Newcastle disease virus (NDV) has been reported to selectively duplicate in and then destroy tumor cells, whilst sparing normal cells. However, the effect of NDV on lung cancer has yet to be elucidated. In the present study, recombinant NDV (rl-RVG) was applied to lung adenocarcinoma A549 cell tumor-bearing mice to explore its effect on the proliferation of the cells and the immune response of the mice. Following rl-RVG transfection, RVG and NDV gene expression, decreased tumor growth, subcutaneous tumor necrosis, tumor apoptosis and an increased number of cluster of differentiation (CD)3-/CD49+ natural killer cells were more evident in the rl-RVG group. The present study demonstrated that rl-RVG transfection effectively restrained lung adenocarcinoma A549 cell growth in vivo, which may have been accomplish by inducing tumor cell apoptosis and regulating the cell immune response.

The aim of the present study was to explore the classification of the internal iliac artery (IIA) and the diagnostic value of the pelvic tumour-feeding artery by multislice computed tomography angiography (MSCTA) compared with digital subtraction angiography (DSA). A total of 43 patients with pelvic tumours were enrolled between January 2013 and August 2017. The classification of the IIA and the quality of the feeding artery of the pelvic tumours were analysed by Yamaki's classification (Groups A-D according to IIA branching) and the 5-point scoring system. The degree of feeding artery stenosis, caused by tumour compression or invasion, was analysed by a 4-point scoring system. The Wilcoxon signed-rank test was used to determine the vascular diagnostic quality identified by MSCTA and DSA. MSCTA of the pelvic arteries was successfully performed in all patients. The main classifications of the IIA were Group A, followed by Group C, then Group B and with no cases of Group D. There was no significant difference in the classification of the IIA between the left and right sides on MSCTA and DSA. The visualization quality of the IIA and its main branches showed excellent consistency, but the difference in the terminal branches of the feeding arteries in the pelvic tumours was statistically significant between MSCTA and DSA. MSCTA has great advantages in evaluating the classification of the IIA, the imaging quality evaluation of the IIA and its main branches, and in the evaluation of the pelvic tumour-feeding artery. However, in the display of the terminal arterial branches of the pelvic tumours, DSA remains irreplaceable, particularly in cases of interventional embolization.

It is widely accepted that immunoglobulin (Ig), the classical immune molecule, is extensively expressed in many cell types other than B-cells (non-B-IgG), including some malignant cells. The expression of Ig in malignant cells has been associated with a poor prognosis. In the present study, immunohistochemical analysis detected strong positive staining of IgG in three bladder cancer cell lines, the cancer cells in 77 bladder cancer patient samples and the cells in 3 cystitis glandularis tissue samples, while negative staining was observed in 4 specimens of normal transitional epithelial tissues. Importantly, functional transcripts of IgG with unique VHDJH rearrangement patterns were also found in bladder cancer cells. The knockdown of IgG in bladder cancer cell lines using small interfering RNA significantly inhibited the proliferation, migration and invasion of the cells. Notably, high IgG expression, as determined by immunostaining, was significantly correlated with a high histological grade and recurrence. The results of the present study suggested that IgG expression is involved in the malignant biological behavior and poor prognosis of bladder cancer. Therefore, IgG may serve as a novel target for bladder cancer therapy.

Various in vitro and in vivo studies have linked mesenchymal stem cells (MSCs) with cancer, but little is known about the effect of MSCs on tumor progression. The present study aimed to analyze the role of the MSCs from different tissues, consisting of human bone marrow, adipose and the umbilical cord tissues, and the heterogeneity of tumors in tumor progression. By collecting the culture supernatants of MSCs as MSC-conditioned media (CMs), the present study found that MSC-CM produces no significant effect on the proliferation of MDA-MB-231 and A549 tumor cells. The migration of MDA-MB-231 cells was enhanced upon incubation with MSC-CM, while that of A549 cells was inhibited. Furthermore, the phosphorylation of insulin receptors (IRs) was upregulated in MSC-CM-treated MDA-MB-231 cells, while in MSC-CM-treated A549 cells, the phosphorylation of human epidermal growth factor receptor 3 (Her3) was downregulated. Taken together, the findings suggest that the phosphorylation of IR and Her3 may contribute to the discrepant effects of MSC-CM on the migration of the 2 cell lines.

Osteosarcoma is an aggressive pediatric tumor affecting growing bones that typically occurs in adolescents and young adults. Although advances in treatment have been made in recent years, a high proportion of patients relapse due to metastases, which are frequently resistant to chemotherapy and pose a significant threat to long-term survival. Previous studies have demonstrated that the epithelial-mesenchymal transition (EMT) is associated with cancer occurrence and metastasis, and our previous study demonstrated the occurrence of EMT in osteosarcoma. Notch is a regulator involved in several cellular processes, and previous studies have identified that the Notch signaling pathway may be activated during chemotherapy. However, whether chemotherapy affects the EMT remains to be elucidated. To address this issue, in the present study osteosarcoma cells were exposed to sublethal doses of doxorubicin, which resulted in upregulation of the expression of genes in the Notch signaling pathway and its target genes. Furthermore, doxorubicin treatment promoted mesenchymal-like properties and enhanced the migration and invasion of cells. In addition, treatment with the selective γ-secretase inhibitor DAPT was able to prevent the EMT and inhibit the in vitro migration of osteosarcoma cells. The results of this study suggested that there is a significant correlation between the Notch signaling pathway and the EMT, and revealed an underlying molecular mechanism by which doxorubicin may induce the EMT via Notch signaling.

A number of studies have demonstrated the crucial functions of GINS2 within the GINS complex in various types of cancer. However, the molecular mechanisms and prognostic value of GINS2 in breast cancer remain unknown. The present study used; BC-GenExMiner, COSMIC, UCSC Xena, The Human Protein Atlas, GEPIA, cBioPortal, GeneMANIA, TIMER and Oncomine, in order to investigate gene expression, co-expression, clinical parameters and mutations in GINS2 in patients with breast cancer. Furthermore, the present study assessed the prognostic value of GINS2 in patients with breast cancer via the Kaplan-Meier plotter database. The results of the present study demonstrated that the mRNA levels of GINS2 were significantly higher in breast cancer tissue compared with normal tissue. In addition, high mRNA expression levels of GINS2 were associated with high Scarff-Bloom-Richardson status grades, a basal-like status and age (≤51 years); however, it was not associated with lymph node metastasis. The survival analysis revealed that increased GINS2 mRNA levels were associated with a worse prognosis for relapse-free survival in all patients with breast cancer, particularly in those with estrogen receptor-positive and progesterone receptor-positive subtypes. In addition, a positive association between the GINS2, CENPM and MCM4 genes was confirmed. The results of the present study suggest that GINS2 could be used as a potential prognostic biomarker for breast cancer. Nevertheless, further studies are necessary to confirm the effects of GINS2 on the pathogenesis and development of patients with breast cancer.

Emerging evidence has revealed that mitochondrial DNA (mtDNA) is encapsulated in plasma extracellular vesicles (EVs). However, the characteristics of mtDNA in EVs from patients with cancer remain largely unexplored, which greatly limits its clinical application. Whole genome and capture-based sequencing found that EV mtDNA covered the whole mitochondrial genome. The medium fragment size in EV mtDNA was significantly larger compared with that in cell-free mtDNA [cfmtDNA; 159 vs. 109 base pairs (bp); P<0.001]. EV DNA appeared to have a higher mtDNA copy number compared with cfDNA. Of note, patients with hepatitis had >300-bp fragments in EV mtDNA compared with patients with hepatocellular carcinoma (HCC) and healthy controls. EV mtDNA fragments >300 bp in length exhibited a significantly higher proportion of EV mtDNA fragment ends than those that were ≤300 bp in length in patients with hepatitis. The EV mtDNA copy number in patients with HCC and hepatitis were significantly lower compared with those in healthy controls. Furthermore, inconsistencies in the mtDNA heteroplasmic variant were observed among HCC tissues, plasma and EVs. In conclusion, EV mtDNA exhibited different characteristics among patients with HCC, hepatitis and healthy controls, indicating the potential value of EV mtDNA as a diagnostic biomarker that complements cfmtDNA.

Dysregulation of cyclin A1 (CCNA1) is implicated in the carcinogenesis, progression and metastasis of many types of solid tumours. In the present study, an mRNA single-channel expression profile chip experiment revealed that the CCNA1 mRNA levels in oesophageal squamous cell carcinoma (ESCC) were increased >10-fold compared with those in the adjacent non-cancer tissues. Reverse transcription-quantitative polymerase chain reaction and immunohistochemistry analyses were performed to additionally investigate the role of CCNA1 in the development and progression of ESCC in patients treated by radical resection of the oesophagus. The association between CCNA1 mRNA expression and the clinicopathological parameters of patients with ESCC was statistically analysed. The results indicated that upregulation of CCNA1 occurred in ~70% of patients with ESCC, and increased CCNA1 mRNA expression was significantly associated with advanced clinical stage, lymph node metastasis, invasiveness and poor clinical outcome, including disease-free survival and overall survival rates. Taken together, the data suggested that CCNA1 had an important function in ESCC development and progression, and may serve as a prognostic biomarker and therapeutic target in ESCC.

Melanocyte proliferating gene 1 (MYG1) is an exonuclease that participates in RNA processing and is required for normal mitochondrial function. However, its role in tumorigenesis remains unknown. The present study aimed to investigate the role of MYG1 and its underlying mechanisms in human lung adenocarcinoma (LUAD). The expression levels of MYG1 in tumor tissues of patients with LUAD were obtained from public cancer databases and analyzed using the UALCAN online software. The association between MYG1 expression levels and the prognosis of patients with LUAD was analyzed using the Kaplan-Meier plotter. In addition, the role of MYG1 in the LUAD A549 and H1993 cell lines was determined by knocking down MYG1 expression with a specific small interfering RNA or by overexpressing it with a MYG1-containing plasmid. The results demonstrated that MYG1 expression levels were upregulated in LUAD tissues compared with those in normal lung tissues from healthy subjects, and high MYG1 expression levels were associated with an unfavorable prognosis. MYG1 promoted the proliferation, migration and invasion of A549 and H1993 cells. In addition, MYG1 inhibited autophagy via the AMP-activated protein kinase/mTOR complex 1 signaling pathway. Collectively, the present results suggested that MYG1 may serve an oncogenic role in LUAD and may be a potential therapeutic target for LUAD.

Human papillomavirus (HPV) infection is one of the main causes of esophageal carcinoma (ESCA), and its carcinogenic mechanisms in ESCA require further investigation. E6 and E7 are HPV oncogenes, and their genomic integration is a crucial reason for the transformation of host cells into cancer cells. In order to reveal the role of oncogenes E6 and E7 in ESCA cells, the RNA-Seq raw data for HPV18-positive and -negative esophageal squamous cell carcinoma (ESCC) samples derived from the NCBI BioProject database were analyzed, and the differentially expressed genes were identified. Moreover, differentially expressed genes were enriched significantly in multiple cell death pathways, including apoptosis (cyclin-dependent kinase inhibitor 2A, plakophilin 1 and desmoglein 3), pyroptosis (gasdermin A, gasdermin C, NLR family pyrin domain containing 3, absent in melanoma 2, NLR family pyrin domain containing 1 and Toll like receptor 1) and autophagy (Unc-51 like autophagy activating kinase 1, adrenoceptor beta 2). Consequently, the effects of cisplatin-induced apoptosis and Hank's balanced salt solution-induced autophagy, and α-ketoglutarate-induced pyroptosis in the ESCC-expressing E6 and E7 cells were verified. Therefore, the expression of E6E7 may culminate in the inhibition of multiple cell death modes, which may also be one of the mechanisms of oncogene-induced carcinogenesis.

This study aimed to explore the exact mechanism of the effect of a furin inhibitor on the migration and invasion of MG-63 and Saos-2 osteosarcoma cells. MG-63 and Saos-2 osteosarcoma cells were treated with regular culture medium in the presence or absence of 480 nM α1-antitrypsin Portland (α1-PDX). Wound-healing and Transwell assays were used for the detection of the effects of α1-PDX on MG-63 and Saos-2 osteosarcoma cell migration and invasion. Western blot analysis and reverse transcription-polymerase chain reaction were performed to detect the expression levels of membrane type I matrix metalloproteinase (MT1-MMP), Wnt and β-catenin. A chromatin immunoprecipitation assay was used for detection of the levels of MT1-MMP gene transcription activity. The results showed that α1-PDX treatment significantly reduced the migration and invasion ability of the cells. Notably, the expression levels of MT1-MMP decreased evidently upon α1-PDX treatment, paralleled with reductions in the expression levels of Wnt and β-catenin. Further analysis of the transcriptional activity of MT1-MMP revealed that the α1-PDX-induced downregulation of the levels of MT1-MMP was mediated by the Wnt signaling pathway. These data suggest that α1-PDX plays a vital role in inhibiting MG-63 and Saos-2 osteosarcoma cell migration and invasion by downregulating the expression levels of MT1-MMP via the Wnt signaling pathway.

The aim of the present study was to investigate the expression of B7-H1 and B7-H4 in ovarian neoplasm tissues and to examine their clinical relevance. A total of 112 ovarian biopsies were collected from patients with epithelial ovarian cancer (EOC) and 10 were taken from ovarian benign neoplasms. The samples were processed in paraffin tissue chips, and subjected to immunohistochemical staining and analysis. Associations of B7-H1 and B7-H4 expression with patients' clinical parameters, such as histological typing, cell grading, International Federation of Gynecology and Obstetrics staging, tumor size, and metastatic status, were examined by statistical analysis. Survival curves were constructed using the Kaplan-Meier method and the log-rank test. Independent prognostic factors were evaluated using the Cox regression model. The results showed an extremely low or negative expression of B7-H1 and B7-H4 in the 10 benign ovarian neoplasm tissues (control): By contrast, a positive expression of B7-H1 and B7-H4 was observed in 55.4% (62/112) and 37.5% (42/112) of the EOC tissues, respectively. The differences between the two groups were significant. In addition, the co-expression of B7-H1 and B7-H4 was found in 31.3% (35/112) of the EOC cases. Furthermore, the progression-free survival and overall survival were significantly lower in EOC patients with a high expression of B7-H1 and B7-H4 (χ2=45.60 and 37.99, respectively). These results demonstrated that the expression of B7-H1 and B7-H4 in EOC tissues was significantly associated with poor prognosis and high relapse rate of EOC. The findings suggest that B7-H1 and B7-H4 is a negative prognostic marker for EOC and a potential immunotherapeutic target for patients with EOC.

Efficacy and safety of paclitaxel/docetaxel + epirubicin (TE), paclitaxel/docetaxel + epirubicin + cytoxan (TEC) and intensive paclitaxel (IP) neoadjuvant chemotherapy (NCT) were compared for the treatment of breast cancer. The clinical data of 326 patients with stage II-III unilateral primary breast cancer treated in Shengjing Hospital of China Medical University from January 2012 to April 2016 were retrospectively analyzed. All patients received NCT for 4 cycles, including 115 cases of TE group, 109 cases of TEC group, and 102 cases of paclitaxel weekly group. The clinical efficacy was evaluated and complete response (CR) + partial response (PR) indicated clinically effective. The pathological effect was evaluated and the grade III+IV+V indicated pathologically effective. The rates of clinical efficacy and pathological CR (pCR) were compared, and the incidence of adverse reactions was also observed. The effects of different molecular typing on clinical efficacy and pCR were compared. Our results showed that the clinical effective rates in TE, TEC and IP groups were 80.9, 89.0 and 77.5%, respectively, and there were no statistically significant differences (P=0.074). The pCR rates in the three groups were 9.57, 8.26 and 5.88%, respectively, and the differences were not statistically significant (P=0.602). The incidence rate of neutropenia was statistically different among the three groups of patients (P<0.001), which was the highest in TEC group and the lowest in IP group. There were no statistically significant differences in the incidence rates of adverse reactions (P>0.05). Estrogen receptor (ER)-negative, progesterone receptor (PR)-negative and human epidermal growth factor receptor-2 (HER-2)-positive states were significantly correlated with the high clinical effective rate and high pCR rate (P<0.05). In conclusion, IP has the lowest incidence rate of neutropenia. Additionally, ER-negative, PR-negative and HER-2-positive states are significantly correlated with the high clinical effective rate and high pCR rate.

MicroRNAs (miRs) are small RNAs that do not code for proteins, but instead decrease the stability and suppress the translation of target mRNAs by binding with complementary sequences in their 3'-untranslated regions (3'-UTRs). In the present study, it is reported that breast cancer tumor tissue, as well as irradiated MCF7 breast cancer cells, exhibit decreased levels of miR-26b expression compared with normal breast tissue and MCF7 cells without exposure to radiation. Additionally, a luciferase reporter assay was used to demonstrate that miR-26b directly targetsDNA damage-regulated autophagy modulator 1 (DRAM1). MCF7 cells that were transfected with an miR-26b mimicexhibited the downregulated expression of DRAM1 protein and a reduced level of irradiation-induced autophagy. Inhibiting miR-26b resulted in the upregulation of DRAM1 and increased levels of irradiation-induced autophagy in MCF7 cells. These results suggest that therapeutic strategies to target miR-26b may increase the efficacy of certain types of cancer therapy.

A number of studies have attempted to elucidate the association between mircoRNAs (miRNAs/miRs) and cancer-associated processes. The aim of the present study was to determine how miR-499a-5p intervenes in human osteosarcoma cell proliferation and differentiation. The cancerous tissues and adjacent non-cancerous tissues of 62 patients with osteosarcoma (OS) were collected. miRNA microarray analysis revealed that 29 miRNAs were upregulated while 26 were downregulated, among which miR-499a-5p expression was the most decreased. Western blot analysis and reverse transcription-quantitative polymerase chain reaction demonstrated that the mRNA and protein expression of miR-499a-5p was lower, while that of protein phosphatase 1D (PPM1D) was higher in OS tissues compared with expression levels in normal tissues. Furthermore, miR-499a-5p expression was markedly decreased in the metastatic tumors and in those at stage III+IV compared with the non-metastatic tumors and those at stage I, respectively. In addition, following transfection of the human OS MG-63 cell line with an miR-499a-5p mimic, the expression of miR-499a-5p was elevated while the protein and mRNA expression of PPM1D was decreased. When combining these findings with the information obtained from the Targetscan predictive software, it was confirmed that PPM1D was targeted by miR-499a-5p. In MG-63 cells transfected with an miR-499a-5p mimic, PPM1D-associated downstream proteins phosphorylated protein kinase B (p-Akt) and phosphorylated glycogen synthase kinase 3β (p-GSK-3β) were significantly downregulated compared with the negative control (NC) group, while the expression of p-Akt and p-GSK-3β were significantly elevated in the tumor tissues compared with the adjacent non-tumor tissues. Simultaneously, the growth and proliferation activity of MG-63 cells were notably reduced when transfected with the miR-499a-5p mimic, compared with the NC group. Therefore, it may be concluded that miR-499a-5p suppresses OS cell proliferation and differentiation by targeting PPM1D through modulation of Akt/GSK-3β signaling.

Rhabdomyosarcoma (RMS) is one of the most common types of soft tissue sarcoma in children; however, the pathogenesis of RMS is unclear. MicroRNAs (miRs) are involved in the development and progression of RMS. The role of miR-410-3p in RMS cell invasion, migration, proliferation and apoptosis, and its possible mechanism were investigated in the current study. Reverse transcription-quantitative polymerase chain reaction and western blot analysis were performed to detect the expression of miR-410-3p in RMS tissues and cells. In addition, the present study investigated the expression levels of molecules associated with the epithelial-mesenchymal transition (EMT), including E-cadherin, N-cadherin, Slug and Snail, and apoptotic factors, including Bcl-2-associated X protein (bax), cleaved-caspase 3, cleaved poly (ADP-ribose) polymerase (PARP), p53 and Bcl-2. Cell Counting Kit-8, terminal deoxynucleotidyl transferase dUTP nick end labeling and Transwell assays were conducted to determine the functional roles of miR-410-3p. Exogenous expression of miR-410-3p inhibited RMS cell invasion, migration and proliferation, induced apoptosis, suppressed the expression of Snail, Slug, N-cadherin and Bcl-2, and increased the expression of E-cadherin, bax, cleaved-caspase 3, cleaved PARP and p53. In summary, it was proposed that miR-410-3p overexpression suppressed invasion, migration and proliferation, downregulated the expression of EMT-associated molecules, and promoted apoptosis and the expression of apoptotic factors in RMS cells. Therefore, miR-410-3p may serve as a novel tumor suppressor gene in RMS, and could possess diagnostic and therapeutic potentials for the treatment of RMS.

Triple negative breast cancer (TNBC) has received increasing attention from oncologists worldwide due to its poor prognosis and paucity of targeted therapies. MicroRNAs (miRs) are a group of small non-coding RNAs that are responsible for the post-transcriptional regulation of various target genes. The present study demonstrated that the expression of miR-199b-5p in breast cancer tissue was significantly reduced compared with that in normal breast tissues by reverse transcription-quantitative polymerase chain reaction. In addition, western blot analysis and luciferase reporter assays revealed that miR-199b-5p in TNBC cells inhibited discoidin domain receptor tyrosine kinase 1 expression by directly targeting its 3'-untranslated region. Furthermore, miR-199b-5p markedly suppressed the proliferation and invasion of TNBC cells, as demonstrated by using wound-healing, migration, invasion and proliferation assays. Collectively, these results indicate that miR-199b-5p may be a novel alternative therapeutic target for TNBC.

A number of studies have revealed the significance of microRNAs (miRs) in tumorigenesis. Cervical cancer (CC) is one of the most malignant cancer types and is associated with a poor overall survival rate. A previous study demonstrated a critical role of miR-214 in the development of multiple cancer types, but its role in CC remains elusive. In the current study, miR-214 was observed to be downregulated in CC tissues compared with the adjacent non-cancerous tissue. Overexpression of miR-214 reduced the proliferation of CC cells, whereas inhibiting its expression resulted in enhanced proliferation. Furthermore, Enhancer of zeste homolog 2 (EZH2) was demonstrated to be a direct target of miR-214 in CC. An MTT assay demonstrated that upregulating miR-214 expression or knocking down the expression of EZH2 impaired the proliferation of a CC cell line. Low expression of miR-214 was positively associated with tumor differentiation (P=0.037) and tumor stage (P=0.012). Notably, low expression of miR-214 predicted poor prognosis of patients with CC. Consequently, the results of the current study demonstrated that miR-214 functions as a tumor suppressor in CC and may be regarded as a potential therapeutic target in CC.

Adenocarcinoma is one of the most common pathological types of human lung cancer and has the highest incidence and mortality rates worldwide. Resistance to paclitaxel (PTX), the standard chemotherapy agent for treatment of lung adenocarcinoma, is a major clinical obstacle. Sensitive markers are urgently required for the diagnosis and characterization of lung cancer, as well as to manage drug resistance. Previous studies have described the activity of long non-coding RNAs (lncRNAs) in human lung cancer and chemotherapy resistance. In previous studies, lncRNA ENST00000500843 was identified to be downregulated in PTX-resistant A549 human lung cancer cells. However, the roles of this lncRNA in the development of lung adenocarcinoma and its mechanism in PTX resistance, to the best of our knowledge, have not been described. In the present study, 56 pairs of lung adenocarcinoma and normal adjacent tissue samples were collected. Reverse transcription-quantitative PCR revealed that the expression levels of lncRNA ENST00000500843 were lower in lung adenocarcinoma tissues and PTX-resistant A549 cells when compared with normal adjacent tissues and A549 cells. Decreased expression levels of lncRNA ENST00000500843 in lung adenocarcinoma tissues were associated with tumor diameter, the degree of pathological differentiation and metastasis of lymph nodes. Additionally, patients with low expression levels of ENST00000500843 exhibited poorer overall survival and progression-free survival rates. Furthermore, the present study demonstrated that knockdown of lncRNA ENST00000500843 with small interfering RNA decreased the likelihood of apoptosis in A549 cells and promoted resistance to PTX. This indicated that lncRNA ENST00000500843 may be a useful diagnostic marker of lung cancer and a good prognostic marker for resistance to treatment with PTX.

Pancreatic cancer is one of the most life-threatening malignancies worldwide. Despite advances in checkpoint immunotherapy for patients with cancer, the current immunotherapies have demonstrated limited benefits for the treatment of pancreatic cancer. Apart from the intricate microenvironments that restrict T-cell function, membrane proteins other than programmed death-ligand 1 may also facilitate immune escape of tumor cells. The present study investigated the membrane proteins of seven paired pancreatic adenocarcinoma (PAAD) and adjacent normal tissues with mass spectrometry, and identified 10 up-and eight downregulated membrane proteins in PAAD. Together with the online database analysis, the results showed that the CASK protein was upregulated in PAAD samples and cell lines, and predicts poor outcomes in patients with PAAD. Furthermore, the results exhibited downregulated CD36 and EPB42 in PAAD samples and cell lines, and higher levels of CD36. EPB42 was shown to predict improved survival outcomes in patients with PAAD. Overall, the results of the present study revealed PAAD-specific membrane proteins as potential diagnostic markers and drug-targets for the immunotherapy of pancreatic cancer.