Quality evaluation of natural monomer flavors for Chinese tobacco industry based on dual mode combined Fourier transform ion cyclotron resonance mass spectrometry and isotopic fine structures.

RATIONALE: Natural monomer flavors can modify the taste of cigarettes. However, no report was published to establish the quality control method for their chemical compositions. METHODS: In this study, licorice, a traditional natural monomer flavor used in tobacco aroma processing, was selected, and the fingerprint was developed by high-performance liquid chromatography (HPLC). Next, the chemical markers of samples from different places of origin were discovered by multivariate statistical analysis. Then, its chemical constituents were identified by combination of HPLC-Fourier transform ion cyclotron resonance mass spectrometry (FT-ICR-MS), direct infusion FT-ICR-MS (DI-FT-ICR-MS), and the technology of isotopic fine structures (IFSs). Moreover, its characteristic constituents were quantitatively analyzed using HPLC. RESULTS: The 14 common peaks were assigned in the fingerprint, and 8 of them were considered as qualitative markers by multivariate statistical analysis. A total of 42 chemical constituents were detected using HPLC-FT-ICR-MS, and 13 of them were unambiguously identified by references. Meanwhile, the elemental compositions of other eight unknown chemical components were decisively determined using IFSs. Subsequently, the contents of five characteristic constituents in 11 batches of samples were determined. CONCLUSIONS: The integration strategy established here can discover and quantify the chemical markers for improving the quality control standard of natural monomer flavor of licorice. It is expected that the strategy will be valuable for further quality control of other natural monomer flavors in Chinese tobacco industry.

Photochemical Difluoromethylation of Quinoxalin-2(1H)-ones with Difluoroacetic Anhydride and Pyridine N-Oxide.

A novel photochemical difluoromethylation of quinoxalin-2(1H)-ones under catalyst-free conditions was achieved with difluoroacetic anhydride and pyridine N-oxide. The green and mild reaction conditions as well as readily attainable difluoroacetic anhydride provide a useful protocol to prepare C3-difluoromethylated quinoxalin-2(1H)-ones.

TAK1 deficiency promotes liver injury and tumorigenesis via ferroptosis and macrophage cGAS-STING signalling.

Background & Aims: Oxidative stress-mediated ferroptosis and macrophage-related inflammation play an important role in various liver diseases. Here, we explored if and how hepatocyte ferroptosis regulates macrophage stimulator of interferon genes (STING) activation in the development of spontaneous liver damage, fibrosis, and tumorigenesis. Methods: We used a transforming growth factor-beta-activated kinase 1 (TAK1) deficiency-induced model of spontaneous liver damage, fibrosis, and tumorigenesis to investigate hepatocyte ferroptosis and its impact on macrophage STING signalling. Primary hepatocytes and macrophages were used for in vitro experiments. Results: Significant liver injury and increased numbers of intrahepatic M1 macrophages were found in hepatocyte-specific TAK1-deficient (TAK1ΔHEP) mice, peaking at 4 weeks and gradually decreasing at 8 and 12 weeks. Meanwhile, activation of STING signalling was observed in livers from TAK1ΔHEP mice at 4 weeks and had decreased at 8 and 12 weeks. Treatment with a STING inhibitor promoted macrophage M2 polarisation and alleviated liver injury, fibrosis, and tumour burden. TAK1 deficiency exacerbated liver iron metabolism in mice with a high-iron diet. Moreover, consistent with the results from single-cell RNA-Seq dataset, TAK1ΔHEP mice demonstrated an increased oxidative response and hepatocellular ferroptosis, which could be inhibited by reactive oxygen species scavenging. Suppression of ferroptosis by ferrostatin-1 inhibited the activation of macrophage STING signalling, leading to attenuated liver injury and fibrosis and a reduced tumour burden. Mechanistically, increased intrahepatic and serum levels of 8-hydroxydeoxyguanosine were detected in TAK1ΔHEP mice, which was suppressed by ferroptosis inhibition. Treatment with 8-hydroxydeoxyguanosine antibody inhibited macrophage STING activation in TAK1ΔHEP mice. Conclusions: Hepatocellular ferroptosis-derived oxidative DNA damage promotes macrophage STING activation to facilitate the development of liver injury, fibrosis, and tumorigenesis. Inhibition of macrophage STING may represent a novel therapeutic approach for the prevention of chronic liver disease. Impact and implications: The precise mechanism by which hepatocyte ferroptosis regulates macrophage STING activation in the progression of liver damage, fibrosis, and tumorigenesis remains unclear. Herein, we show that deletion of TAK1 in hepatocytes caused oxidative stress-mediated ferroptosis and macrophage-related inflammation in the development of spontaneous liver injury, fibrosis, and hepatocellular carcinoma.

Searching for the true origin of the red fluorescence of leaf-derived carbon dots.

We report for the first time that the red fluorescence of leaf-derived carbon dots is derived from chlorophyll, and a possible formation structure is proposed. By controlling the solvothermal reaction temperature, the new luminescence center of CDs can be adjusted. This work provides unprecedented insights into the luminescence mechanism of biomass-derived CDs.

Comprehensive analyses of intraoral spindle cell carcinoma: A rare disease entity revisited.

OBJECTIVE: The present study was aimed to comprehensively characterize the epidemiological, clinicopathological characteristics, treatments, and prognosis of intraoral spindle cell carcinoma (SpCC). MATERIALS AND METHODS: Patients diagnosed with intraoral SpCC at our institution in the past 15 years (2005-2019) were screened from inpatient disease registry. All relevant data concerning patients with intraoral SpCC were retrieved. Previous reports about intraoral SpCC with adequate clinicopathological data in both English literature and Chinese literature were collected. Eligible cases were further reviewed and pooled for statistical analyses. RESULTS: Six patients (5 females and 1 male; average age: 59 years) with intraoral SpCC were histopathologically diagnosed and surgically treated at our institution. The literature review identified another 63 published cases from 34 articles. Most cases were presented in the fifth to seventh decade of life with a male preponderance. Gingiva (23/69, 33.3%) was the most common site followed by the tongue (19/69, 27.5%) and buccal mucosa (8/69, 11.6%). Complete surgical ablation remains the primary treatment option. Tumor size, pathological grades, cervical node metastasis, and distant metastasis were significantly associated with reduced survival. CONCLUSIONS: Intraoral SpCC is an uncommon and aggressive malignancy with dismal prognosis. Much attention and effort are needed to characterize this rare entity and improve its clinical outcomes.

Influence of Nitrogen-Doped Carbon Quantum Dots on the Electrocatalytic Performance of the CoP Nanoflower Catalyst for OER.

Cobalt phosphides modified by nitrogen-doped carbon quantum dots (CoP-NCQDs) were successfully constructed by a facile and low-cost hydrothermal treatment, which is expected to replace traditional noble-metal oxygen evolution reaction electrode materials. Detailed experiments and findings show that nitrogen-doped carbon quantum dots (NCQDs) have a significant impact on the morphology of the CoP catalyst, and nitrogen doping can regulate the surface-active sites to obtain the catalyst with abundant structural defects. Simultaneously, nitrogen doping can regulate the content of pyridinic N and pyrrolic N, which exerts positive effects on the formation of the bond structure and electron conduction between NCQDs and CoP.

[Effect of electroacupuncture on gastrointestinal function of patients after laparoscopic cholecystectomy under general anesthesia].

OBJECTIVE: To observe the effects of electroacupuncture at bilateral Zusanli(ST36), Shangjuxu(ST37), and Sanyinjiao (SP6) acupoints on gastrointestinal function after laparoscopic cholecystectomy under general anesthesia. METHODS: A total of 150 patients(American Society of Anesthesiologists［ASA］ grades Ⅰ and Ⅱ) undergoing laparoscopic cholecystectomy in the Department of Hepatobiliary Surgery of the First Affiliated Hospital of Guangzhou University of Chinese Medicine were randomly assigned into three groups: electroacupuncture group (n=50), simple acupuncture group (n=50), and control group (n=50). Patients in the control group received routine treatment；on the basis of routine treatment, patients in the simple acupuncture group were acupunctured at bilateral ST36, ST37 and SP36；patients in the electroacupuncture group were treated with electroacupuncture at bilateral ST36, ST37 and SP36（50 Hz，5 mA）. In both simple acupuncture group and electroacupuncture group, the corresponding treatments were conducted 1 h after surgery, Patients as well as in the morning (8:00-10:00) and afternoon (14:00-16:00) on the first day after surgery, 30 min each time. The time of bowel sound recovery, the time to the first postope-rative exhaust and defecation, the time of postoperative fluid diet recovery, abdominal pain score, and gastrointestinal reaction score were recorded and analyzed. RESULTS: Compared with the control group, the electroacupuncture group and the simple acupuncture group showed shortened time of bowel sound recovery, shortened time to the first postoperative exhaust and defecation, and shortened time of postoperative liquid diet recovery (P<0.01), as well as decreased postoperative abdominal pain score and gastrointestinal reaction score (P<0.01). Furthermore, the time of bowel sound recovery, the time to the first postoperative exhaust and defecation, and the time of postoperative liquid diet recovery were shortened in the electroacupuncture group compared with those in the simple acupuncture group (P<0.01). The total effective rate of electroacupuncture group was 94.0% (47/50), the total effective rate of simple acupuncture group was 88.0% (44/50), significantly higher than 78.0% (39/50) in the control group (P<0.05). CONCLUSION: Both electroacupuncture and simple acupuncture can promote the recovery of gastrointestinal function in patients after laparoscopic cholecystectomy under general anesthesia, and electroacupuncture is superior to simple acupuncture,but they have no significant difference in alleviating postoperative abdominal pain and gastrointestinal reactions.

Simple Strategy for Scalable Preparation Carbon Dots: RTP, Time-Dependent Fluorescence, and NIR Behaviors.

Transforming carbon dots (CDs) fluorescent materials into smart materials with complex functions is a topic of great interest to nanoscience. However, designing CDs with regulating fluorescence/phosphorescence that can be visually monitored with the environment changes in real-time remains a challenge. Here, a very simple strategy, one-step solvent-free catalytic assistant strategy, which is low cost, facile, environment-friendly, and high throughput, is put forward. Hydrogen bond is used to manipulate nanostructure of CDs, and the obtained carbon dots (M-CDs) show a series of attractive properties including matrix-free room-temperature phosphorescence, time-dependent fluorescence, and near-infrared emissive characteristics. Different from the traditional aggregation caused quenching or aggregation-induced emission fluorescent materials, M-CDs exhibit unprecedented and unique dispersion induced redshift fluorescence phenomenon, promoting the studies of fluorescence from static to dynamic. The causes of this phenomenon are further analyzed in detail. As a kind of intelligent fluorescent materials, this new designed CDs greatly enrich the basic recognition of CDs by illustrating the relationship between redshift fluorescence behaviors and the dispersion states, and may provide with an opportunity for solid-state fluorescent materials, anti-counterfeiting, cellular imaging, and hopefully many others.

Long noncoding RNA matrilineal expression gene 3 inhibits hepatocellular carcinoma progression by targeting microRNA-5195-3p and regulating the expression of forkhead box O1.

We investigated the effect of the long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) on hepatocellular carcinoma (HCC) tumorigenesis and progression by targeting miR-5195-3p and transcription factor forkhead box O1 (FOXO1) to identify a novel target for HCC treatment. HCC clinical samples were collected, and cell counting kit-8 (CCK-8), and transwell migration and invasion assays were performed. Furthermore, interaction was detected via double luciferase reporter and RNA pull-down assays. MEG3, miR-5195-3p, and FOXO1 expression was determined by quantitative real-time polymerase chain reaction (RT-qPCR) and Western blotting. Xenograft tumor models were established to investigate the effect of MEG3 in vivo. Compared with normal tissues, MEG3 expression was significantly downregulated in HCC tissues. MEG3 overexpression inhibited the viability and migration of HCC cells. Double luciferase reporter and RNA pull-down assays confirmed the binding between MEG3 and miR-5195-3p as well as between miR-5195-3p and FOXO1. RT-qPCR and Western blotting results showed that MEG3 inhibited the expression of miR-5195-3p and promoted that of FOXO1. Additionally, MEG3 overexpression inhibited HCC tumorigenesis and progression in xenograft tumor models while depletion of MEG3 exerted the opposite way. Therefore, the lncRNA MEG3 inhibits HCC tumorigenesis and progression through the miR-5195-3p/FOXO1 signaling axis.

Analysis of the efficacy and prognostic factors of PD-1 inhibitors in advanced gallbladder cancer.

BACKGROUND: Gallbladder cancer (GBC) is highly malignant, its early diagnosis is difficult, and the 5-year survival rate is less than 5%. For patients with advanced GBC (GBCa), combined chemotherapy, radiotherapy, targeted therapy, and immunotherapy are needed to improve the overall survival (OS) rate of patients. METHODS: Data were collected from 53 patients with GBCa who had volunteered to receive programmed death protein-1 (PD-1)-based treatment at the First Affiliated Hospital of Nanjing Medical University from February 2018 to February 2021. Statistical analysis of the collected data, including Kaplan-Meier method, log-rank test, Cox proportional hazard regression model and other methods. RESULTS: The objective response rates (ORRs) and disease control rates (DCRs) of 53 participants 3 months after receiving immunotherapy were 30.2% and 79.2%, respectively. The ORRs and DCRs of the combined treatment group were higher than those of the camrelizumab group (CG) (P<0.05). The DCRs of the camrelizumab plus apatinib group (CAG) at 3 and 6 months were 90.9% and 45.5% (P=0.003), respectively, while the DCRs at 3 and 6 months of the camrelizumab plus chemotherapy group (CCG) were 85.7% and 71.4% (P=0.450), respectively. After treatment, there were statistically significant differences before and after CA199 for each group (P<0.05). The median progression-free survival (mPFS) of the 53 participants was 7 months, and the median overall survival (mOS) was 12 months. The mPFS and mOS of the CAG and the CCG were greater than those in the CG (6 vs. 3 months, P<0.001, 12 vs. 8 months, P=0.019; 9 vs. 3 months, P<0.001, 13 vs. 8 months, P<0.001, respectively). A total of 16 cases had grade 1 or 2 adverse events, and 3 cases had grade 3 and higher adverse events. CONCLUSIONS: For GBCa patients, PD-1 combined with targeted therapy or chemotherapy is more effective than immunotherapy alone. The targeted therapy group has more obvious early effects on the disease control rate, and combined chemotherapy can achieve sustained effects, providing new ideas for the future GBCa application of immune, targeted, and chemotherapy sequential therapy.

RCN1 induces sorafenib resistance and malignancy in hepatocellular carcinoma by activating c-MYC signaling via the IRE1α-XBP1s pathway.

The increasing incidence of hepatocellular carcinoma (HCC) is of great concern globally, but the molecular pathogenesis of these tumors remains unclear. Sorafenib is a first-line drug for the treatment of advanced HCC. However, the efficacy of sorafenib in improving patient survival is limited, and most patients inevitably develop resistance to this drug. Recent studies have demonstrated that the activation of the IRE1α-XBP1s pathway might play a protective role in the response to sorafenib and contribute to malignancy in HCC. Here, we found that RCN1, an endoplasmic reticulum resident protein, is significantly upregulated in sorafenib-resistant HCC cells and promotes tumor progression. Our analysis showed that RCN1 may be an independent predictor of tumor recurrence and overall survival. Mechanistically, RCN1 promotes the dissociation of GRP78 from IRE1α in sorafenib-resistant cells by interacting with GRP78 through its EFh1/2 domain. Subsequently, the IRE1α-XBP1s pathway, a branch of the unfolded protein response, is sustainably activated. Interestingly, IRE1α-XBP1s pathway activity is required for c-MYC signaling, one of the most highly activated oncogenic pathways in HCC. These results suggest that RCN1-targeted therapy might be a feasible strategy for the treatment of HCC.

Postoperative liver metastasis of primary inflammatory pseudotumorous follicular dendritic cell sarcoma of the spleen: a case report.

Follicular dendritic cell sarcoma (FDCS) is a rare and low incidence tumor. So far, there is no standard treatment for the disease. Surgery is the main treatment for FDCS. Here, we report the case of a 51-year-old woman who was admitted with the chief complaint of "spleen-occupying lesion detected via physical examination more than 1 month ago". Spiral plain scan and enhanced computed tomography (CT) of the upper abdomen showed a vascular-derived tumor, with a high possibility of hemangioma or hemangiolymphangioma. Later, on 25 December 2019, the patient underwent laparoscopic splenectomy, and the pathological diagnosis of primary splenic FDCS was made. The patient did not receive adjuvant chemotherapy or radiotherapy. At a regular follow-up inspection 11 months later, on 18 December 2020, an abdominal scan + enhanced CT revealed multiple new abnormal intrahepatic nodules, which combined with her history, indicated the possibility of metastases. Subsequently, she was readmitted to hospital and surgical treatment was decided upon after multi-disciplinary consultation and discussion. Laparoscopic S1/S3/S4/S5 hepatectomy plus cholecystectomy was performed on 31 December 2020. The postoperative pathology findings revealed (liver tumor, S3, S4, S5) metastatic inflammatory pseudotumor follicular dendritic sarcoma, tumor diameter 0.6-1.2 cm. Due to the lack of clinical reports on postoperative organ metastasis of this disease, less experience, and controversy in drug selection of radiotherapy and chemotherapy, the patient refused to receive radiotherapy and chemotherapy. She now undertakes regular outpatient reexamination, and has been followed-up until now, during which time she has not progressed, and the efficacy is considered satisfactory.

m6A-Induced LncRNA MEG3 Suppresses the Proliferation, Migration and Invasion of Hepatocellular Carcinoma Cell Through miR-544b/BTG2 Signaling.

OBJECTIVE: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors. Long non-coding RNA plays an important role in the development of HCC. This study analyzed the impact of MEG3 on malignant behavior of HCC and explored its possible molecular mechanism. METHODS: Expression of MEG3 in HCC tissues and cell lines was measured by qRT-PCR. Transfection efficiency of MEG3 was verified by qRT-PCR. Cell proliferation, transwell migration, invasion and cell cloning assays were used to detect the effect of MEG3 on the proliferation, migration and invasion ability of HCC cells. The bioinformatics analysis was applied to predict the binding between miR-544b and MEG3 as well as BTG2. Luciferase reporter assay was performed to verify their interaction. Finally, the m6A modification of MEG3 by METTL3 was identified through RIP experiments. RESULTS: MEG3 was lowly expressed in HCC tissues and cells. Overexpression of MEG3 inhibits the proliferation, migration and invasion of HCC cells. MiR-544b can be sponged by MEG3, and overexpression of miR-544b reverses the anti-cancer effect of MEG3. We further confirmed that BTG2 gene is the target gene of miR-544b. Epigenetic studies have shown that METTL3-mediated N6-methyladenosine modification led to MEG3 downregulation. CONCLUSION: In HCC, MEG3 and BTG2 are lowly expressed while miR-544b is highly expressed. MEG3 regulates the expression of BTG2 through miR-544b, thus affecting the malignant behavior of HCC. METTL3 regulates the m6A modification of MEG3 and its expression. This study clarified the role of MEG3/miR-544b/BTG2 axis in HCC and also provided new targets for HCC research.

IL-10 derived from Hepatocarcinoma cells improves human induced regulatory T cells function via JAK1/STAT5 pathway in tumor microenvironment.

Forkhead box P3 (Foxp3) expressing CD4+CD25+ regulatory T cells (Tregs), an essential subset of immune T cells for maintaining immune homeostasis is implicated as a negative regulator in an anti-tumor immune response. Current researches suggest that reducing tumor-infiltrating Tregs contribute to enhanced anti-cancer effect. However, the mechanism of infiltration of a large number of Tregs into tumor tissues is still unclear. In this study, human induced Tregs (iTregs) were co-cultured with human hepatocytes and various types of cancer cells (HepG2, NSCLC, and AsPC-1) supernatants. Foxp3, multiple cytokines, levels of apoptosis and suppressive ability of iTregs were detected by FACS. Western blot was employed to test of proteins. Impact of HepG2 supernatants on T cell subpopulations differentiation, cytokines in supernatants were examed by FACS and ELISA respectively. Anti-IL-10R antibody and JAK1 inhibitor were used to reconfirm the role of tumor-derived IL-10 play in the regulation on iTregs. Hepatocarcinoma cells (HCC) supernatants treatment increases Foxp3 stability and reduces apoptosis level in human iTregs without influencing its differentiation trend. Furthermore, IL-10 was found to be extremely higher in HCC supernatants than other groups, IL-10R blockade neutralize the effect of HCC supernatants on iTregs in vitro obviously. HCC supernatants also reversed IL-1ß/6 triggered decline on Foxp3 which may be related to higher expression of JAK1 and elevated phosphorylation level of STAT5 induced by IL-10. Our results suggest that improved stability and abnormal accumulation of Tregs in tumor microenvironment is IL-10/JAK1/STAT5 signal pathway-dependent and provide a novel approach for improving the efficiency of anti-tumor immunotherapy.

Establishment of Myotis myotis cell lines--model for investigation of host-pathogen interaction in a natural host for emerging viruses.

Bats are found to be the natural reservoirs for many emerging viruses. In most cases, severe clinical signs caused by such virus infections are normally not seen in bats. This indicates differences in the virus-host interactions and underlines the necessity to develop natural host related models to study these phenomena. Due to the strict protection of European bat species, immortalized cell lines are the only alternative to investigate the innate anti-virus immune mechanisms. Here, we report about the establishment and functional characterization of Myotis myotis derived cell lines from different tissues: brain (MmBr), tonsil (MmTo), peritoneal cavity (MmPca), nasal epithelium (MmNep) and nervus olfactorius (MmNol) after immortalization by SV 40 large T antigen. The usefulness of these cell lines to study antiviral responses has been confirmed by analysis of their susceptibility to lyssavirus infection and the mRNA patterns of immune-relevant genes after poly I:C stimulation. Performed experiments indicated varying susceptibility to lyssavirus infection with MmBr being considerably less susceptible than the other cell lines. Further investigation demonstrated a strong activation of interferon mediated antiviral response in MmBr contributing to its resistance. The pattern recognition receptors: RIG-I and MDA5 were highly up-regulated during rabies virus infection in MmBr, suggesting their involvement in promotion of antiviral responses. The presence of CD14 and CD68 in MmBr suggested MmBr cells are microglia-like cells which play a key role in host defense against infections in the central nervous system (CNS). Thus the expression pattern of MmBr combined with the observed limitation of lyssavirus replication underpin a protective mechanism of the CNS controlling the lyssavirus infection. Overall, the established cell lines are important tools to analyze antiviral innate immunity in M. myotis against neurotropic virus infections and present a valuable tool for a broad spectrum of future investigations in cellular biology of M. myotis.

[Chromosomal alterations analyzed by comparative genomic hybridization in primary gastric carcinoma].

OBJECTIVE: To identify genetic abnormalities in primary gastric carcinoma. METHODS: Comparative genomic hybridization (CGH) was used in screening DNA copy number changes along all chromosomes in 23 cases of primary gastric cancer. RESULTS: Twenty-one out of 23 cases showed chromosomal losses and gains for at least one of the chromosomal arms in primary gastric cancer. The mean number of chromosomal alterations was 7.52. Chromosomal gains predominated over chromosomal losses in a ratio of 5.38:2.14. The most often involved chromosomal gains were observed in 8q (9/21, 42.9%), 20q (9/21, 42.9%), 17q (8/21, 38.1%), 3q (7/21, 33.3%), 7q (7/21, 33.3%), 11q (6/21, 28.6%), 13q (6/21, 28.6%), 1q (5/21, 23.8%) and 20p (5/21, 23.8%). The chromosomal arms with frequent losses were 17p (7/21, 33.3%), 18q (6/21, 28.6%), 5q (5/21, 23.8%), 8p (5/21, 23.8%), and 9p (5/21, 23.8%). CONCLUSIONS: The phenomenon of gain and loss of chromosomal regions is observed in primary gastric cancer, which may induce the amplification of oncogenes and the loss of tumor suppressor genes to regulate the development and progression of gastric cancer.

[Study on amplification of ZNF217 in primary gastric carcinoma].

OBJECTIVE: To investigate amplification of zinc finger protein 217(ZNF217) and its association with clinicopathologic parameters in primary gastric carcinoma. METHODS: Semiquantitative polymerase chain reaction (PCR) was used to determine DNA copies of ZNF217 in the specimens from forty- seven cases with primary gastric carcinoma. RESULTS: There was no difference in DNA copies between tumor specimens and paratumor normal tissues. The incidence of ZNF217 amplification was 11.36% in gastric cancer. The amplification of ZNF217 was significantly associated with tumor size(P< 0.01) and intestinal type of stomach cancer(P< 0.05). CONCLUSION: Oncogene ZNF217 may play a role in specific tumor types or subtypes of gastric cancer. There may be other oncogenes associated with gastric carcinoma in 20(q)13.