Immune reactions following intestinal transplantation: Mechanisms and prevention.

For patients with intestinal failure, small bowel transplantation remains one of the most effective treatments despite continuous advancements in parenteral nutrition techniques. Long-term use of parenteral nutrition can result in serious complications that lead to metabolic dysfunction and organ failure. However, the small intestine is a highly immunogenic organ with a large amount of mucosa-associated lymphoid tissue and histocompatibility antigens; therefore, the small intestine is highly susceptible to severe immune rejection. This article discusses the mechanisms underlying immune rejection after small bowel transplantation and presents various options for prevention and treatment. Our findings offer new insights into the development of small bowel transplantation.

Chemotherapy-induced pneumatosis intestinalis followed by hepatic portal venous gas. A case report.

Pneumatosis intestinalis (PI) is a rare disease, and there are many theories about its pathogenesis. Hepatic portal venous gas (HPVG), is thought to occur secondary to intramural intestinal gas emboli migrating through the portal venous system via the mesenteric veins. PI accompanied by HPVG is usually a sign of bowel ischaemia and is associated with a high mortality rate. We report here, a patient with liver metastases from colorectal cancer who developed PI followed by HPVG after treatment with 5-Fluorouracil, leucovorin, and oxaliplatin (mFOLFOX6). Timely attention and management of gastrointestinal symptoms following chemotherapy are essential in the treatment of this type of patient.

Extracellular vesicle-mediated pre-metastatic niche formation via altering host microenvironments.

The disordered growth, invasion and metastasis of cancer are mainly attributed to bidirectional cell-cell interactions. Extracellular vesicles (EVs) secreted by cancer cells are involved in orchestrating the formation of pre-metastatic niches (PMNs). Tumor-derived EVs mediate bidirectional communication between tumor and stromal cells in local and distant microenvironments. EVs carrying mRNAs, small RNAs, microRNAs, DNA fragments, proteins and metabolites determine metastatic organotropism, enhance angiogenesis, modulate stroma cell phenotypes, restructure the extracellular matrix, induce immunosuppression and modify the metabolic environment of organs. Evidence indicates that EVs educate stromal cells in secondary sites to establish metastasis-supportive microenvironments for seeding tumor cells. In this review, we provide a comprehensive overview of PMN formation and the underlying mechanisms mediated by EVs. Potential approaches to inhibit cancer metastasis by inhibiting the formation of PMNs are also presented.

Effects of surgical management for gastrointestinal stromal tumor patients with liver metastasis on survival outcomes.

Purpose: To investigate the effect of surgical resection on survival in gastrointestinal stromal tumors synchronous liver metastasis (GIST-SLM) and to develop clinically usable predictive models for overall survival (OS) and cancer-specific survival (CSS) in patients. Methods: We identified patients in the SEER database diagnosed with GISTs from 2010 to 2019. We used propensity score matching (PSM) to balance the bias between the Surgery and No surgery groups. Kaplan-Meier(K-M) analysis was used to detect differences in OS and CSS between the two groups. The nomogram to predict 1, 3, and 5-year OS and CSS were developed and evaluated. Results: After PSM, 228 patients were included in this study. There were significant differences in 1, 3, and 5-year OS and CSS between the two groups (OS: 93.5% vs. 84.4%, 73.2% vs. 55.3%, 60.9% vs. 36.9%, P=0.014; CSS: 3.5% vs.86.2%,75.3% vs.57.9%, 62.6% vs. 42.9%, P=0.02). We also found that patients who received surgery combined with targeted therapy had better OS and CSS at 1, 3, and 5 years than those who received surgery only (OS: 96.6% vs.90.9%, 74.9% vs. 56.8%, 61.7% vs. 35.5%, P=0.022; CSS: 96.6% vs. 92.1%, 77.4% vs.59.2%,63.8% vs. 42.0%, P=0.023). The area under the curve (AUC) was 0.774, 0.737, and 0.741 for 1, 3, and 5-year OS, respectively, with 0.782 and 0.742 for 1, 3, and 5-year CSS. In the model, C-index was 0.703 for OS and 0.705 for CSS and showed good consistency. Conclusion: Surgical treatment can improve the OS and CSS of patients with GIST-SLM. In addition, the combination with chemotherapy may be more favorable for the long-term survival of patients. Meanwhile, we constructed the nomograms for predicting OS and CSS at 1, 3, and 5-year, and validated them internally. Our model can contribute to clinical management and treatment strategy optimization.

DNA damage repair molecular subtype derived immune signature applicable for the prognosis and immunotherapy response prediction in colon cancer.

Background: The DNA damage repair (DDR) pathway is one of the pathways of tumor pathogenesis, but its relationship with the immunophenotype has not been clarified in colon cancer (CC). Methods: We identified the differentially expressed immune-related genes (DEIRGs) between two DDR molecular subtypes, namely, C1 and C2, and used univariate Cox analysis and least absolute shrinkage and selection operator (LASSO) penalized Cox regression analysis to construct the risk score in the training cohort [n=1,009, a combination of The Cancer Genome Atlas (TCGA) and GSE39582]. Regarding the median risk score as the unified cutoff to classify the patients into high- and low-risk groups. Two independent cohorts (GSE17538, n=232; GSE38832, n=122) were used for external validation of the prognostic value of the risk score. The IMvigor210 cohort (n=348) was used to test the predictive value of the risk score for immunotherapy response. Gene set variation analysis (GSVA) and gene set enrichment analysis (GSEA) were performed to discover the underlying mechanism. Immune cell infiltration was quantified by the single sample gene set enrichment analysis (ssGSEA) algorithm. Results: The high-risk group showed significantly reduced overall survival (OS), disease-specific survival (DSS), disease-free survival (DFS), progression-free survival (PFS), and relapse-free survival (RFS) compared to the low-risk group, and the two groups differed significantly in lymphatic invasion, American Joint Committee on Cancer (AJCC) TNM stage, preoperative carcinoembryonic antigen (CEA) level, etc. The enrichment levels of pathways related to colorectal cancer, epithelial-mesenchymal transition (EMT), angiogenesis, hypoxia, P53, TGF-ß, KRAS signaling, etc., were upregulated in the high-risk group, but DDR-related pathways were defective in the high-risk group. The immunophenotypes of the high-risk group tended to be desert and excluded, and the risk score of patients who responded to immunotherapy was significantly lower than that of patients who did not respond to immunotherapy. The higher the infiltration levels of gamma delta T cells (γδ T cells), immature dendritic cells, and T follicular helper (Tfh) cells, the more significant adverse impact on the prognosis of CC patients was exhibited and an obviously positive correlation with the risk score was showed. Conclusions: An immune gene risk score associated with the DDR molecular subtype was built and verified herein; that is applicable to the prognosis and immunotherapy response prediction in CC.

Higher anthocyanin intake is associated with a lower risk of non-alcoholic fatty liver disease in the United States adult population.

Background: Flavonoids are a class of plant chemicals known to have health-promoting properties, including six subclasses. Anthocyanin is one of the subclasses that have anti-inflammatory and antioxidant activities. However, the relationship between flavonoid subclass intake and the risk of non-alcoholic fatty liver disease (NAFLD) and liver fibrosis has not been verified in representative samples of the United States. Methods: This is a cross-sectional study based on the data from the National Health and Nutrition Examination Survey (NHANES) and the Food and Nutrient Database for Dietary Studies (FNDDS) in 2017-2018. The intake of flavonoid subclasses of the participants was obtained from two 24 h dietary recalls. The NAFLD and liver fibrosis were defined based on the international consensus criteria. The relationship between flavonoid subclass intake and NAFLD and liver fibrosis was evaluated using a multivariate logistic regression model corrected for multiple confounding factors. Subgroup analysis, trend tests, interaction tests and restricted cubic spline were carried out to further explore this relationship. In addition, we also explored the relationship between anthocyanin and liver serum biomarkers, dietary total energy intake and healthy eating index (HEI)-2015 scores. Results: A total of 2,288 participants were included in the analysis. The intake of anthocyanin was significantly negatively associated with the risk of NAFLD, but not other flavonoid subclasses. A higher anthocyanin intake was significantly associated with a lower risk of NAFLD (quartile 4, OR 0.470, 95% CI 0.275-0.803). The results of subgroup analysis showed that the protective effect of dietary anthocyanin intake on NAFLD was more pronounced in participants of non-Hispanic whites, with hypertension and without diabetes (P for interaction <0.05). Alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), dietary total energy intake was significantly negatively correlated with dietary anthocyanin intake. We did not find any protective effect of flavonoid subclass intake on liver fibrosis. Conclusion: Anthocyanin, but not other flavonoid subclasses, can significantly reduce the risk of NAFLD. The protective effect was more pronounced in non-Hispanic whites, participants without diabetes and those with hypertension. Our study provides new evidence that anthocyanin intake has a reverse significant association with the risk for NAFLD.

Prognostic Analysis of Prophylactic Hyperthermic Intraperitoneal Chemotherapy for Advanced Gastric Cancer: a Propensity Score-Matched Analysis.

PURPOSE: To investigate the efficacy of prophylactic hyperthermic intraperitoneal chemotherapy (HIPEC) for advanced gastric cancer (AGC). METHODS: We included 198 patients treated from December 2016 to January 2019; of these patients, the 132 who had clinical T4 gastric cancer were divided into a hyperthermic intraperitoneal chemotherapy group (HIPEC group) and a radical gastrectomy and D2 lymph node dissection group (control group). Because this study was retrospective, we used propensity score matching (PSM) to reduce selectivity bias; we then assessed risk factors for recurrence and compared prognosis in terms of survival in the gastrectomy and prophylactic HIPEC groups. RESULTS: Prophylactic HIPEC reduced the risk of postoperative peritoneal metastasis (PM: 27.5% vs. 10.5%, P = 0.015) and did not increase the risk of postoperative complications, but there was no significant difference in the effect on hepatic metastases or other distant metastases. Risk factors for recurrence included pT4 staging and positive lymph node metastases. Both disease-free survival (DFS: HR 0.592; 95% CI 0.354-0.990; P = 0.042) and peritoneal recurrence-free survival (PFS: HR 0.314; 95% CI 0.127-0.774; P = 0.008) were better in the prophylactic HIPEC group than in the gastrectomy-only group. In addition, there was no difference in the prognosis of patients between the two groups of raltitrexed (RT) and paclitaxel (PTX) for perfusion dosing. CONCLUSION: Our study showed that prophylactic HIPEC could prevent postoperative PM in patients with AGC and did not increase the incidence of postoperative complications. However, it was not found to be effective in the prevention of other metastases, such as hepatic metastases.

Combined detection of SDC2/ADHFE1/PPP2R5C methylation in stool DNA for colorectal cancer screening.

BACKGROUND: Colorectal cancer (CRC) is a disease of global concern, and its increasing incidence suggests the need for early and accurate diagnosis. The aim of this study was to investigate the value of combined detection of SDC2, ADHFE1 and PPP2R5C gene methylation in stool samples for early CRC screening. METHODS: Stool samples from patients with CRC (n = 105), advanced adenoma (AA) (n = 54), non-advanced adenoma (NA) (n = 57), hyperplastic or other polyps (HOP) (n = 47) or no evidence of disease (NED) (n = 100) were collected from September 2021 to September 2022. The methylation levels of SDC2, ADHFE1 and PPP2R5C were quantified by quantitative methylation-specific polymerase chain reaction (qMSP), and faecal immunochemical testing (FIT) was performed. The diagnostic value was assessed using reporter operating characteristic (ROC) curve analysis. RESULTS: The sensitivity of combined detection of SDC2/ADHFE1/PPP2R5C methylation in predicting CRC (0-IV) was 84.8%, the specificity was 98.0%, and the AUC was 0.930 (95% CI 0.889-0.970). Compared to FIT and serum tumour biomarkers, it showed better diagnostic performance for different stages of CRC. CONCLUSION: The results of this study verified that the methylation levels of SDC2, ADHFE1 and PPP2R5C in stool DNA were significantly increased in CRC patients. Combined detection of SDC2/ADHFE1/PPP2R5C methylation is a potential non-invasive diagnostic method for CRC and precancerous lesion screening. CLINICAL TRIAL REGISTRATION: Chinese Clinical Trials Registry, ChiCTR2100046662, registered on 26 May 2021, prospective registration.

Prognostic value of systemic immune inflammation index and geriatric nutrition risk index in early-onset colorectal cancer.

Background: Systemic nutritional and inflammatory markers, which are easy to measure are associated with the progression and prognosis of many cancers. Nevertheless, among the various available indicators, optimal prognostic indicators for patients with early-onset colorectal cancer have not been identified. Therefore, the aim of this study was to identify optimal nutritional and inflammatory markers for early-onset colorectal cancer and examine the relationship between systemic nutritional and inflammatory markers before treatment and survival in patients with early-onset colorectal cancer. Methods: We retrospectively collected data from 236 eligible patients with early-onset colorectal cancer. Area under the prognostic curve (AUC) and concordance index (C-index) were used to compare seven systemic nutritional and inflammatory markers to identify the optimal inflammatory immune markers. Univariate and multivariate COX regression analyses were used to evaluate the prognostic value of indicators in the total study population and different subgroups. Results: The AUC and C-index showed that the systemic immune inflammation index (SII) and geriatric nutrition risk index (GNRI) had higher prognostic values than other systemic nutritional and inflammatory indicators. Compared with patients in the low SII group, those in the high SII group had lower overall survival (HR, 4.42, 95% CI, 2.36-8.27, p = 0.000). Compared with patients in the high GNRI group, those in the low GNRI group had lower overall survival (HR, 0.33, 95% CI, 0.19-0.56, p = 0.000). SII was negatively associated with GNRI (R = -0.3, p < 0.001), and both were correlated with the tumor stage. Conclusion: SII and GNRI are suitable nutritional and inflammatory factors for predicting OS in patients with early-onset colorectal cancer; high SII and low GNRI were correlated with worse prognoses. Identifying the high inflammatory state and low nutritional state of patients before surgery and conducting active and timely therapeutic interventions could improve patient prognosis.

Targeting tumor immunosuppressive microenvironment for pancreatic cancer immunotherapy: Current research and future perspective.

Pancreatic cancer is one of the most malignant tumors with increased incidence rate. The effect of surgery combined with chemoradiotherapy on survival of patients is unsatisfactory. New treatment strategy such as immunotherapy need to be investigated. The accumulation of desmoplastic stroma, infiltration of immunosuppressive cells including myeloid derived suppressor cells (MDSCs), tumor associated macrophages (TAMs), cancer-associated fibroblasts (CAFs), and regulatory T cells (Tregs), as well as tumor associated cytokine such as TGF-ß, IL-10, IL-35, CCL5 and CXCL12 construct an immunosuppressive microenvironment of pancreatic cancer, which presents challenges for immunotherapy. In this review article, we explore the roles and mechanism of immunosuppressive cells and lymphocytes in establishing an immunosuppressive tumor microenvironment in pancreatic cancer. In addition, immunotherapy strategies for pancreatic cancer based on tumor microenvironment including immune checkpoint inhibitors, targeting extracellular matrix (ECM), interfering with stromal cells or cytokines in TME, cancer vaccines and extracellular vesicles (EVs) are also discussed. It is necessary to identify an approach of immunotherapy in combination with other modalities to produce a synergistic effect with increased response rates in pancreatic cancer therapy.

Cancer-associated fibroblast-secreted miR-421 promotes pancreatic cancer by regulating the SIRT3/H3K9Ac/HIF-1α axis.

This study was designed to explore the effects of exosomal miR-421 secreted by cancer-associated fibroblasts (CAFs) on pancreatic cancer (PC) progression and the mechanisms involved. CAFs and exosomes (exos) were isolated and identified. PC cells were treated with CAF-derived exos (CAF-exos). Western blotting and quantitative polymerase chain reaction (qPCR) were used to measure miR-421, sirtuin-3 (SIRT3), and hypoxia duciblefactors-1 alpha (HIF-1α) levels. Cell counting kit-8 (CCK-8), wound-healing, and transwell migration assays were used to measure proliferation, migration, and invasion abilities of the cells. Dual-luciferase assay and RNA immunoprecipitation (RIP) experiment analyzed the relationship between miR-421 and SIRT3. Chromatin immunoprecipitation (f)-verified H3K9Ac enrichment in the HIF-1α promoter region. In vivo tumorigenesis experiments were performed to further explore the effects of exosomal miR-421 from CAFs on PC. CAFs and exos were successfully isolated. CAF-exo-treated PC cells highly expressed miR-421 and had increased cell proliferation, migration, and invasion abilities. Knocking down miR-421 increased the expression of SIRT3. SIRT3 is a target of miR-421, and inhibiting the expression of SIRT3 reversed the negative effects of miR-421 knockdown on PC cell. Knocking down miR-421 in CAF-exo inhibited the expression of HIF-1α in PC cells. Moreover, SIRT3-mediated HIF-1α expression by regulating H3K9Ac. HIF-1α overexpression reversed the inhibiting effects of SIRT3 overexpression on PC progression and counteracted the inhibiting effects of miR-421 knockdown on glycolysis. Moreover, in vivo tumorigenesis experiments showed that knocking down miR-421 attenuated CAF-exo induced tumor growth. Exosomal miR-421 from CAFs promoted PC progression by regulating the SIRT3/H3K9Ac/HIF-1α axis. This study provided insights into the molecular mechanism of PC.

Development and validation of a nomogram to predict anastomotic leakage in colorectal cancer based on CT body composition.

Background: Anastomotic leakage (AL) is one of the most serious postoperative complications. This study aimed to investigate the predictive value of preoperative body composition for AL in patients with colorectal cancer (CRC). Methods: We first reviewed data from 3,681 patients who underwent radical CRC resection 2013-2021 in our hospital, and 60 patients were diagnosed with AL after surgery. We designed a nested case-control study and two controls were randomly selected for each case according to the time and position of surgery. Body composition was measured at the level of the third lumbar vertebra based on computed tomography (CT) images. The risk factors of AL were analyzed by univariate and multivariate analysis. Nomogram was built using binary regression analysis and assessed for clinical usefulness, calibration, and discrimination. Results: In the multivariate analysis, gender, blood glucose, nutrition risk screening (NRS), skeletal muscle area (SMA) and visceral fat area (VFA) were independent risk factors for developing anastomotic leakage after surgery. The prognostic model had an area under the receiver operating characteristic curve of 0.848 (95% CI, 0.781-0.914). The calibration curve showed good consistency between the predicted and observed outcomes. Decision curve analysis indicated that patients with colorectal cancer can benefit from the prediction model. Conclusions: The nomogram that combined with gender, blood glucose, NRS, SMA, and VFA had good predictive accuracy and reliability to AL. It may be conveniently for clinicians to predict AL preoperatively and be useful for guiding treatment decisions.

LINC00960 regulates cell proliferation and glycolysis in pancreatic cancer through the miR-326-3p/TUFT1/AKT-mTOR axis.

Pancreatic cancer (PC) is a common malignant cancer characterized by high mortality and poor prognosis. LINC00690 was involved in the occurrence and progression of PC, but the underlying mechanisms require further investigation. The goal of this study was to figure out how LINC00960 mediates glycolysis in PC. LINC00960, miR-326-3p, and Tuftelin 1 (TUFT1) expression levels were detected in PC cell lines. LINC00960 and TUFT1 expression levels were increased in PC cells when compared with normal pancreatic cells, whereas miR-326-3p expression levels were decreased. The expression levels of LINC00690 affected glycolysis in PC, and inhibition of LINC00960 inhibited tumor growth in vivo. LINC00690 targeted and suppressed the expression of miR-326-3p. MiR-326-3p bound to TUFT1, and miR-326-3p inhibited AKT-mTOR pathway activation via TUFT1. In conclusion, the depletion of LINC00960 repressed cell proliferation and glycolysis in PC by mediating the miR-326-3p/TUFT1/AKT-mTOR axis. Thus, we present a novel mechanism underlying the progression of PC that suggests LINC00960 is a potential therapeutic target for this cancer.

Extracellular vesicle-mediated crosstalk between pancreatic cancer and stromal cells in the tumor microenvironment.

Pancreatic ductal adenocarcinoma (PDAC) interacts closely with the tumor microenvironment (TME). The TME is remodeled by crosstalk between pancreatic cancer cells and stromal cells, and is critical for cancer progression. Extracellular vesicles (EVs), including exosomes and microvesicles, help facilitate an exchange of information both within the TME and to distant organs. EVs have also been identified as potential diagnostic biomarkers, therapeutic targets, and drug carriers for pancreatic cancer treatment. Thus, understanding the selective packaging of EVs cargo and its mechanistic impact will increase our understanding of cancer biology. In this review, we collect and analyze recent findings of the pancreatic cancer-stromal cell interactions mediated by EVs and the mechanisms involved in cancer-related immunity and chemoresistance. These studies demonstrate the vital role of EVs in pancreatic cancer reprogramming and TME remodeling. We also summarize the EVs identified as potential PDAC diagnostic biomarkers and possible therapeutic targets. This greater understanding is a promising avenue for transitioning EVs from bench to bedside.

The Interplay Between Inflammation and Stromal Components in Pancreatic Cancer.

Inflammation involves interactions between various immune cells, inflammatory cells, chemokines and cytokines in pancreatic cancer. Cancer cells as well as surrounding stromal and inflammatory cells establish an inflammatory tumor microenvironment (TME). Inflammation is closely associated with immunity. Meanwhile, immune cells are involved in both inflammation and immune response. Tumor-promoting inflammation and tumor-suppressive immunity are two main characteristics of the tumor microenvironment in pancreatic cancer. Yet, the mechanism of inflammation and immune response in pancreatic cancer development is still unclear due to the dual role of some cytokines and the complicated crosstalk between tumor and stromal components in TME. In this review, we outline the principal cytokines and stromal cells in the pancreatic TME that are involved in the tumor-promoting and immunosuppressive effects of inflammation, and discuss the interaction between inflammation and stromal components in pancreatic cancer progression. Moreover, the clinical approaches based on targeting TME in pancreatic cancer are also summarized. Defining the mechanisms of interplay between inflammation and stromal components will be essential for further development of anti-cancer therapies.

Imaging Features for Predicting High-Grade Dysplasia or Malignancy in Branch Duct Type Intraductal Papillary Mucinous Neoplasm of the Pancreas: A Systematic Review and Meta-Analysis.

BACKGROUND: The consensus guidelines for branch-duct intraductal papillary mucinous neoplasm (BD-IPMN) of the pancreas are mostly based on imaging features. This study aimed to determine imaging features and their diagnostic accuracy for predicting high-grade dysplasia (HGD)/malignancy in BD-IPMN, including mixed type. METHODS: The PubMed, Embase, and Cochrane databases were searched, and data were extracted from relevant studies. As the main diagnostic accuracy index, diagnostic odds ratios (DORs) of imaging features for diagnosing HGD/malignancy in BD-IPMNs were pooled using the random-effects model. A bivariate random-effects approach was used to construct summary receiver operating characteristic curves for sensitivity and specificity estimation. RESULTS: The pooled DOR was the highest for the enhanced solid component/mural nodule (MN) (DOR, 12.21; 95 % confidence interval [CI], 6.14-24.27), followed by a main pancreatic duct (MPD) diameter of 10 mm or greater (DOR, 7.93; 95 % CI, 3.02-20.83), solid component (DOR, 4.85; 95 % CI, 2.49-9.42), lymphadenopathy (DOR, 4.84; 95 % CI, 1.11-21.06), MN (DOR, 4.48; 95 % CI, 3.15-6.39), an MPD diameter of 5 mm or greater (DOR, 3.69; 95 % CI, 2.62-5.19), abrupt change in MPD caliber with distal pancreatic atrophy (DOR, 2.65; 95 % CI, 1.66-4.24), thickened/enhancing walls (DOR, 2.38; 95 % CI, 1.57-3.60), and cyst size of 3 cm or larger (DOR, 1.98; 95 % CI, 1.48-2.64). The largest area under the curve (0.89 and 0.95, respectively) and high specificity (0.95 and 0.98, respectively) also were found for enhanced solid component/MN and an MPD diameter of 10 mm or greater, albeit with low sensitivity (0.38 and 0.14, respectively). CONCLUSIONS: The aforementioned imaging features could aid in predicting HGD/malignancy of BD-IPMN. Furthermore, enhanced solid component/MN and an MPD diameter of 10 mm or greater were the most important predictors of HGD/malignancy in BD-IPMN and should be considered as indications for surgery.

Detection and analysis of null alleles of amelogenin in gender identification.

In this study, we located eight samples with null alleles of amelogenin out of 10,750 cases, and discussed the influence in gender identification and forensic personal identification. Amelogenin was detected and retested by several autosomal STR kits and sex chromosomal STR kits, and the causes were analyzed by chromosome karyotype analysis and Y chromosome microdeletion detection if necessary. Suspected AMEL-X loss was observed in five samples, but no abnormality was detected in the X-STR loci. AMEL-X was recovered when samples were retested by other detection systems designed with different primers. One sample had AMEL-X and X-STR loci loss, and the karyotype was chimeric 45,X0[70]/46,X,+mar[13].Two male samples lost AMEL-Y fragment, and both of them lost DYS522-DYS570-DYS576 loci, but no abnormalities were found in the STS loci of SRY and AZF regions. Therefore, when carrying out gender identification by using amelogenin, it is essential to focus on null alleles of amelogenin. In especially, deal with the samples collected from the individuals who had chromosomal hereditary disorders(e.g. Turner Syndrome and Oligospermia / Azoospermia). In order to achieve this, laboratories should have various techniques to verify the null alleles of amelogenin and ensure accurate genotyping. Accurate genotyping of amelogenin and DNA database establishment are vital for personal identification.

Establishment and clinical application value of an automatic diagnosis platform for rectal cancer T-staging based on a deep neural network.

BACKGROUND: Colorectal cancer is harmful to the patient's life. The treatment of patients is determined by accurate preoperative staging. Magnetic resonance imaging (MRI) played an important role in the preoperative examination of patients with rectal cancer, and artificial intelligence (AI) in the learning of images made significant achievements in recent years. Introducing AI into MRI recognition, a stable platform for image recognition and judgment can be established in a short period. This study aimed to establish an automatic diagnostic platform for predicting preoperative T staging of rectal cancer through a deep neural network. METHODS: A total of 183 rectal cancer patients' data were collected retrospectively as research objects. Faster region-based convolutional neural networks (Faster R-CNN) were used to build the platform. And the platform was evaluated according to the receiver operating characteristic (ROC) curve. RESULTS: An automatic diagnosis platform for T staging of rectal cancer was established through the study of MRI. The areas under the ROC curve (AUC) were 0.99 in the horizontal plane, 0.97 in the sagittal plane, and 0.98 in the coronal plane. In the horizontal plane, the AUC of T1 stage was 1, AUC of T2 stage was 1, AUC of T3 stage was 1, AUC of T4 stage was 1. In the coronal plane, AUC of T1 stage was 0.96, AUC of T2 stage was 0.97, AUC of T3 stage was 0.97, AUC of T4 stage was 0.97. In the sagittal plane, AUC of T1 stage was 0.95, AUC of T2 stage was 0.99, AUC of T3 stage was 0.96, and AUC of T4 stage was 1.00. CONCLUSION: Faster R-CNN AI might be an effective and objective method to build the platform for predicting rectal cancer T-staging. TRIAL REGISTRATION: chictr.org.cn: ChiCTR1900023575; http://www.chictr.org.cn/showproj.aspx?proj=39665.

Establishment and Clinical Application of an Artificial Intelligence Diagnostic Platform for Identifying Rectal Cancer Tumor Budding.

Tumor budding is considered a sign of cancer cell activity and the first step of tumor metastasis. This study aimed to establish an automatic diagnostic platform for rectal cancer budding pathology by training a Faster region-based convolutional neural network (F-R-CNN) on the pathological images of rectal cancer budding. Postoperative pathological section images of 236 patients with rectal cancer from the Affiliated Hospital of Qingdao University, China, taken from January 2015 to January 2017 were used in the analysis. The tumor site was labeled in Label image software. The images of the learning set were trained using Faster R-CNN to establish an automatic diagnostic platform for tumor budding pathology analysis. The images of the test set were used to verify the learning outcome. The diagnostic platform was evaluated through the receiver operating characteristic (ROC) curve. Through training on pathological images of tumor budding, an automatic diagnostic platform for rectal cancer budding pathology was preliminarily established. The precision-recall curves were generated for the precision and recall of the nodule category in the training set. The area under the curve = 0.7414, which indicated that the training of Faster R-CNN was effective. The validation in the validation set yielded an area under the ROC curve of 0.88, indicating that the established artificial intelligence platform performed well at the pathological diagnosis of tumor budding. The established Faster R-CNN deep neural network platform for the pathological diagnosis of rectal cancer tumor budding can help pathologists make more efficient and accurate pathological diagnoses.

The Metabolism Symbiosis Between Pancreatic Cancer and Tumor Microenvironment.

Complex interactions occur between tumor cells and the tumor microenvironment. Studies have focused on the mechanism of metabolic symbiosis between tumors and the tumor microenvironment. During tumor development, the metabolic pattern undergoes significant changes, and the optimal metabolic mode of the tumor is selected on the basis of its individual environment. Tumor cells can adapt to a specific microenvironment through metabolic adjustment to achieve compatibility. In this study, the effects of tumor glucose metabolism, lipid metabolism, and amino acid metabolism on the tumor microenvironment and related mechanisms were reviewed. Selective targeting of tumor cell metabolic reprogramming is an attractive direction for tumor therapy. Understanding the mechanism of tumor metabolic adaptation and determining the metabolism symbiosis mechanism between tumor cells and the surrounding microenvironment may provide a new approach for treatment, which is of great significance for accelerating the development of targeted tumor metabolic drugs and administering individualized tumor metabolic therapy.