was the downstream target of circ_KIAA1429. Up-regulation of Zeb1 led to HCC cells metastasis induced by circ_KIAA1429. In addition, YTHDF3 enhanced Zeb1 mRNA stability via an m6A dependent manner. SIGNIFICANCE: This study revealed that circ_KIAA1429 could accelerate HCC advancement, maintained the expression of Zeb1 through the mechanism of m6A-YTHDF3-Zeb1 in HCC. What's more, it might represent a potential therapeutic target in HCC.

Benign testicular cavernous hemangioma presenting with acute onset: A case report.

Cavernous hemangioma is a congenital, benign vascular tumor that occurs in the deep dermis and subcutaneous tissue. Testicular cavernous hemangioma is extremely rare, mostly occurring during childhood or adolescence. Testicular cavernous hemangioma is a benign tumor that appears as a slowly growing painless mass. In rare cases, it may be associated with acute testicular infarction or torsion with acute onset. We herein report the case of a patient with an atypical presentation of testicular cavernous hemangioma, characterized by acute painful testicular enlargement triggered by minor injury. The patient underwent right radical orchiectomy, and histopathological examination confirmed the diagnosis of testicular cavernous hemangioma. Although this is a rare tumor, it should be considered in the differential diagnosis of testicular tumors.

Comparison of MRI and MRA for the diagnosis of rotator cuff tears: A meta-analysis.

BACKGROUND: Numerous quantitatively based studies measuring the accuracy of MRI and MRA for the diagnosis of rotator cuff tears remain inconclusive. In order to compare the accuracy of MRI with MRA in detection of rotator cuff tears a meta-analysis was performed systematically. METHODS: PubMed/Medline and Embase were utilized to retrieve articles comparing the diagnostic performance of MRI and MRA for use in detecting rotator cuff tears. After screening and diluting out the articles that met inclusion criteria to be used for statistical analysis the pooled evaluation indexes including sensitivity and specificity as well as hierarchical summary receiver operating characteristic (HSROC) curves with 95% confidence interval (CI) were calculated. RESULTS: Screening determined that 12 studies involving a total of 1030 patients and 1032 shoulders were deemed viable for inclusion in the meta-analysis. The results of the analysis showed that MRA has a higher sensitivity and specificity than MRI for the detection of any tear; similar results were observed in the detection of full-thickness tears. However, for the detection of partial-thickness tear, MRI has similar performance with MRA. CONCLUSION: MRI is recommended to be a first-choice imaging modality for the detection of rotator cuff tears. Although MRA have a higher sensitivity and specificity, it cannot replace MRI after the comprehensive consideration of accuracy and practicality.

Depiction of Vaginal Microbiota in Women With High-Risk Human Papillomavirus Infection.

Persistent infection with the carcinogenic human papillomavirus (HPV) is a prerequisite for the progression of cervical lesions and cancer. A growing body of research has focused on the functional role of the vaginal microbiota in the persistence of HPV infection. Understanding the microbial composition and structure in women with high-risk (hr)-HPV infection may help reveal associations between the vaginal microbiota and HPV infection, and identify potential biomarkers. Our study investigated the vaginal microbial community in women with and without hr-HPV infection, by using 16s rRNA gene sequencing. We found that microbial perturbations occurred in the early phase of hr-HPV infection. Lactobacillus and Sporolactobacillus were decreased, while bacteria related to bacterial vaginosis (BV), such as Gardnerella, Prevotella, Dialister, Slackia, Actinomyces, Porphyromonas, Peptoniphilus, Anaerococcus, Peptostreptococcus, Streptococcus, Ureaplasma, Megasphaera, and Mycoplasma were increased. Our results could offer insights into the correlations between hr-HPV and the vaginal microbiota in the early infection period, and provide indications that the predominance of some BV-associated bacteria during hr-HPV infection may increase the risk for cervical neoplasia.

Chaperone-mediated autophagy regulates apoptosis and the proliferation of colon carcinoma cells.

Chaperone-mediated autophagy (CMA) is one of the three types of autophagy. In recent years, CMA has been shown to be associated with the pathogenesis of several types of cancer. However, whether CMA is involved in the pathogenesis of colorectal cancer (CRC) remains unclear. In this study, we investigated CMA activity in tissue specimens from CRC patients and mouse models of colitis-associated CRC (induced by administration of AOM plus DSS). In addition, we down-regulated CMA in CT26 colon carcinoma cells stably transfected with a vector expressing a siRNA targeting LAMP-2A, the limiting component in the CMA pathway, to explore the role of CMA in these cells. Apoptosis was detected using TUNEL assay, and the apoptosis-related proteins were detected using western blotting. Cell proliferation was assessed using MTT assay, Ki-67 labelling and western blotting for PCNA. We found that LAMP-2A expression was significantly increased in CRC patients and mouse models and varied according to the stage of the disease. Inhibition of CMA in CT26 cells facilitated apoptosis, as evidenced by increased TUNEL immunolabeling, increased expression of Bax and Bnip3, and decreased expression of Bcl-2. Cell proliferation assays showed that inhibition of CMA impeded the proliferation of CT26 cells. These data support the hypothesis that CMA is up-regulated in CRC, and inhibition of CMA may be a new therapeutic strategy for CRC patients.

Concurrent apatinib and docetaxel vs apatinib monotherapy as third- or subsequent-line therapy for advanced gastric adenocarcinoma: a retrospective study.

PURPOSE: The aim of this study was to assess the efficacy and safety of concurrent apatinib and docetaxel therapy vs apatinib monotherapy as third- or subsequent-line treatment for advanced gastric adenocarcinoma (GAC). METHODS: Patients, who had received apatinib with or without docetaxel as third or more line therapy for advanced GAC, were retrospectively reviewed. Propensity score matching (PSM) analysis was performed to minimize the potential confounding bias. Kaplan-Meier curve and log-rank test were used to analyze the survival. Prognostic factors were estimated by Cox regression. Adverse events (AEs) were evaluated using CTCAE 4.0. RESULTS: Thirty-four patients received concurrent therapy, whereas 31 received monotherapy. The median progression-free survival (PFS) and overall survival (OS) in monotherapy and con-therapy groups were 2.5 and 4 months (P=0.002), 3.3 and 6 months (P=0.004), respectively. After PSM, the median PFS and OS in the con-therapy group were also superior to the monotherapy group (P=0.004 and P=0.017). Cox regression suggested that Eastern Cooperative Oncology Group performance status (ECOG PS; HR =2.437, 95% CI: 1.349-4.404, P=0.003), CA199 (HR =1.001, 95% CI: 1.000-1.002, P=0.016), and treatment options (HR =0.388, 95% CI: 0.222-0.679, P=0.001) had significant effects on OS. Grade 3/4 toxicities in the monotherapy and con-therapy groups were as follows: leukopenia (0% vs 8.8%), neutropenia (3.2% vs 2.9%), anemia (9.8% vs 8.8%), thrombocytopenia (6.4% vs 2.9%), proteinuria (3.2% vs 2.9%), aminotransferase (0% vs 11.8%), hyperbilirubinemia (9.8% vs 5.9%), hypertension (9.8% vs5.9%), hand-foot syndrome (3.2% vs 8.8%), nausea and vomiting (0% vs 11.8%), diarrhea (0% vs 5.9%), and fatigue (6.5% vs 2.9%). CONCLUSION: Patients with advanced GAC benefit more from concurrent apatinib and docetaxel therapy than apatinib monotherapy.