SLC38A1 has been identified as a carcinogenic factor in the progression of colorectal, gastric, pancreatic, and other cancers. However, its involvement in lung adenocarcinoma (LUAD) remains unexplored in the literature. The expression levels, diagnostic relevance, and clinical significance of SLC38A1 in LUAD were evaluated using data from the TCGA, XENA, and LCE databases, along with validation in samples from 10 LUAD patients at our hospital. Prognostic nomograms and risk models based on SLC38A1 were constructed. The functional roles and mechanisms of SLC38A1 in LUAD were investigated through CCK-8 assays, migration and invasion assays, Western blotting, GO and KEGG pathway analyses, and correlation analysis to explore its relationship with the immune microenvironment. SLC38A1 was overexpressed in both unpaired and paired LUAD samples, with a marked increase in early-stage LUAD. Overexpression of SLC38A1 correlated with diagnostic accuracy and poor overall survival (HR = 1.53; 95

This study aims to evaluate whether the amount of fibroglandular tissue (FGT) and the level of background parenchymal enhancement (BPE) on magnetic resonance imaging (MRI) are associated with synchronous contralateral breast cancer (CBC) during preoperative MRI staging of newly diagnosed breast cancer patients. From January 2010 to December 2019, core needle biopsy-confirmed newly diagnosed breast cancer patients who underwent preoperative bilateral breast MRI were screened. 61 eligible patients with pathologically proven synchronous CBC were enrolled as the study group, while 122 matched primary breast cancer patients without synchronous CBC were selected as the control group.Odds ratios (ORs) and corresponding 95

To investigate the CT and MRI features of pancreatic colloid carcinoma (PCC) and to correlate imaging findings with histopathological characteristics. The CT and MRI images and clinical data of 15 patients with PCC confirmed by surgical resection and histopathological examination from August 2009 to October 2023 were retrospectively analyzed. All 15 PCC lesions presented as single masses, occurring in 8 males and 7 females (mean age 66 ± 8.4 years). The majority of lesions (73

Background The impact of ischemic heart disease (IHD) on the brain glymphatic MRI indices and risk of Alzheimer's disease (AD) remains largely unclear. This study aimed to investigate the associations between IHD, brain glymphatic MRI indices and risk of AD. Methods A total of 1385 non-dementia subjects (55.2 % male, mean age 73.53) were included. Diffusivity along the perivascular space (DTI-ALPS), free water (FW) and choroid plexus volume were used to reflect glymphatic function. The associations of IHD with MRI derived glymphatic indices, PET amyloid, tau and cognitive performance were explored by multiple regression analysis. IHD were tested as predictors of clinical progression using cox proportional hazards modeling. The mediation effect of MRI derived glymphatic indices on the relationship between IHD and cognitive changes was investigated. Results Individuals with IHD exhibited glymphatic dysfunction revealed by lower DTI-ALPS (p = 0.035), higher FW (p < 0.001), and higher choroid plexus volume (p = 0.019). IHD had poorer cognitive performance in MMSE (p = 0.022), ADNI-MEM (p = 0.001) and ADNI-MF (p = 0.006), and more amyloid deposition (p = 0.007). IHD had a higher diagnostic conversion risk (HR = 1.321, 95 % CI = 1.003–1.741). IHD was associated with longitudinal cognitive decline in all cognitive tests (p < 0.05 for all) and FW (β = 0.012, 95 % CI 0.001, 0.023, p = 0.038). FW demonstrated an indirect effect (β = -0.0009, 95 % CI: -0.0034, -0.0001) and mediated 13.85 % effect for the relationship between IHD and ADNI-EF decline. Conclusion IHD is independently associated with AD risk, and brain glymphatic dysfunction may partially mediate this relationship.

Laparoscopic surgery has been widely used in various surgical fields due to its minimally invasive and rapid recovery benefits. However, it demands a high level of technical expertise from surgeons. While advancements in computer vision and deep learning have significantly contributed to surgical action recognition, the effectiveness of these technologies is hindered by the limitations of existing publicly available datasets, such as their small scale, high homogeneity, and inconsistent labeling quality. To address the above issues, we developed the SLAM dataset (Surgical LAparoscopic Motions), which encompasses various surgical types such as laparoscopic cholecystectomy and appendectomy. The dataset includes annotations for seven key actions: Abdominal Entry, Use Clip, Hook Cut, Suturing, Panoramic View, Local Panoramic View, and Suction. In total, it includes 4,097 video clips, each labeled with corresponding action categories. In addition, we comprehensively validated the dataset using the ViViT model, and the experimental results showed that the dataset exhibited superior training and testing capabilities in laparoscopic surgical action recognition, with the highest classification accuracy of 85.90%. As a publicly available benchmark resource, the SLAM dataset aims to promote the development of laparoscopic surgical action recognition and artificial intelligence-driven surgery, supporting intelligent surgical robots and surgical automation.

Abstract Background Pyroptosis belongs to a unique type of programmed cell death among which GSDME is reported to exert anti-tumor immunity. However, the underlying mechanisms of how to boost tumor-infiltrating lymphocytes and whether it could benefit the efficacy of ICIs are still unknown. Methods CRC samples were used to analyze its relationship with CD8+T cells. GSDME in mouse CRC cell lines CT26/MC38 was overexpressed. The infiltration of CD8+T cells in grafted tumors was determined by multiplex flow cytometric analysis and immunohistochemistry. Transcriptomic analysis was performed in cell lines to define key signatures related to its overexpression. The mechanism of how mtDNA was released by GSDME-induced mitochondrial damage and activated cGAS-STING pathway was observed. Whether GSDME benefited ICIs and the relationships with the genotypes of CRC patients were investigated. Results It had favorable prognostic value in CRC and was positively associated with increased number and functionality of CD8+T cells both in human samples and animal models. This was due to mitochondrial damage and activation of cGAS-STING-IFNβ pathway for the recruitment of CD8+T cells. Mechanically, GSDME overexpression enhanced N-GSDME level, leading to the mitochondrial damage and mtDNA was released into cytosol. Finally, GSDME benefited with ICIs and exhibited positive relationships with MSI in CRC patients. Conclusion We presented the mechanism of GSDME in anti-tumor immunity through activating cGAS-STING-IFNβ axis mediated by mitochondrial damage, leading to more infiltration of CD8+T cells with synergistic efficacy with ICIs.

The expression level of PD-L1 does not accurately predict the prognosis of advanced colorectal cancer (CRC) patients, but it still reflects the tumor microenvironment to some extent. By stratifying PD-L1 status, gene subtypes in PD-L1 positivity-related pathological pathways were analyzed for their relationship to MSI or TMB to provide more individualized treatment options for CRCs. A total of 752 advanced CRCs were included, and their genomic variance was measured by a targeted next generation sequencing panel in this study. MSI and TMB were both measured by NGS, while PD-L1 expression level was measured using the PD-L1 colon 22C3 pharmDx kit. We found RTK/RAS pathway was positively related to high PD-L1 expression, with BRAF V600E and most KRAS mutations (G12 and G13) subtypes showing a significant correlation. Conversely, the Wnt and p53 pathways were negatively related to high PD-L1 expression, with APC C-terminal alterations and other non-inactivation mutations in TP53 making a primary contribution with significant statistical significance. Major subtypes showing a significantly higher proportion of TMB-H or MSI-H were irrespective of PD-L1 status. These findings demonstrate pathological pathways associated with high PD-L1 expression, suggesting that pathway-induced oncogenic constructive PD-L1 upregulation may be the reason for the corresponding patients' primary resistance to immune checkpoint inhibitors (ICIs), rather than a lack of pre-existing immune responses.

BackgroundLipoprotein(a) (Lp[a]) is associated with an increased risk of myocardial infarction (MI). However, the mechanism underlying this association has yet to be fully elucidated.ObjectivesThis multicenter study aimed to investigate whether association between Lp(a) and MI risk is reinforced by the presence of low-attenuation plaque (LAP) identified by coronary computed tomography angiography (CCTA).MethodsIn a derivation cohort, a total of 5,607 patients with stable chest pain suspected of coronary artery disease who underwent CCTA and Lp(a) measurement were prospectively enrolled. In validation cohort, 1,122 patients were retrospectively collected during the same period. High Lp(a) was defined as Lp(a) ≥50 mg/dL. The primary endpoint was a composite of time to fatal or nonfatal MI. Associations were estimated using multivariable Cox proportional hazard models.ResultsDuring a median follow-up of 8.2 years (Q1-Q3: 7.2-9.3 years), the elevated Lp(a) levels were associated with MI risk (adjusted HR [aHR]: 1.91; 95% CI: 1.46-2.49; P < 0.001). There was a significant interaction between Lp(a) and LAP (Pinteraction <0.001) in relation to MI risk. When stratified by the presence or absence of LAP, Lp(a) was associated with MI in patients with LAP (aHR: 3.03; 95% CI: 1.92-4.76; P < 0.001). Mediation analysis revealed that LAP mediated 73.3% (P < 0.001) for the relationship between Lp(a) and MI. The principal findings remained unchanged in the validation cohort.ConclusionsElevated Lp(a) augmented the risk of MI during 8 years of follow-up, especially in patients with LAP identified by CCTA. The presence of LAP could reinforce the relationship between Lp(a) and future MI occurrence.

Objective:The aim was to explore the effects of preoperative calcium and activated vitamin D3 supplementation on post-thyroidectomy hypocalcemia and hypo-parathyroid hormone-emia (hypo-PTHemia). Methods:A total of 209 patients were randomly divided into control group (CG) and experimental group (EG). Oral calcium and activated vitamin D3 supplementation were preoperatively administered to EG, whereas a placebo was administered to CG. Data on serum calcium, phosphorus, and PTH concentrations before operation, on postoperative day 1 (POPD1), at postoperative week 3 (POPW3), and on the length of postoperative hospitalization were collected. Results:The serum calcium, phosphorus, and PTH concentrations, as well as the incidence of postoperative hypocalcemia and hypo-PTHemia, did not significantly differ between EG and CG. Subgroup analysis revealed that the serum calcium concentrations of the experimental bilateral thyroidectomy subgroup (eBTS) on POPD1 and POPW3 were higher than that of the control bilateral thyroidectomy subgroup (cBTS) (P < 0.05); the reduction of serum calcium in eBTS on POPD1 and POPW3 was less than those in cBTS (P < 0.05). However, significant differences were not observed between the unilateral thyroidectomy subgroups (UTS) (P > 0.05). Moreover, the incidence of postoperative hypocalcemia in cBTS on POPD1 was significantly higher than that in eBTS (65.9% vs 41.7%) (P < 0.05). The length of hospitalization in cBTS (3.55 ± 1.89 days) was significantly longer than that (2.79 ± 1.15 days) in eBTS (P < 0.05). Conclusion:Short-term preoperative prophylactic oral calcium and activated vitamin D3 supplementation could effectively reduce the incidence of postoperative hypocalcemia and decrease the length of postoperative hospitalization in patients who have undergone bilateral thyroidectomy.

Objective To compare the clinical efficacy between air-free trans-axillary laparoscopic thyroidectomy and open thyroidectomy. Methods A retrospective analysis was performed on the data of both 96 patients who underwent air-free trans-axillary laparoscopic thyroidectomy (laparoscopic group) and 232 patients who underwent open thyroidectomy (open group) from August 2015 to July 2020. Comparative analysis were performed on operative data, the postoperative data of recovery and complications between two groups. Results The operative time in laparoscopic group was longer significantly than that in open group [(168±23) min vs. (95±18) min, P=0.022]. There was no significantly difference in the rate of recognition of recurrent laryngeal nerve between two groups (100.0% vs. 99.1%, P=0.138). The rate of recognition of both superior (98.0% vs. 97.0%, P=0.003) and inferior parathyroid glands (95.8% vs. 99.1%, P=0.028) in laparoscopic group was higher significantly than those in open group. The amount of drain of the first day after operation in laparoscopic group was more significantly than that in open group[(42±22) mL vs. (25±10) mL, P=0.006]. The postoperative length of hospital stay in laparoscopic group was longer significantly [(2.8±0.6) d vs. (1.8±1.2) d, P=0.016]. The cost of hospital stay was (13 186±1 015) yuan vs. (12 632±1 456) yuan （P=0.365） and the rate of postoperative complication was 10.4% vs. 9.1%（P=0.126）, which all showed no significant difference between two groups. Conclusions Air-free trans-axillary laparoscopic thyroidectomy could be feasible and safe, and have better appearance. However, both operative time and hospital stay were longer.

Rationale and Objectives: To investigate the relationship between upper-thigh intermuscular fat, subcutaneous fat measured by CT and major complications after primary total hip arthroplasty (THA). Materials and Methods: Between 2015 and 2021, consecutive patients who had primary THA and preoperative hip CT were retrospec-tively included. Upper-thigh muscle cross-sectional intermuscular fat, subcutaneous fat, and muscle area were measured on hip CT images. The major complications included dislocation, aseptic loosening, infection, and periprosthetic fracture. The effect of upper-thigh intermuscular fat, subcutaneous fat and muscle area on the outcome was analyzed using multivariable cox proportional hazards analysis. Adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated. Results: A total of 3028 patients were included and 71 (2.34%) of them had major complications. During a median of 25 months of follow-up, patients showed increased incidence of total major complications with increased intermuscular fat area (log-rankp = 0.012). The multi-variable cox regression revealed that per SD increment in intermuscular fat area was associated with higher risk of total major complica-tions (HR = 2.04, 95% CI = 1.71-2.43, p < 0.001), dislocation (HR = 1.96, 95% CI = 1.44-2.66, p < 0.001), aseptic loosening (HR = 2.02, 95% CI = 1.30-3.16, p = 0.002), infection (HR = 1.94, 95% CI = 1.24-3.05, p = 0.004), and periprosthetic fracture (HR = 2.26, 95% CI = 1.67-3.07, p < 0.001). Conclusion: Upper-thigh intermuscular fat, but not subcutaneous fat measured on CT associated with the risk of major complications after primary THA.

Chronic inflammation promotes the tumorigenesis and cell stemness maintenance of colorectal cancer (CRC). However, the bridge role of long noncoding RNA (lncRNA) in linking chronic inflammation to CRC development and progression needs better understanding. Here, we elucidated a novel function of lncRNA GMDS-AS1 in persistently activated signal transducer and transcription activator 3 (STAT3) and Wnt signaling and CRC tumorigenesis. Interleukin-6 (IL-6) and Wnt3a induced lncRNA GMDS-AS1 expression, which was highly expressed in the CRC tissues and plasma of CRC patients. GMDS-AS1 knockdown impaired the survival, proliferation and stem cell-like phenotype acquisition of CRC cells in vitro and in vivo. We performed RNA sequencing (RNA-seq) and mass spectrometry (MS) to probe target proteins and identify their contributions to the downstream signaling pathways of GMDS-AS1. In CRC cells, GMDS-AS1 physically interacted with the RNA-stabilizing protein HuR, thereby protecting the HuR protein from polyubiquitination- and proteasome-dependent degradation. HuR stabilized STAT3 mRNA and upregulated the levels of basal and phosphorylated STAT3 protein, persistently activating STAT3 signaling. Our research revealed that the lncRNA GMDS-AS1 and its direct target HuR constitutively activate STAT3/Wnt signaling and promote CRC tumorigenesis, the GMDS-AS1-HuR-STAT3/Wnt axis is a therapeutic, diagnostic and prognostic target in CRC.

BACKGROUND:Colon cancer is characterized by a sophisticated tumor microenvironment (TME). Cancer-associated fibroblasts (CAFs), which make up the majority of the stromal cells in TME, participate in tumor development and immune regulation. Further investigations of CAFs would facilitate an in-depth understanding of its role in colon cancer TME.METHODS:In this study, we estimated CAF abundance based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases using the Microenvironment Cell Populations-counter (MCP-counter) algorithm. CAF-related genes were identified by differential gene expression analysis combined with weighted gene coexpression network analysis. For further selection, the least absolute shrinkage and selection operator (LASSO)-Cox regression was used, and the prognostic value of the selected gene was confirmed in numerous external cohorts. The function enrichment, immunological characteristics, tumor mutation signature, immunotherapy response, and drug sensitivity of the selected gene were subsequently explored. The bioinformatics analysis results were validated using immunohistochemistry on clinical samples from our institution.RESULTS:According to our findings, cartilage oligomeric matrix protein (COMP) was uncovered as a candidate CAFs-driven biomarker in colon cancer and plays an important role in predicting prognosis in colon cancer. COMP upregulation was associated with enhanced stromal and immune activation, and immune cell infiltration, especially M2 macrophages. Genes that mutated differently between the high- and low-COMP expression subgroups may be correlated with TME change. Following verification, COMP reliably predicted the immunotherapy response and drug response. In addition, our experimental validation demonstrated that COMP overexpression is associated with colon cancer carcinogenesis and is strongly associated with CAFs and M2 macrophage infiltration.CONCLUSION:Our study uncovered that COMP was a key CAFs-driven gene associated with M2 macrophage infiltration and acted as a convincing predictor for prognosis and immunotherapy response in colon cancer patients.

A 19-year-old man presents to the emergency room with migraine headaches seven days after a blow to the head during martial arts competition. His neurologic examination is normal. The patient wishes to resume normal activities, including martial arts practice. As the radiologist, what imaging test, if any, do you recommend?

SHP2, a protein tyrosine phosphatase, plays a critical role in fully activating oncogenic signaling pathways such as Ras/MAPK downstream of cell surface tyrosine receptors (e.g., EGFR), which are often activated in human cancers, and thus has emerged as an attractive cancer therapeutic target. This study focused on evaluating the therapeutic potential of the novel SHP2 degrader, SHP2-D26 (D26), either alone or in combination, against non-small cell lung cancer (NSCLC) cells. While all tested NSCLC cell lines responded to D26 with IC 50 s of < 8 μM, a few cell lines (4/14) were much more sensitive than others with IC 50 s of ≤ 4 μM. There was no clear association between basal levels of SHP2 and cell sensitivities to D26. Moreover, D26 rapidly and potently decreased SHP2 levels in different NSCLC cell lines in a sustained way regardless of cell sensitivities to D26, suggesting that additional factors may impact cell response to D26. We noted that suppression of p70S6K/S6, but not ERK1/2, was associated with cell responses to D26. In the sensitive cell lines, D26 effectively increased Bim levels while decreasing Mcl-1 levels accompanied with the induction of apoptosis. When combined with the third generation EGFR inhibitor, osimertinib (AZD9291), synergistic effects on decreasing the survival of different osimertinib-resistant cell lines were observed with enhanced induction of apoptosis. Although D26 alone exerted moderate inhibition of the growth of NSCLC xenografts, the combination of osimertinib and D26 effectively inhibited the growth of osimertinib-resistant xenografts, suggesting promising efficacy in overcoming acquired resistance to osimertinib.

Colorectal cancer (CRC) is one of the prevalent malignant tumors. This study is aimed at evaluating the mechanism of anlotinib (anlo) on tumor microenvironment (TME) in CRC, and its effects in combination with immune checkpoint inhibitors (ICIs) therapy. Firstly, MC38 and CT26 cells were both exposed to different gradient concentrations of anlo for 72 h, to investigate the cell viability and synergetic therapy efficacy with ICIs by CCK8. The results showed that anlo could obviously inhibit cell growth and showed no synergistic efficacy therapy in combination with αPDL1 in vitro. Then, we found the upregulation of programmed cell death ligand 1(PDL1) expression both in vitro and in vivo after anlo treatment. In vivo, anlo could enhance the percentage of natural killer (NK) cells and M1 macrophage cells and decrease the percentage of M2 macrophage cells in TME. Moreover, we explored the mechanism and we proved that anlo could activate reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK)/activator protein-1 (AP-1) signaling pathway to increase the expression levels of PDL1, IFN-α/β/γ, and CXCL2 in two cell lines in vitro. We also proved that anlo had synergistic effects with ICIs in vivo. Finally, it could also increase the mRNA and protein PDL1 expression levels in human cell lines, which was consistent with mouse CRC cell lines. However, there are still a few limitations. On one hand, the ROS/JNK/AP-1 pathway needs to be proved whether it can be activated in human cell lines. On the other hand, the mechanism behind ROS promoting phosphorylation of JNK needs to be explored.

(1) Background: This study aimed to investigate the prevalence and risk factors for enlarged perivascular spaces (EPVS) in young adults from a neurology clinic-based cohort (≤45 years old) via unenhanced brain MRI. (2) Methods: A total of 931 young adults from a neurology clinic-based cohort who underwent unenhanced brain MRI between 1 January 2021 and 30 June 2021 were retrospectively included in this study. The EPVS were rated in the centrum semiovale (CSO-EPVS), basal ganglia (BG-EPVS), and midbrain (MB-EPVS) using a visual rating scale. The degrees of the CSO-EPVS, BG-EPVS, and MB-EPVS were all divided by a cutoff value of 1. Demographic factors, vascular risk factors, and symptoms were analyzed using the chi-square test and logistic regression to determine the risk factors of EPVS. (3) Results: The overall prevalence of EPVS was 99.8% (929/931). The CSO-EPVS, BG-EPVS, and MB-EPVS were predominantly scored as 1 (52.1%, 79.1%, and 58.3%, respectively). Logistic regression analysis identified age and hypertension as factors affecting the degrees of CSO-EPVS and BG-EPVS (p < 0.05). Hypertension (p < 0.001) and diabetes (p = 0.014) were revealed to be factors affecting the degree of BG-EPVS. Furthermore, patients with headache (OR = 1.807; p = 0.001) and dizziness (OR = 1.574; p = 0.025) were associated with MB-EPVS. (4) Conclusions: EPVS were frequently found in young adults and could be related to the symptoms. Age, hypertension, and diabetes were the risk factors for the severity of EPVS in the corresponding brain regions.

Objective The aim of this study was to investigate the distribution characteristics of enlarged perivascular spaces (EPVS) and white matter hyperintensities (WMH) and their associations with disease severity across the frontotemporal lobar degeneration (FTLD) syndromes spectrum. Methods This study included 73 controls, 39 progressive supranuclear palsy Richardson’s syndrome (PSP-RS), 31 corticobasal syndrome (CBS), 47 behavioral variant frontotemporal dementia (bvFTD), 36 non-fluent variant primary progressive aphasia (nfvPPA), and 50 semantic variant primary progressive aphasia (svPPA). All subjects had brain magnetic resonance imaging (MRI) and neuropsychological tests, including progressive supranuclear palsy rating scale (PSPRS) and FTLD modified clinical dementia rating sum of boxes (FTLD-CDR). EPVS number and grade were rated on MRI in the centrum semiovale (CSO-EPVS), basal ganglia (BG-EPVS), and brain stem (BS-EPVS). Periventricular (PWMH) and deep (DWMH) were also graded on MRI. The distribution characteristics of EPVS and WMH were compared between control and disease groups. Multivariable linear regression analysis was performed to evaluate the association of EPVS and WMH with disease severity. Results Compared with control subjects, PSP-RS and CBS had more BS-EPVS; CBS, bvFTD, and nfvPPA had less CSO-EPVS; all disease groups except CBS had higher PWMH (p < 0.05). BS-EPVS was associated with PSPRS in PSP-RS (β = 2.395, 95% CI 0.888–3.901) and CBS (β = 3.115, 95% CI 1.584–4.647). PWMH was associated with FTLD-CDR in bvFTD (β = 1.823, 95% CI 0.752–2.895), nfvPPA (β = 0.971, 95% CI 0.030–1.912), and svPPA (OR: 1.330, 95% CI 0.457–2.204). Conclusion BS-EPVS could be a promising indicator of disease severity in PSP-RS and CBS, while PWMH could reflect the severity of bvFTD, nfvPPA, and svPPA.

Background:Programmed death ligand 1 (PD-L1) immunohistochemistry (IHC) has been proposed as a predictive biomarker to predict response to immunotherapy. Given the limitations of IHC test in PD-L1 detection, this study aimed to investigate the technical feasibility of using quantitative RT-PCR (qRT-PCR) to replace IHC in PD-L1 detection in gastrointestinal tumors.Materials and methods:The Cancer Genome Atlas database was used to evaluate the relationship between PD-L1 expression in tumor tissue and the patient prognosis. In addition, 52 patients with gastrointestinal cancer were enrolled and divided into the stomach (STAD), colon (COAD), and rectum (READ) adenocarcinoma cohorts. IHC test was used to determine the PD-L1 level of the tissue specimens, and the qRT-PCR test was used to analyze the mRNA expression in both blood and tissue specimens. Moreover, the correlation between blood PD-L1 mRNA expression and immunotherapy efficacy was investigated in additional 15 patients with gastric cancer that further enrolled.Results:The expression level of PD-L1 in tumor tissue is related to the tumor stage of COAD (p-value = 0.001) and primary therapy outcomes in patients with READ (p-value = 0.003) but not significantly correlated to the overall survival (OS) time of patients with gastrointestinal cancer. Moreover, the concordance of PD-L1 mRNA expression level of tissue and paired blood samples is low, despite a weak linear relationship that was found in the STAD cohort (r = 0.43, p-value = 0.049). We further demonstrated that qRT-PCR results in both tissue and blood specimens were numerically but not statistically significant consistent with IHC results (corresponding to a p-value of 0.84 and 0.55, respectively). Remarkably, high PD-L1 expression in blood of patients with STAD shows a better response to immunotherapy (p-value = 0.04), which could be well identified at the relative expression cutoff of 1.5 (sensitivity of 85.7%, specificity of 75.0%, and AUC of 0.82).Conclusions:Our study established a novel strategy for rapidly distinguishing patients with gastrointestinal cancer with the response to immunotherapy and has potential clinical benefits.