Tumors Of Digestive Tract Research Articles

Colangitis crónicas: diagnóstico diferencial y papel de la resonancia magnética

The idiopathic chronic cholangitides comprise a group of hepatobiliary diseases of probable autoimmune origin that are usually asymptomatic in the initial stages and can lead to cirrhosis of the liver. Elevated cholestatic enzymes on blood tests raise suspicion of these entities. Among the idiopathic cholangitides, the most common is primary sclerosing cholangitis, which is associated with inflammatory bowel disease and with an increased incidence of hepatobiliary and digestive tract tumors. It is important to establish the differential diagnosis with IgG4-associated cholangitis, primary biliary cholangitis, and secondary cholangitides, because the therapeutic management is different. Magnetic resonance cholangiopancreatography (MRCP) is the best test to evaluate the intrahepatic and extrahepatic biliary tract, and MRI also provides information about the liver and other abdominal organs. An appropriate MRCP protocol and knowledge of the different findings that are characteristic of each entity are essential to reach the correct diagnosis.

Detection of genes responsible for cetuximab sensitization in colorectal cancer cells using CRISPR-Cas9.

Colorectal cancer (CRC) is a common malignant tumor in digestive tract with highly invasive and metastatic capacity. Drug sensitivity remains a significant obstacle to successful chemotherapy in CRC patients. The present study aimed to explore genes related to cetuximab (CTX) sensitivity in CRC by clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9. Celigo image cytometer was used to detect suitable cells and optimal dosage of CTX. Inhibition rate of CTX on Caco-2 cells was evaluated by cell counting kit-8 (CCK-8) method before and after transfection. 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyl tetrazolium bromide (MTT) was performed to explore suitable concentration of puromycin and multiplicity of infection (MOI). CRISPR-Cas9, sequencing data quality analysis and cell viability test were used for the selection of genes related to CTX sensitivity in CRC cells. Finally, the selected genes associated with CTX sensitivity in CRC cells were further validated by colony formation and CCK-8 assays. In the present study, Caco-2 cells had a better prolificacy, and CTX 100 μg/ml exhibited a good inhibition trend on the 7th and 14th days of infection. MTT assay indicated that the minimum lethal concentration of puromycin was 2.5 μg/ml. Forty-six candidate genes were preliminarily screened via sequencing data quality analysis. Subsequently, we found that knockout of any of the four genes (MMP15, MRPL48, CALN1 and HADHB) could enhance CTX sensitivity in Caco-2 cells, which was further confirmed by colony formation assay. In summary, MMP15, MRPL48, CALN1 and HADHB genes are related to the mediation of CTX sensitivity in CRC.

Pulchinenoside B4 exerts the protective effects against cisplatin-induced nephrotoxicity through NF-κB and MAPK mediated apoptosis signaling pathways in mice

Cisplatin (cis-Dichlorodiammine platinum, CP), as the first-line chemotherapy drug of choice for many cancers such as urogenital system tumors and digestive tract tumors, also causes toxicity and side effects to the kidney. Previous studies have shown that Pulsatilla chinensis has significant anti-inflammatory and antioxidant activities, but the mechanism of cisplatin induced acute kidney injury (AKI) in vivo has not been thoroughly studied. The purpose of this study is to investigate the protective effect of pulchinenoside B4 (PB4), a representative and major component with a content of up to 10% in root of P. chinensis, on AKI induced by CP in mice. Our results indicated the significant protective effect of PB4 by evaluating renal function indicators, inflammatory factor levels and renal histopathological changes. In addition, PB4 may mainly act on NF-κB signaling pathway to reduce the levels of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) in the kidney after CP exposure, thus exerting anti-inflammatory activity. Furthermore, PB4 regulated MAPK signaling pathway and its downstream apoptotic factors to inhibit the occurrence of apoptosis, such as Bax, Bcl-2, caspase 3 and caspase 9. Notably, the activations of caspase 3 induced by cisplatin were strikingly reduced in PB4-treated mice. Therefore, the above evidence suggested that PB4 is a potential renal protectant with significant anti-inflammatory and anti-apoptotic effects.

Ultrasound Image-Based Radiomics: An Innovative Method to Identify Primary Tumorous Sources of Liver Metastases.

To develop radiomic models of B-mode ultrasound (US) signatures for determining the origin of primary tumors in metastatic liver disease. A total of 254 patients with a diagnosis of metastatic liver disease were included in this retrospective study. The patients were divided into 3 groups depending on the origin of the primary tumor: group 1 (digestive tract versus non-digestive tract tumors), group 2 (breast cancer versus non-breast cancer), and group 3 (lung cancer versus other malignancies). The patients in each group were allocated to a training or testing set (a ratio of 8:2). The region of interest of liver metastasis was determined through manual differentiation of the tumors, and radiomic signatures were acquired from B-mode US images. Optimal features were selected to develop 3 radiomic models using multiple-dimensionality reduction and classifier screening. The area under the curve (AUC) of the receiver operating characteristic curve was applied to assess each model's performance. A total of 5936 features were extracted, and 40, 6, and 14 optimal features were sequentially identified for the development of radiomic models for groups 1, 2, and 3, respectively, with training set AUC values of 0.938, 0.974, and 0.768 and testing set AUC values of 0.767, 0.768, and 0.750. The differences in age, sex, and number of liver metastatic lesions varied greatly between the 4 primary tumors (P < .050). B-mode US radiomic models could be effective supplemental means to identify the origin of hepatic metastatic lesions (ie, unknown primary sites).

Sepsis en pacientes con tumores sólidos en quimioterapia

El cáncer constituye un problema de salud mundial. Múltiples factores relacionados con la enfermedad y los tratamientos provocan predisposición a las infecciones en el paciente oncológico. La sepsis, constituye una importante causa de morbimortalidad. Se realizó un estudio descriptivo de corte transversal, con el objetivo de describir el comportamiento de las infecciones en pacientes con tumores sólidos en quimioterapia, atendidos en el servicio de Oncología Médica del Hospital Clínico Quirúrgico Hermanos Ameijeiras, de enero 2015 a enero 2017. La media de edad fue 53 años (32,3 %) y predominaron los pacientes masculinos (56.5 %). Los tumores de vías digestivas, carcinomas de pulmón y sarcomas de partes blandas representaron el 32.3, 25 y 13.7 %, respectivamente. De los 124 eventos de sepsis reportados, el 39.5 % fueron neutropenia febril, seguido por sepsis urinaria (34.7 %). En pacientes con otras infecciones, predominaron la nuemopatía inflamatoria y la mucositis grado IV. No existió asociación estadística significativa entre el esquema de quimioterapia y la aparición de infección. El avance y perfeccionamiento de los tratamientos han prolongado la vida de los pacientes y esto ha favorecido el mejor estudio y compresión de los diferentes eventos adversos, relacionados con la administración de quimioterapia.

A Glycosylated Covalent Organic Framework Equipped with BODIPY and CaCO3 for Synergistic Tumor Therapy.

Ca2+ , a ubiquitous but nuanced modulator of cellular physiology, is meticulously controlled intracellularly. However, intracellular Ca2+ regulation, such as mitochondrial Ca2+ buffering capacity, can be disrupted by 1 O2 . Thus, the intracellular Ca2+ overload, which is recognized as one of the important cell pro-death factors, can be logically achieved by the synergism of 1 O2 with exogenous Ca2+ delivery. Reported herein is a nanoscale covalent organic framework (NCOF)-based nanoagent, namely CaCO3 @COF-BODIPY-2I@GAG (4), which is embedded with CaCO3 nanoparticle (NP) and surface-decorated with BODIPY-2I as photosensitizer (PS) and glycosaminoglycan (GAG) targeting agent for CD44 receptors on digestive tract tumor cells. Under illumination, the light-triggered 1 O2 not only kills the tumor cells directly, but also leads to their mitochondrial dysfunction and Ca2+ overload. An enhanced antitumor efficiency is achieved via photodynamic therapy (PDT) and Ca2+ overload synergistic therapy.

Recent Advances in Digestive Tract Tumors: Updates From the 5th Edition of the World Health Organization "Blue Book".

The World Health Organization Classification of Tumours: Digestive System Tumors, 5th edition, was published in 2019 and shows several impactful changes as compared with the 4th edition published in 2010. Changes include a revised nomenclature of serrated lesions and revamping the classification of neuroendocrine neoplasms. Appendiceal goblet cell adenocarcinoma is heavily revised, and intrahepatic cholangiocarcinoma is split into 2 subtypes. New subtypes of colorectal carcinoma and hepatocellular carcinoma are described. Precursor lesions are emphasized with their own entries, and both dysplastic and invasive lesions are generally recommended to be graded using a 2-tier system. Hematolymphoid tumors, mesenchymal tumors, and genetic tumor syndromes each have their own sections in the 5th edition. New hematolymphoid lesions include monomorphic epitheliotropic intestinal T-cell lymphoma; duodenal-type follicular lymphoma; intestinal T-cell lymphoma, not otherwise specified; and indolent T-cell lymphoproliferative disorder of the gastrointestinal tract. This paper will provide an in-depth look at the changes in the 5th edition as compared with the 4th edition. To provide a comprehensive, in-depth update on the World Health Organization classification of digestive tumors, including changes to nomenclature, updated diagnostic criteria, and newly described entities. The 5th edition of the World Health Organization Classification of Tumours: Digestive System Tumours, as well as the 4th edition. The World Health Organization has made many key changes in its newest update on tumors of the digestive system. Pathologists should be aware of these changes and incorporate them into their practice as able or necessary.

Expression and function of transmembrane 4 superfamily proteins in digestive system cancers

BackgroundAlthough the medical level is constantly improving, cancer is still a major disease that threatens human health, and very effective treatments have not been found. In recent years, studies have found that four-transmembrane superfamily proteins are involved in multiple stages of tumorigenesis and development, but their expression and function in tumors have not been systematically studied.MethodsWe used the Oncomine database to analyze the mRNA expression levels of TSPAN family in various cancers. Then differentially expressed genes were screened out and verified by liver cancer, colorectal cancer, and gastric cancer cells by q-PCR and Western blot analysis. CCK8 and EDU analysis are used to detect cell proliferation, Cell wound scrape assay and Cell invasion assay are used to analyze cell invasion and metastasis. Nude tumor formation test used to verify the tumor suppressive effect of TSPAN7 in vivo.ResultsDifferential analysis of 33 TSPAN proteins revealed that a total of 11 proteins showed differential expression in 10% of independent analyses, namely TSPAN1, TSPAN3, TSPAN5, TSPAN6, TSPAN7, TSPAN8, TSPAN13, TSPAN25, TSPAN26, TSPAN29, TSPAN30. TSPAN7 is the only four-transmembrane protein with reduced expression in three types of digestive tract tumors, so we chose TSPAN7 to be selected for cellular and molecular level verification. We found that compared with normal cells, the expression of TSPAN7 in liver cancer cells was significantly reduced, while the expression of gastric and colon cancer was not significantly different from that of normal cells. In addition, we also found that the high expression of Tspan7 not only inhibited the proliferation of HCC-LM3 cells, but also inhibited its invasion and metastasis.ConclusionsOur study evaluated the expression and function of the TSPANs family in digestive cancers and explored TSPAN7 in hepatoma cells in detail. We found some members of the TSPAN family show significant expression differences between cancer and normal tissues, of which TSPAN7 may be a potential biomarker for liver cancer.

Chinese expert consensus and practice guideline of totally implantable access port for digestive tract carcinomas.

Totally implantable access port is a fully implantable drug delivery system that is implanted subcutaneously and can be retained for a long time. Advantages of ports include a simple nursing process, low risk of infection and embolism, and high patient comfort. In order to promote the standardized application of ports in the treatment of digestive tract tumors and reduce port-related complications, the Chinese Research Hospital Association Digestive Tumor Committee, the Chinese Association of Upper Gastrointestinal Surgeons, the Chinese Gastric Cancer Association, and the Gastrointestinal Surgical Group of Chinese Surgical Society Affiliated to Chinese Medical Association have organized multidisciplinary expert discussions at the General Hospital of the People’s Liberation Army and nation-wide expert letter reviews and on-site seminars, and formulated an expert consensus of the operation guidelines.

Effect of family support on quality of postoperative life in patients with digestive cancer.

Digestive tumors are malignant tumors of epithelial origin with high rates of morbidity and mortality worldwide. At present, surgery is the main treatment for patients with digestive tumors. In this study, we conducted a survey of patients with digestive cancers to explore the influence of family support on postoperative quality of life, with the aim of providing a basis of reference for further improvement of the quality of life of such patients. A total of 82 patients with digestive cancer who underwent surgery in Hospital of Chengdu University of Traditional Chinese Medicine between October, 2018 and April, 2019 were selected to take part. The self-made questionnaire, the European Cancer Research and Treatment Organization's Core Quality of Life Questionnaire for Cancer Patients, and the Family Support Scale were used to investigate the patients, and the collected data were statistically analyzed. The family support scores of the 82 enrolled patients ranged from 5 to 15 points, with an average score of (8.86±2.47) points; 60 cases (73.17%) scored ≥10 points and 12 cases (26.83%) scored <10 points. Patients who were married, aged under 30 years old, or employed as civil servants had higher family support scores than other patients (P<0.05). The scores for physical function, emotional function, and overall health status/quality of life in patients who had a high family support score were higher than those in patients who had a low family support score (P<0.05). According to the logistic regression model, Patients with higher age, getting married, with education level of bachelor degree or above, occupation as farmer and with other digestive tract tumor got higher family support score. (P<0.05). Good family support can effectively improve quality of postoperative life for patients with digestive cancer. Education, age, occupation and marriage are all independent factors that affect family support.

Роль мультидисциплинарных центров в диагностике и лечении нейроэндокринных опухолей: опыт работы Российского экспертного центра по морфологической диагностике нейроэндокринных опухолей пищеварительного тракта на базе Московского областного научно-исследовательского клинического института им. М.Ф. Владимирского (МОНИКИ)

Роль мультидисциплинарных центров в диагностике и лечении нейроэндокринных опухолей: опыт работы Российского экспертного центра по морфологической диагностике нейроэндокринных опухолей пищеварительного тракта на базе Московского областного научно-исследовательского клинического института им. М.Ф. Владимирского (МОНИКИ)

DCLK1 inhibition attenuates tumorigenesis and improves chemosensitivity in esophageal squamous cell carcinoma by inhibiting β-catenin/c-Myc signaling.

Doublecortin-like kinase 1 (DCLK1) is involved in tumorigenesis, tumor growth and metastasis, and epithelial-to-mesenchymal transition in many digestive tract tumors. It is reportedly highly expressed in Barrett's esophagus and esophageal adenocarcinoma, but its effects on the occurrence and progression of esophageal squamous cell carcinoma (ESCC) remain unclear. In this study, real-time PCR and western blot analysis confirmed significant upregulation of DCLK1 expression in human ESCC tissues and cell lines. CCK-8 assay showed that transfection with siRNA against DCLK1 (si-DCLK1) markedly inhibited cell proliferation and colony formation in the ESCC cell lines Eca109 and TE1. Transwell assay revealed that si-DCLK1 transfection inhibited the migratory and invasive capacities of Eca109 and TE1 cells. Moreover, si-DCLK1 increased the chemosensitivity of these cells to cisplatin, as indicated by inhibited cell viability and colony formation, and increased ROS and apoptosis in cisplatin-treated cells. Western blot assay revealed that expression of nuclear β-catenin and c-Myc was significantly increased in ESCC tissues and that si-DCLK1 markedly downregulated nuclear β-catenin and c-Myc in Eca109 cells. Treatment with lithium chloride, an activator of β-catenin signaling, partially abolished the si-DCLK1-induced inhibition of proliferation, migration, invasion, and chemoresistance of ESCC cells. These findings suggest that knockdown of DCLK1 may inhibit the progression of ESCC by regulating proliferation, migration, invasion, and chemosensitivity via suppressing the β-catenin/c-Myc pathway, supporting a promising therapeutic target against ESCC.

Tumor circulome in the liquid biopsies for digestive tract cancer diagnosis and prognosis.

Digestive tract cancer is one of the main diseases that endanger human health. At present, the early diagnosis of digestive tract tumors mainly depends on serology, imaging, endoscopy, and so on. Although tissue specimens are the gold standard for cancer diagnosis, with the rapid development of precision medicine in cancer, the demand for dynamic monitoring of tumor molecular characteristics has increased. Liquid biopsy involves the collection of body fluids via non-invasive approaches, and analyzes biological markers such as circulating tumor cells, circulating tumor DNA, circulating cell-free DNA, microRNAs, and exosomes. In recent years, liquid biopsy has become more and more important in the diagnosis and prognosis of cancer in clinical practice due to its convenience, non-invasiveness, high specificity and it overcomes temporal-spatial heterogeneity. Therefore, this review summarizes the current evidence on liquid biopsies in digestive tract cancers in relation to diagnosis and prognosis.

Role of gut microbiota in carcinogenesis and treatment for colorectal cancer

Colorectal cancer is one of the most common malignant tumors of digestive tract. There are a large number of microorganisms in the digestive tract. Under normal physiological conditions, intestinal microorganisms can help with digestion and absorption, resist pathogen invasion and regulate the proliferation of intestinal mucosal cells. However, intestinal microflora imbalance will affect the intestinal microenvironment and intestinal cell function, and is closely related to the incidence and progression of colorectal cancer. Firstly, this paper introduces the changes of intestinal flora in patients with colorectal cancer, and then summarizes the mode of intestinal flora participating in the occurrence of colorectal cancer from the macro level. Then, we elaborate the involvement of intestinal flora in colorectal cancer from the aspects of cytokine-dependent chronic inflammation, DNA damage of intestinal epithelial cells, carcinogenic metabolites of intestinal flora and cellular enzymes, and changes of intestinal immune system. The pathogenesis of colorectal cancer provides a reference for further study of the pathogenesis of colorectal cancer. Finally, from the perspective of intestinal flora and colorectal cancer treatment, we analyze the significance of probiotics and bacterial flora transplantation for the treatment of colorectal cancer, and provide some new treatment ideas and methods that may be useful for the treatment of colorectal cancer.

Lentiviral-Mediated Beclin-1 Overexpression Inhibits Cell Proliferation and Induces Autophagy of Human Esophageal Carcinoma Eca109 Cell Xenograft in Nude Mice.

Esophageal carcinoma is one of the common malignant tumors in digestive tract. BECLIN-1 is a key gene that regulates autophagy, and its abnormal expression may be related with many human tumors. However, the mechanism of BECLIN-1 in esophageal carcinoma remains unknown. In this study, we explored the effect of BECLIN-1 overexpression on tumor growth in mice with esophageal carcinoma and its mechanism. Recombined lentiviral vector containing BECLIN-1 was used to transfect human esophageal carcinoma Eca109 cells and establish stable cell line. qRT-PCR was used to detect BECLIN-1 mRNA level in the transfected Eca109 cells, CCK-8 assay was used to detect cell proliferation. Beclin-1, P62 and LC3-II protein expression levels in Eca109 cells were detected using Western blot analysis. Subcutaneous xenograft nude mice model of human esophageal carcinoma was established, and the tumor growths in Beclin-1 group, control group and empty vector group were monitored. Beclin-1 protein expression in vivo was detected by immunohistochemistry. Beclin-1 mRNA and protein were overexpressed in Eca109 cells. Compared with empty vector group, the growth rate of cells transfected with BECLIN-1 decreased significantly. Compared with the control group and empty vector group, the expression level of P62 protein in beclin-1 group was significantly decreased, while the expression level of LC3-II protein was significantly increased. The tumor growth rate in nude mice of Beclin-1 group was significantly lower than that of the control group and empty vector group, and Beclin-1 protein was mainly expressed in Beclin-1 group in vivo. BECLIN-1 can induce autophagy in esophageal carcinoma Eca109 cells, and it can significantly inhibit the growth of esophageal carcinoma.

Clinical Efficacy of Metoprolol Succinic Acid Sustained Release Tablets Combined with Trimetazidine in the Treatment of Gastrointestinal Tumors with Angina Pectoris

Objective: To investigate the clinical efficacy of metoprolol succinate sustained-release tablets combined with trimetazidine in the treatment of gastrointestinal tumors with angina pectoris. Methods: We enrolled the 58 patients with digestive tract tumor merger angina in November 2017 - October 2019 and analysis the hospital clinical data by retrospective method. We included patients with routine treatment in control group (n = 31 cases) and the subjects treated with increased dose of succinic acid metoprololzyban joint with trimetazidineinobservation group (n = 27 cases) according to the different treatment group. Results: The effective rate of angina pectoris treatment in the observation group was higher than that in the control group. Furthermore, the incidence of adverse reactions was lower than that in the control group and the difference was statistically significant (P &lt; 0.05). Conclusion: Metoprolol succinic acid sustained release tablets combined with trimetazidine in the treatment of gastrointestinal tumors with angina pectoris can improve the efficacy of angina pectoris. The drug use is safe and worthy of clinical use.

Value of long non-coding RNA Rpph1 in esophageal cancer and its effect on cancer cell sensitivity to radiotherapy.

BACKGROUNDEsophageal cancer is a common digestive tract tumor that is generally treated with radiotherapy. Poor responses to radiotherapy in most patients generally result in local radiotherapy failure, so it is essential to find new radiosensitizers that can enhance the response of cancer cells to radiotherapy and improve the survival of esophageal cancer patients with radiation resistance. The long non-coding RNA (lncRNA) Rpph1 is highly expressed in human gastric cancer tissues, and represses breast cancer cell proliferation and tumorigenesis. However, the expression of lncRNA Rpph1 in esophageal cancer and its relationship with radio-sensitivity has not been studied.AIMTo explore the value of lncRNA Rpph1 in esophageal cancer and its effect on cancer cell sensitivity to radiotherapy.METHODSEighty-three patients with esophageal cancer admitted to Qilu Hospital of Shandong University and 90 healthy participants who received physical examinations were collected as research participants. The expression of Rpph1 was determined by qRT-PCR. siRNA-NC and siRNA-Rpph1 were transfected into esophageal cancer cell lines, and cells without transfection were designated as the blank control group. Cell survival was tested by colony formation assays, and the levels of proteins related to apoptosis and epithelial-mesenchymal transitions were determined by Western blot assays. Cell proliferation was assessed by MTT assays, cell apoptosis by flow cytometry, and cell migration by wound-healing assays. Changes in cell cycle distribution were monitored.RESULTSRpph1 was highly expressed in esophageal carcinoma, making it a promising marker for the diagnosis of esophageal cancer. Rpph1 could also be used to distinguish different short-term responses, T stages, N stages, and clinical stages of esophageal cancer patients. The results of 3-year overall survival favored patients with lower Rpph1 expression over patients with higher Rpph1 expression (P < 0.05). In vitro and in vivo experiments showed that silencing Rpph1 expression led to higher sensitivity of esophageal cancer cells to radiotherapy, stronger apoptosis in esophageal cancer cells induced by radiotherapy, higher expression of Bax and caspase-3, and lower expression of Bcl-2 (Bax, caspase-3, and Bcl-2 are apoptosis-related proteins). Additionally, silencing Rpph1 attenuated radiation-induced G2/M phase arrest, and significantly inhibited the expression of proteins involved in cell proliferation, migration, and epithelial-mesenchymal transition regulation in esophageal cancer cells.CONCLUSIONRpph1 is highly expressed in esophageal cancer. Silencing Rpph1 expression can promote cell apoptosis, inhibit cell proliferation and migration, and increase radio-sensitivity.

Auxiliary role and application prospects of immune nutrition and traditional Chinese medicine in comprehensive treatment of digestive tract tumors

Auxiliary role and application prospects of immune nutrition and traditional Chinese medicine in comprehensive treatment of digestive tract tumors

What is New in the 2019 World Health Organization (WHO) Classification of Tumors of the Digestive System: Review of Selected Updates on Neuroendocrine Neoplasms, Appendiceal Tumors, and Molecular Testing.

The 5th edition of the World Health Organization classification of digestive system tumors discusses several advancements and developments in understanding the etiology, pathogenesis, and diagnosis of several digestive tract tumors. To provide a summary of the updates with a focus on neuroendocrine neoplasms, appendiceal tumors, and the molecular advances in tumors of the digestive system. English literature and personal experiences. Some of the particularly important updates in the 5th edition are the alterations made in the classification of neuroendocrine neoplasms, understanding of pathogenesis of appendiceal tumors and their precursor lesions, and the expanded role of molecular pathology in establishing an accurate diagnosis or predicting prognosis and response to treatment.

Identification of pathways and genes in the process of E6/E7-induced carcinogenesis of esophageal epithelial cells.

Human papillomavirus (HPV) infection was associated with some carcinomas, especially malignant tumors in upper digestive tract, upper respiratory tract, and genitourinary system. The mechanism of the viral transformation of normal cells is still not very clear. To investigate the tumorigenesis of epithelial cells, E6/E7-induced malignant transformation model cells were used for expression profiling analysis by performing RNA expression microarray detection. Bioinformatics analysis was applied to investigate the cellular process changes along with the E6/E7 expression in SHEE cells. The differentially expressed genes were further grouped and uploaded for Search Tool for the Retrieval of Interacting Genes analysis. The protein-protein interaction results were visualized. The hub genes and their first-neighbors genes were selected, followed by gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis. The obtained results demonstrated that tumor-related biological processes began to emerge during the carcinogenesis process from 48th passage to 76th passage of SHEE cells after E6/E7 expression. Ten hub genes were identified and analyzed during the E6/E7-induced tumorigenesis. This study explores the gene expression network in the progressive transformation of immortalized esophageal epithelial cells induced by E6/E7 expression. Understanding the biological processes and hub genes that first appear during the transformation will provide some clues to the mechanism of E6/E7-induced carcinogenesis of esophageal epithelial cells.