Objective: To investigate the repair of spinal cord injury (SCI) in rats using 3D bioprinted decellularized extra-cellular matrix (dECM) hydrogel, neural stem cells (NSCs), and TGF-(31 monoclonal antibody. Methods: The spinal cord-derived dECM hydrogel (SC-dECM-gel) was optimized for 3D printing. Rheological tests established a 3 % concentration as optimal. In vitro tests assessed the effects of TGF-(31 monoclonal antibody on NSC viability and differentiation. A rat SCI model was treated with the printed gel, and recovery was monitored using the Basso-Beattie-Bresnahan test and evoked potentials. Results: The 3 % SC-dECM-gel showed superior rheological properties. TGF-(31 monoclonal antibody enhanced NSC survival and differentiation in vitro. In vivo, the 3D bioprinted gel significantly improved motor function and promoted neuronal regeneration. Conclusion: 3D bioprinted SC-dECM-gel loaded with NSCs and TGF-(31 monoclonal antibody effectively restores motor function and promotes regeneration in SCI rats, offering a promising approach for SCI treatment.

Table contains sequences of primers and probes used to amplify the nine markers and ACTB in the LBx-BCM assay

The miR-497-195 cluster facilitates the occurrence and development of cancer. This study aims to investigate whether the miR-195-497 cluster could regulate the progression of colorectal cancer by regulating the common target gene, FOS-related antigen 1 ( FRA1 ). Overexpression of the miR-195/497 vector was used to evaluate the effect of overexpression of miR-195-497 clusters on the biological behavior of colon cancer cells. In animal experiments, tumor growth and metastasis were recorded by constructing a nude mouse model of a subcutaneously implanted tumor. miR-195 and miR-497 were expressed to varying degrees in Caco-2, LoVo, and HT-29 cells. Overexpression of miR-195/497 and inhibition of FRA1 decreased HT-29 cell proliferation, inhibited cell invasion and migration, and promoted Epithelial-mesenchymal transition (EMT). In vivo experiments showed that the overexpression of miR-195/497 or inhibition of FRA1 inhibited tumor growth, affected EMT in tumor cells, and inhibited the expression of FRA1 . Additionally, the aforementioned conditions had the best effect when used together. The miR-195-497 cluster can regulate the proliferation, EMT, invasion, and migration of colorectal cancer cells by regulating the common target gene FRA1 , thereby affecting the development of colorectal cancer.

Figure shows changes in LBx-BCM methylation in response to chemotherapy in 7 additional patient longitudinal serial samples. LBx-BCM was performed and cumulative methylation (CM) (Y-axis) is plotted from serum samples drawn at baseline (0 days) and immediately before each treatment cycle (X-axis). For each patient, treatment cycles are shown as a shaded area. PD, progressive disease; SD, stable disease (SD).

Figure shows ACTB reference gene DNA levels plotted for each of the 132 study samples. Stage IV breast cancer patient sera had significantly higher total ACTB DNA (lower Ct) compared to normal (Mann Whitney P < 0.0001). Descriptive statistics are shown for normal vs. cancer and for methylation Cartridge A vs Cartridge B

Figure shows the relationship between PCR Cycle threshold (Ct) and target DNA copy (0-300 copies) input

Figure shows the analytical sensitivity of LBx-BCM based detection of fully methylated DNA (0-300 copies) spiked into normal serum separately for each gene in the panel in 10-11 replicate assays

Figure shows the perfomance of LBx-BCM in the training set samples. A histogram shows cumulative methylation for each sample, and a box plot shows significnt difference of methylation in serum of metastatic breast cancer patients compared to normal individuals (Mann Whitney p= 0.002)

The table provides descriptive statistics and coefficient of variation for methylation in each gene in replicate LBx-BCM analyses of 300 copies of fully methylated DNA spiked into normal serum or plasma

The table provides a step by step guide to calculate methylation in each gene followed by cumulative methylation using the algorithm derived in this paper.

Current molecular liquid biopsy assays to detect recurrence or monitor response to treatment require sophisticated technology, highly trained personnel, and a turnaround time of weeks. We describe the development and technical validation of an automated Liquid Biopsy for Breast Cancer Methylation (LBx-BCM) prototype, a DNA methylation detection cartridge assay that is simple to perform and quantitatively detects nine methylated markers within 4.5 hours. LBx-BCM demonstrated high interassay reproducibility when analyzing exogenous methylated DNA (75–300 DNA copies) spiked into plasma (coefficient of variation, CV = 7.1%–10.9%) and serum (CV = 19.1%–36.1%). It also demonstrated high interuser reproducibility (Spearman r = 0.887, P < 0.0001) when samples of metastatic breast cancer (MBC, N = 11) and normal control (N = 4) were evaluated independently by two users. Analyses of interplatform reproducibility indicated very high concordance between LBx-BCM and the reference assay, cMethDNA, among 66 paired plasma samples [MBC N = 40, controls N = 26; Spearman r = 0.891; 95% confidence interval (CI) = 0.825–0.933, P < 0.0001]. LBx-BCM achieved a ROC AUC = 0.909 (95% CI = 0.836–0.982), 83% sensitivity and 92% specificity; cMethDNA achieved a ROC AUC = 0.896 (95% CI = 0.817–0.974), 83% sensitivity and 92% specificity in test set samples. The automated LBx-BCM cartridge prototype is fast, with performance levels equivalent to the highly sensitive, manual cMethDNA method. Future prospective clinical studies will evaluate LBx-BCM detection sensitivity and its ability to monitor therapeutic response during treatment for advanced breast cancer.Significance:We technically validated an automated, cartridge-based, liquid biopsy prototype assay, to quantitatively measure breast cancer methylation in serum or plasma of patients with MBC, that demonstrated high sensitivity and specificity.

Background: Increased detection of ductal carcinoma in situ (DCIS) has been a consequence of mammographic screening. Currently there is a reappraisal of the necessity of aggressive treatment, with their attendant toxicities for a preneoplastic lesion with 15-20% chance of recurrence or progression. The recombinant immunotoxin, TFR(fv)PE40, binds to the abundantly expressed transferrin receptors on cancer cells, is internalized, processed and trafficked to the cytosol. The released Pseudomonas exotoxin (PE) catalyzes the transfer of ADP-ribose from NAD to elongation factor 2 (EF2), inactivates EF2, and leads to an arrest in protein translation, and cell death by apoptosis. However, TFR(fv)PE40 is toxic to liver cells. We hypothesized that, when administered via the opening at the mammary teat, the immunotoxin will destroy preneoplasias in the entire ductal tree. Because of the closed nature of the ductal system, the toxic effects of the TFR(fv)PE40 will be confined to the tumor cells alone, and systemic effects will be minimal or absent. The intraductal approach, we proposed, will provide a direct, safe and effective treatment for DCIS. Methods: We tested this concept in two models of DCIS using two luc-tagged cell lines-SUM225-luc, derived from a human DCIS, and in MCF-7-luc. In both cell lines, the IC50 of the toxin was in the nM range. DCIS develop within one week in MIND models following intraductal (i.duc) injection of tumor cells (right and left 4th mammary gland) of ex-breeder NSG mice. DCIS progressed to invasive cancer in 2-3 weeks. At day 7, mice were administered vehicle, TFR mAb alone, or the HB21(fv)PE40 conjugate at two doses (0.15 or 1.5 ug per teat x 2) by the i.duc route, 3 times at weekly intervals, and observed for 1-3 months. Mice treated with the TFR-Ab showed no significant reduction in tumor size. Treated with HB21(fv)PE40 i.duc, by IVIS imaging, tumors were undetectable in both models (P<0.0001) within two weeks. No recurrence was observed during 3 months of followup. Mammary whole mount analysis and histopathology showed that i.duc toxin rendered more than 90% of the mice cancer-free. Immunohistochemical analysis of tumor sections for huTFR (CD71), Ki67, and CD31 supported the loss of TFR-expressing and proliferating cancer cells, and reduction of blood vessels. Pharmacokinetics studies showed that toxin was detectable by TFR-ELISA in blood 5, 30 and 60 min after i.p injection, but was undetectable in the blood of i.duc-treated mice. Conclusions: Overall, we have shown that i.duc HB21(fv)PE40 has remarkable antitumor activity in cell culture with an IC50 in the nM range, and in two MIND models of DCIS. Blood levels of the toxin after i.duc injection were undetectable, suggesting that the toxin remains inside the ductal system during its 30 min half-life, and its effect occurs during this time. This preclinical study provides a strong basis for conducting human trials. The toxicity of HB21(Fv)PE40 by the i. duc route of drug administration could be determined in dose escalation studies in patients with DCIS and early breast cancer who will undergo mastectomy as part of their treatment regimen, using a previously successful study design (PMID:2230751). This design will allow detailed examination of the local and systemic effects of HB21(fv)PE40 administered i.duc and reintroduce a very potent agent into DCIS treatment, and in the future, cancer prevention in women at high risk of developing breast cancer. Citation Format: Saraswati Sukumar, Guannan Wang, Alok Kumar, Wanjun Ding, Preethi Korangath, Priya Pai, Kathleen Gabrielson, Ira Pastan. Intraductal administration of a Transferrin Receptor-directed immunotoxin eliminates ductal carcinoma in situ in preclinical mammary in-duct (MIND) models of breast cancer [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P5-08-03.

The human transferrin receptor (TFR) is overexpressed in most breast cancers, including preneoplastic ductal carcinoma in situ (DCIS). HB21(Fv)-PE40 is a single-chain immunotoxin (IT) engineered by fusing the variable region of a monoclonal antibody (HB21) against a TFR with a 40 kDa fragment of Pseudomonas exotoxin (PE). In humans, the administration of other TFR-targeted immunotoxins intrathecally led to inflammation and vascular leakage. We proposed that for treatment of DCIS, intraductal (i.duc) injection of HB21(Fv)-PE40 could avoid systemic toxicity while retaining its potent antitumor effects on visible and occult tumors in the entire ductal tree. Pharmacokinetic studies in mice showed that, in contrast to intravenous injection, IT was undetectable by enzyme-linked immunosorbent assay in blood following i.duc injection of up to 3.0 μg HB21(Fv)-PE40. We demonstrated the antitumor efficacy of HB21(Fv)-PE40 in two mammary-in-duct (MIND) models, MCF7 and SUM225, grown in NOD/SCID/gamma mice. Tumors were undetectable by In Vivo Imaging System (IVIS) imaging in intraductally treated mice within 1 wk of initiation of the regimen (IT once weekly/3 wk, 1.5 μg/teat). MCF7 tumor-bearing mice remained tumor free for up to 60 d of observation with i.duc IT, whereas the HB21 antibody alone or intraperitoneal IT treatment had minimal/no antitumor effects. These and similar findings in the SUM225 MIND model were substantiated by analysis of mammary gland whole mounts, histology, and immunohistochemistry for the proteins Ki67, CD31, CD71 (TFR), and Ku80. This study provides a strong preclinical foundation for conducting feasibility and safety trials in patients with stage 0 breast cancer.

Background Definitive diagnosis of primary central nervous system lymphoma (PCNSL) requires invasive surgical brain biopsy, causing treatment delays. In this paper, we identified and validated tumor-specific markers that can distinguish PCNSL from other CNS tumors in tissues. In a pilot study, we tested these newly identified markers in plasma. Results The Methylation Outlier Detector program was used to identify markers in TCGA dataset of 48 diffuse large B-cell lymphoma (DLBCL) and 656 glioblastomas and lower-grade gliomas. Eight methylated markers clearly distinguished DLBCL from gliomas. Marker performance was verified (ROC-AUC of ≥ 0.989) in samples from several GEO datasets (95 PCNSL; 2112 other primary CNS tumors of 11 types). Next, we developed a novel, efficient assay called Tailed Amplicon Multiplexed-Methylation-Specific PCR (TAM-MSP), which uses two of the methylation markers, cg0504 and SCG3 triplexed with ACTB . FFPE tissue sections (25 cases each) of PCNSL and eight types of other primary CNS tumors were analyzed using TAM-MSP. TAM-MSP distinguished PCNSL from the other primary CNS tumors with 100% accuracy (AUC = 1.00, 95% CI 0.95–1.00, P < 0.001). The TAM-MSP assay also detected as few as 5 copies of fully methylated plasma DNA spiked into 0.5 ml of healthy plasma. In a pilot study of plasma from 15 PCNSL, 5 other CNS tumors and 6 healthy individuals, methylation in cg0504 and SCG3 was detectable in 3/15 PCNSL samples (20%). Conclusion The Methylation Outlier Detector program identified methylated markers that distinguish PCNSL from other CNS tumors with accuracy. The high level of accuracy achieved by these markers was validated in tissues by a novel method, TAM-MSP. These studies lay a strong foundation for a liquid biopsy-based test to detect PCNSL-specific circulating tumor DNA.

目的:探讨原发中枢神经系统淋巴瘤合并胃弥漫大B细胞淋巴瘤（DLBCL）的临床特征及治疗。方法:回顾分析武汉大学人民医院收治的1例原发中枢神经系统小B细胞淋巴瘤（PCNSL-SBC）合并胃DLBCL患者临床资料及诊疗经过，并复习相关文献。结果:患者初诊为PCNSL-SBC，经手术、大剂量甲氨蝶呤化疗及局部放疗，颅内病变完全缓解并持续22个月。诊断为胃DLBCL时颅内磁共振成像无异常，CHOP（环磷酰胺、长春地辛、吡柔比星、泼尼松）方案化疗4个周期胃部病灶缓解，但颅内病灶出现进展，再予大剂量甲氨蝶呤+大剂量阿糖胞苷化疗4个周期，神经系统症状缓解，颅内病灶缩小，但合并Ⅳ级骨髓抑制且胃部病灶进展，出现多浆膜腔积液，病情迅速恶化。结论:复合型淋巴瘤临床少见，针对一种类型淋巴瘤有效的治疗方案对另一种类型基本无效，由于严重骨髓抑制，患者不能耐受两种方案同时应用。

目的 探讨基于网络平台的个性化营养管理对维持性血液透析(MHD)营养不良患者的影响.方法 选取2016年1月～2017年12月武汉大学人民医院MHD营养不良患者100例,根据随机数字表法分为对照组和观察组,每组各50例.对照组给予常规营养管理(口头宣教及营养宣教手册)+随访6个月,观察组给予常规营养管理+6个月的网络延伸个性化营养管理及随访(微信及QQ平台).于营养管理前、营养管理后6个月分别进行营养学评估:改良定量主观整体评估表(MQSGA)营养状态评分、人体学测量、血生化检测;同时行个体化食谱的平均执行天数比较.结果 营养管理前两组MQSGA评分比较,差异无统计学意义(P＞0.05);营养管理后6个月两组MQSGA评分均低于营养管理前(均P＜0.05);且观察组MQSGA评分显著低于对照组(P＜0.01).营养管理前两组肱三头肌皮皱厚度(TSF)比较,差异无统计学意义(P＞0.05).营养管理后6个月两组TSF值较营养管理前均明显增加,且观察组明显高于对照组(P＜0.05).营养管理前两组上臂肌围(AMC)比较,差异无统计学意义(P＞0.05).营养管理后6个月,观察组AMC较营养管理前明显增加(P＜0.05),但对照组营养管理前后比较,差异无统计学意义(P＞0.05),且观察组AMC明显高于对照组(P＜0.05).营养管理前,两组患者血清白蛋白(ALB)、转铁蛋白(TF)、血红蛋白(Hb)比较,差异无统计学意义(P＞0.05),营养管理后6个月,观察组ALB、TF、Hb均高于对照组(均P＜ 0.05).营养管理后6个月,观察组ALB、TF、Hb较营养管理前明显增加(P＜0.05);对照组营养管理后6个月较营养管理前ALB值比较(P＞0.05),对照组TF、Hb值较营养管理前增加(P＜0.05).营养管理后6个月营养食谱每月平均执行天数,观察组平均执行天数为(29.4±0.5)d高于对照组[(22.6±5.7)d](P＜0.05),观察组患者营养管理依从性明显优于对照组.结论 基于网络平台的个性化营养管理对MHD患者开展院外延续护理,可提高护理依从性,改善患者营养状态.

To the Editor: The outbreak of the coronavirus disease 2019 (COVID-19) has brought great challenges to the routine diagnosis and treatment of patients.1 It has been proved in our clinical practice that the buffer ward, as the intermediate platform of pre-examination and risk screening for patients requiring hospitalization, was an effective way to control the COVID-19 transmission in hospitals.2 However, limited literatures reported the operation and efficiency of the buffer ward. We therefore summarized the admission, characteristics, and outcomes of the patients in buffer wards in our hospital. A total of 1003 patients were included (median age 57 years [interquartile range, IQR, 48–65; range 2–95 years]; 49.5% female; 36.0% cancer) between March 11 and April 23, 2020 (Table 1). Cancer patients, who were vulnerable to COVID-19, were also the focus of this study. Subgroup analyses were performed between cancer and noncancer patients. The demographic distribution between two groups was well balanced (median age 57 years [IQR 50–64; range 3–88 years] and 51.3% female vs median age 57 years [IQR 47–67; range 2–95 years] and 48.4% female; P = .68 for age and P = .39 for gender). Among all the 361 cancer patients, those with thoracic tumors (98, 27.2%), mainly lung cancer, have the most urgent need for hospitalization, followed by gastrointestinal tumors (67, 18.6%) and breast cancer (56, 15.5%) (Table 1). Among the 642 noncancer patients, those with chronic cardio-cerebrovascular diseases (115, 31.2%) were the most affected population, which mirrors findings of other literatures.3, 4 In addition, 19 (3.0%) patients were admitted for thrombotic disease, reflecting the inevitable reality of limited social activities under the epidemic.5 The process of hospitalization and risk stratification of COVID-19 is shown in Figure 1. All patients would undergo two rounds of risk screening in outpatient and emergency department and buffer ward, respectively. Patients with confirmed infection would be reported immediately and sent to designated hospitals, meanwhile the suspicious close contacts would be isolated for another 14-day quarantine. As an important gateway to control the epidemic in hospitals, the buffer ward was temporarily constructed based on the principle of three zones and two channels, and was under closed-end management to reduce the nosocomial cross-infection (Figure 1). Specialist consultation became the bridge of communication. A standard two- or six-occupant ward can only accommodate a maximum of one or two patients, respectively, and those previously infected patients must be admitted to a separate ward. To improve efficiency and save medical resources, we classified buffer wards into subspecialties for centralized management of similar patients. It was reported that the viral load of asymptomatic patients was no less than that of symptomatic patients.8 Close monitoring and preventing them from gathering remains the priority. Three months ago, the Wuhan Health Committee had organized the nucleic acid test of COVID-19 for nearly 10 million residents, and only 300 (0.003%) asymptomatic infected individuals were eventually detected. In our study, the asymptomatic infection rate of hospitalized patients was relatively higher, at 3.8% (Table 2). And of the 38 asymptomatic infected patients, two developed a confirmed infection. Among all admitted patients, only one newly confirmed and one re-positive cases were found. Of all the nine close contacts, none has developed symptoms or confirmed to be infected after rigorous medical observation (Table 2). Therefore, despite relatively high density of asymptomatic individuals in hospitals, the transmission of the virus was effectively blocked, and that is maybe what the buffer wards were for. As expected, most patients were transferred to inpatient wards after 3 days of transition in buffer wards, three patients were transferred to designated hospitals, one was transferred to community hospital, three were readmitted, 12 were discharged, and six died. Fever and cough are the most typical clinical manifestations of COVID-19, while shortness of breath, sore throat, nasal congestion, diarrhea, nausea, vomiting, fatigue, anorexia, headache, myalgias, dysosmia, dysgeusia, hearing loss, ischemic and hemorrhagic stroke, encephalopathy, encephalitis, and thyroid inflammation are other atypical symptoms that should also be taken seriously. Here, lymphopenia and fever were two statistically significant indicators between cancer and noncancer patients (P = .01, 31.9% vs 24.5% and P = .03, 1.4% vs 3.7%; Table 2). The former may be associated with the immunosuppressive status in cancer patients, whereas the latter may be related to acute abdomen such as pancreatitis and appendicitis in noncancer patients.6, 7 But what is interesting to note here is that cancer patients in buffer wards did not show a higher risk of infection (P = .45, 0% vs 0.2%), indicating that immunodeficiency may not be the only susceptibility factor for them, and that active hospitalization for primary disease was feasible under the current objective conditions. A recent analysis showed that 22 million cancer screenings may have been canceled or delayed between March and June 2020, which directly contributed to 80 000 missed cancer cases.9 Therefore, with hospital's prevention and control measures in place, we encourage cancer patients to overcome panic caused by COVID-19 and actively seek medical treatment under the premise of adequate self-protection. For the general population, it is also recommended to face the need of seeking care and put the routine cancer screening on the agenda. As a model hospital in Hubei province, our hospital had a good representation of patients and the management of buffer wards was also a typical demonstration. But, as a single-center retrospective study, the interpretation of findings may be limited by the observational design. In conclusion, this is the first dedicated case series observing patients who were admitted to buffer wards during the epidemic remission stage. Our data suggest that for patients requiring hospitalization, especially cancer patients, the buffer wards can effectively cut off the route of transmission, classify asymptomatic cases, and control the spread of COVID-19. It offers useful practical experience to others globally to fight against the pandemic. In short, we advocate setting up buffer wards wherever possible on the basis of the principle of "three zones and two channels" and closed-end management, but it also depends on various external conditions. This work was supported by the National Natural Science Foundation of China (No. U1604175 to YC) and Fundamental Research Funds for the Central Universities of China (2042020kf0110 to Wensi Zhao). We thank all the patients involved in the study. The authors declare that there is no conflict of interest. This study was approved by the Medical Ethics Committee of Renmin Hospital of Wuhan University. All the patients gave their written informed consent in accordance with the Declaration of Helsinki. The authors have obtained consent from the participants to publish/report individual patient data. National Natural Science Foundation of China, Grant Number: U1604175; Fundamental Research Funds for the Central Universities of China, Grant Number: 2042020kf0110 Yongshun Chen and Qian Chen conceived and designed the clinical study; Wanjun Ding and Dedong Cao conducted quality control and supervision; Wensi Zhao, Yi Gao, Zhuya Xiao, Jayu Chen, Li Yan, and Chen Zhao performed statistical analyses; Wensi Zhao and Yongshun Chen drafted and revised the manuscript; all the authors collected clinical data, analyzed, discussed, and revised the important intellectual content of the manuscript. The published data are available upon request from the corresponding authors.

骨肉瘤是一种多发于儿童和青少年的原发性恶性骨肿瘤.既往采用截肢术等单纯手术治疗骨肉瘤的疗效欠佳,术后易出现复发和转移,患者的术后5年生存率低.随着肿瘤化疗技术的不断发展,化疗联合保肢手术已成为目前临床治疗骨肉瘤的重要手段.但多药耐药(MDR)的出现常导致骨肉瘤患者化疗失败,已成为骨肉瘤致死的主要原因之一.MDR的发生机制较为复杂,骨肉瘤的MDR与药物排出增加、细胞解毒作用增强、细胞凋亡抑制、骨肉瘤干细胞相关化疗耐药、自噬相关化疗抵抗、DNA损伤修复增强、长链非编码RNA异常等多种机制有关.本文将针对骨肉瘤MDR形成的相关机制和研究进展作一综述.

Carboxymethylated chitosan (CMCS) has many beneficial effects, including anti-oxidant and anti-apoptotic actions. However, the mechanisms by which CMCS protect against oxidative stress induced damage to Schwann cells (SCs) remains unclear. The present study aimed to investigate the mechanism by which CMCS protects SCs against hydrogen peroxide (H2O2) induced damage. H2O2 was used to establish a model of oxidative stress injury in SCs to mimic the development of nerve injury in vitro. Different concentrations (50, 100 and 200 µg/ml) of CMCS were added to test whether CMCS was capable of protecting SCs from H2O2 induced damage. MTT, LDH release and Annexin V/FITC assays were then performed. Levels of reactive oxygen species were detected using a reactive oxygen species assay kit, the mitochondrial membrane potential (ΔΨm) of SCs was analyzed by rhodamine123 fluorescence staining, the synthesis of Bcl-2, Bax, cytochrome c and caspase-3 were analyzed by real-time PCR and Western blot analysis. The results showed that CMCS protected SCs from apoptosis, decreased LDH release and enhanced cell viability, also decreased reactive oxygen species levels and increased ΔΨm. Additional experiments demonstrated that CMCS could decrease protein expression of Bax, cytochrome c and caspase-3, while promote Bcl-2 protein expression induced by H2O2. Taken together, the finding of this study indicated that CMCS prevented H2O2-induced damage to SCs through the mitochondrial dependent pathway.

Objective To detect the expression of phosphatidylinositol 3-kinase (PIK3CA) and glutathione-S transferase-π (GST-π) in osteosarcoma tissues and to explore its effect on the multidrug resistance of osteosarcoma.Methods Thirty-three cases of pathological tissue specimens of osteosarcoma from Renmin Hospital of Wuhan University from January 2009 to June 2017 were collected.The expression of PIK3CA and GST-π of 33 cases of osteosarcoma specimens was detected by immunohistochemistry (Envision method) and Western blot method.The differences between the chemotherapy-resistant group (7 cases) and the chemotherapy-effective group (26 cases) were compared.The results were analyzed combined with clinicopathological factors.Results The average optical density of PIK3CA in the chemotherapy-resistant group and chemotherapy-effective group was (11.089±2.147) and (6.938±2.065) respectively,and there was a significant difference between the two groups (P ＜ 0.05);the average optical density of GST-π in the chemotherapy-resistant group and chemotherapy-effective group was (15.871±2.678) and (7.693±2.443),and there was a significant difference between the two groups (P ＜ 0.05).The average optical density of PIK3CA and GST-π by Western blot method had significant differences between the two groups (P ＜ 0.05).The expression of PIK3CA and GST-π in osteosarcoma was correlated (r =0.68,P ＜ 0.01).Conclusion PIK3CA and GST-π are over expressed in osteosarcoma chemotherapy-resistant group,and the expression of PIK3CA and GST-π is positively correlated with each other,which may be one of the mechanisms of drug resistance in osteosarcoma.