To identify the clinical pathological characteristics and prognostic factors in patients with gastrointestinal stromal tumors of the stomach.The data of 98 patients of gastric stromal tumors, leiomyomas, leiomyosarcomas, leiomyoblastomas, schwannomas and neurofibromas, collected from Mar. 1983 to Dec. 2001 in our hospital with complete clinical and pathological data, were investigated retrospectively. Gastric stromal tumors were diagnosed by reviewing the tumor slides stained with hematoxylin and eosin (H&E). Two histomorphologically representative areas of each tumor slides were identified and arrayed on a tissue microarray. Immunohistochemistry staining were performed using antibodies to c-kit (CD117), CD34, smooth muscle actin (SMA), Desmin and S-100 proteins. The relations of various clinicopathologic characteristics and outcomes were tested by univariate analysis and multivariate analysis.Ninety-one patients were clearly identified as gastric stromal tumors from the 98 patients, who were diagnosed as gastric stromal tumor, leiomyoma, leiomyosarcoma, leiomyoblastoma schwannoma and neurofibroma (92.9%). The follow-up rate was 91% and the median follow up time was 54 months. The patient survival rates at 1, 5 and 10 years were 88.8%, 79.6% and 63.7% respectively. Univariate analysis showed that tumor size, mitotic count, tumor necrosis, nuclear pleomorphism, cell type, cell density, surgical procedure, mucosal invasion, age and lable index of Ki-67 were associated with prognosis (P<0.05). Multivariate analysis showed that tumor size, mitotic count, mucosal invasion and tumor necrosis were predictors of prognosis (P<0.05).Tumor size of >10 cm, mitotic count of >10 mitoses per 50 high power fields, necrosis and mucosal invasion are often associated with an aggressive clinical course in gastric stromal tumors.
Objective To investigate the prognostic implication of common bile duct infiltration in the adenocarcinoma of the ampulla of Vater after panreaticoduodenectomy. Methods A retrospective study was conducted on clinical manifestation, pathological behavior and survival data in 102 patients with Vater＇s ampulla adenocarcinoma, who underwent pancreaticoduodenectomy from Jan 1980 to Dec 2003. The result of patients with the common bile duct infiltration were compared with that of those without. Results There were 42 cases in stage Ⅰ （41.2%）, 32 in stage Ⅱ （31.3%）, 27 in stage Ⅲ （26.5%）, and 1 in stage Ⅳ （1.0%）. As for T stage ： 9 cases in stage T1 （8.8%）,40 in T2 （39.2%）,25in T3 （24.5%）, and 28 in T4 （27.5%）. As regarding to N stage： 76 cases in stage NO （74.5%） and 26 in N1 （25.5%）. Of these 102 cases, microscopic infiltration in the common bile duct （25.0%） was identified in 26 cases. A significant difference was observed between the patients with bile duct infiltration and those without, in the proportion of pancreatic medullae infiltration： 84.6% （ infiltration group） versus 34.2% （ non-infiltration group, P 〈 0. 001 ）. Twenty-five cases （24.5%） had recurrence and/or metastases postoperatively, with a median survival of 20 months （ range, 2 to 93 months）. The overall median survival of the whole group was 46.0 months （2 - 192 months） , with a significant difference between the common bile duct infiltration group （36 months） and the non-infiltration group （49 months, P = 0. 0061 ）. The median non-recurrence survival of the whole group was 43 months （2 -192 months）, and a significant difference was observed between the common bile duct infiltration group （35 months） and non-infiltration group （ 47 months, P = 0. 0002）. Conclusion If the adenocarcinoma of the Vater＇s ampulla infiltrated the common bile duct, the invasion to the pancreatic medulla is likely developed, and usually with a poor non-recurrence and overall survival. Therefore, postoperative chemotherapy/radiotherapy is suggested.
Key words:
Ampulla of Vater; Adenocarcinoma; Common bile duct infiltration; Panceaticoduodenectomy; Prognosis
To assess the clinical value of sigmoid coloplasty of super-lower anastomosis.Thirty-five patients underwent sigmoid coloplasty (treatment group), while 33 patients received straight sigmoidorectostomy (control group). Complication rate and anal function were observed and compared between the two groups.The complication rate was 17.1% and 21.2% in the study group and control group respectively (P> 0.05). Average stool frequency were 2 times (1-5.5 times) a day in the study group and 3.5 times (1-9 times) a day in the control group 12 months after operation (P< 0.01). The fecal continence and self-satisfaction were improved significantly in the study group than that of the control group(P< 0.01, respectively). The postoperative anal function score was 2.57 in the study group and 7.21 in the control group, there was significant difference between the two groups (P< 0.01).Compared with straight sigmoidorectostomy, sigmoid coloplasty applied in super-lower anastomosis can significantly improve the recovery of anal function without increasing complication rates.
Large pedunculated colorectal polyps are not frequent among colonic polyps. We present a clinical case of a large pedunculated colorectal polyp with signet ring cell cancer infiltrating the submucosa and lymph node invasion in a patient who ultimately underwent additional surgery. Clinicians should attach importance to pedunculated colorectal polyps and choose the most appropriate therapy.A 52-year-old female farmer underwent routine screening colonoscopy and denied constipation, diarrhea, hematochezia, or other gastrointestinal symptoms. Her past medical history and general biochemical examination results were unremarkable. During the colonoscopy, a 25-mm pedunculated polyp in the sigmoid colon was identified. The superficial epithelium was macroscopically congestive, rough, and granular, showing characteristic features of adenoma. We first ligated the root of the pedunculated polyp using nylon loops as well as a titanium clip. Histopathological examination revealed high-grade intraepithelial neoplasia of the tumor surface and a negative margin with signet ring cell adenocarcinoma infiltrating the submucosal layer. The deepest infiltration was approximately 0.9 cm from the tumor surface and 0.55 cm from the stratum basale. We performed radical resection of the left colon with lymph node dissection after two weeks. The lesion was completely resected, and pathological assessment revealed signet ring cell adenocarcinoma infiltrating the submucosal layer as well as lymph node invasion (stage PT1N1M0 and grade IIIA in pathological grading, NRAS-, BRAF V600E-, KRAS-).This case highlights the importance of paying attention to the malignancy of large pedunculated polyps. Polyps or adenomas removed via endoscopy must be evaluated histologically. Even if adenomas may be fragile, endoscopy doctors should still remove polyps as completely as possible and choose perpendicular sections through the stalk and base to fix by formaldehyde solution.
To investigate the clinical pathological characteristics and treatment of primary splenic tumor.The clinical data of 43 patients with primary splenic rumors, 23 males and 20 females, aged 44.7 (19 - 66), treated in the Cancer Hospital, Chinese Academy of Medical Science from Feb 1972 through Mar 2006 were analyzed.Of the 43 cases, 21 cases (48.8%) were found in physical examination. 42 cases underwent splenectomy and 1 case underwent rumor biopsy. Sixteen cases were with benign splenic tumors, including 15 cases of hemangioma and 1 case of lymphangioma. Of the 24 malignant cases, 16 suffered from splenic lymphoma and 8 from angiosarcoma. Most lymphoma cases survived and the mean three year surviving rate was 88.7%. The mean surviving time of angiosarcoma was only 10.4 months.Primary splenic tumors lack specificity; B-ultrasonography and CT are primary examination methods. Surgery is an effective method in treatment of primary splenic tumors.
Molecular biological studies indicated that abnormal expression of cyclooxygenase-2(COX-2), p53, proliferating cell nuclear antigen(PCNA), and nm23 correlate with the development of gastric cancer, but the relationship between abnormal expression of above gene proteins and the biological behavior of gastric cancer was not yet clear. This study was designed to investigate the relationship between expressions of COX-2, p53, PCNA, and nm23 and the clinicopathological behavior in gastric cancer.The expressions of COX-2, p53, PCNA, and nm23 were detected by using immunohistochemical(SP) method.(1) The overexpression rate of COX-2 in gastric cancer was 70.4% (50/71), and the overexpression of COX-2 was correlated to tumor size, gross morphology, histological type, lymph node metastases, and clinicopathological stage of gastric cancer (P < 0.05, or P < 0.01). (2) The overexpression rates of p53 and PCNA in 71 surgically removed specimens from the patients with gastric cancer were 74.6% and 78.9%, respectively. And the expressions of p53 (86.7%) and PCNA (88.8%) in gastric cancer patients with lymph node metastasis were significantly higher than those in patients without lymph node metastasis (53.8% and 61.5%) (both, P < 0.05), respectively. Moreover, expressions of p53(52.2%) and PCNA(60.9%) in stage I + II patients were lower than those(85.4% and 87.5%) in stage III + IV (both, P < 0.05). (3) The low-expression of nm23 in gastric cancer was 71.8%, and its low-expression rate of nm23 in patients without lymph node metastasis(88.5%) and in stage I + II (91.3%) were much higher than those in the patients with lymph node metastasis (62.2%) and in stage III + IV (62.5%) (respectively, P < 0.05). (4) The differences of histological types, depth of invasion, lymph node metastasis and clinical stage were significantly different(P < 0.05 or P < 0.001), between the patients with two or more genes expression of COX-2, p53, PCNA, and nm23 and those with less one gene expression.Our results suggest that abnormal expressions of COX-2, p53, PCNA, and nm23 associate with malignant potential, lymph node metastasis and clinical stage, and they might therefore play a role in development of gastric cancer.
Background: Hepatocellular carcinoma (HCC) remains notorious for its high malignancy, poor prognosis and high mortality. The exploration of novel therapeutic agents for HCC has remained challenging due to its complex aetiology. Therefore, it is necessary to elucidate the pathogenesis and mechanism of HCC for clinical intervention. Methods: We collected data from several public data portals and systematically analysed the association between transcription factors (TFs), eRNA-associated enhancers and downstream targets. We next filtered the prognostic genes and established a novel prognosis-related nomogram model. Moreover, we explored the potential mechanisms of the identified prognostic genes. The expression level was validated by several ways. Results: We first constructed a significant TF-enhancer-target regulatory network and identified DAPK1 as a coregulatory differentially expressed prognosis-related gene. We combined common clinicopathological factors and built a prognostic nomogram model for HCC. We found that our regulatory network was correlated with the processes of synthesizing various substances. Moreover, we explored the role of DAPK1 in HCC and found that it was associated with immune cell infiltration and DNA methylation. Several immunostimulators and targeting drugs could be promising immune therapy targets. The tumor immune microenvironment was analyzed. Finally, the lower DAPK1 expression in HCC was validated via the GEO database, UALCAN cohort, and qRT-PCR. Conclusion: In conclusion, we established a significant TF-enhancer-target regulatory network and identified downregulated DAPK1 as an important prognostic and diagnostic gene in HCC. Its potential biological functions and mechanisms were annotated using bioinformatics tools.
Gastric cancer (GC) is known for its high heterogeneity, presenting challenges in current clinical treatment strategies. Accurate subtyping and in-depth analysis of the molecular heterogeneity of GC at the molecular level are still not fully understood. This study categorized GC into two subtypes based on apoptosis-related genes (ARGs) and investigated differences in tumor immune microenvironment, intratumoral microorganisms distribution, gene expression, and signaling pathways. Key prognostic genes related to apoptosis in GC were identified through random survival forest analysis, and their specific signaling mechanisms were explored. Expression levels of key genes were validated through PCR in paired GC tissues and cancer cell lines. Moreover, biological functions of these key genes were verified in vitro experiments. A consistent clustering of GC was conducted using 161 apoptosis-related genes (ARGs), resulting in the identification of two subtypes, C1 and C2. Subsequently, significant differences were found in the tumor immune microenvironment, intratumoral microorganisms, gene expression, signaling pathways, and protein interaction networks between the two subtypes. GPX3, PLAT, and CAV1 were identified as key prognostic genes related to apoptosis in GC, with a focus on their impact on disease progression-related pathways. Furthermore, PCR assays validated that these three key genes exhibited significantly low expression levels in both GC cell lines and tissues. Finally, knocking down key genes expression significantly promoted cell proliferation, colony formation and invasion of GC. Our study conducted a comprehensive analysis of the molecular characteristics of ARGs in GC, revealed their association with the tumor immune microenvironment and intratumoral microorganisms. These findings provide new ideas for the molecular classification of GC.
Background: Worldwide, gastric cancer (GC) remains intractable due to its poor prognosis and high morbidity and mortality.Disulfidptosis is a novel kind of cell death mediated by abnormal accumulation of intracellular disulphides.The correlation between disulfidptosis and GC is still unknown.Therefore, it is necessary to elucidate the pathogenesis and mechanism of disulfidptosis and GC for clinical diagnosis and intervention.Methods: RNA-sequencing data from several public data portals and clinical samples were collected.We compared the expression levels of four key genes of disulfidptosis, including SLC7A11, SLC3A2, RPN1, and NCKAP1, in GC and selected prognostic genes to build a novel GC prognosis-related nomogram model.The biological functions and immune landscape of the identified prognostic genes were explored.Results: Overexpressed NCKAP1 and SLC7A11 were prognostic disulfidptosis-related genes in GC.We combined these genes and several clinicopathological factors to build a prognostic nomogram model for GC.Meanwhile, the ROC curves showed that NCKAP1 and SLC7A11 were promising biomarkers for GC screening.The biological and cellular functions were focused on actin activities, GTPase and immunoreaction.The tumour immune microenvironment and immune therapy targets were identified.Competing endogenous RNA network was built to explore the downstream regulatory mechanisms.Finally, the elevated NCKAP1 and SLC7A11 expression in GC was validated via qRT-PCR in a cell line and tissue line. Conclusion:In conclusion, NCKAP1 and SLC7A11 are promising prognostic and diagnostic biomarkers for GC that correlate with the activities of actin, energy metabolism of GTPase, immune infiltration and immunotherapy.
Worldwide, gastric cancer (GC) is a common lethal solid malignancy with a poor prognosis. Cuproptosis is a novel type of cell death mediated by protein lipoylation and may be related to GC prognosis.To offer new insights to predict GC prognosis and provide multiple therapeutic targets related to cuproptosis-related genes (CRGs) for future therapy.We collected data from several public data portals, systematically estimated the expression level and prognostic values of CRGs in GC samples, and investigated related mechanisms using public databases and bioinformatics.Our results revealed that FDX1, LIAS, and MTF1 were differentially expressed in GC samples and exhibited important prognostic significance in The Cancer Genome Atlas (TCGA) cohort. We constructed a nomogram model for overall survival and disease-specific survival prediction and validated it via calibration plots. Mecha-nistically, immune cell infiltration and DNA methylation prominently affected the survival time of GC patients. Moreover, protein-protein interaction network, KEGG pathway and gene ontology enrichment analyses demonstrated that FDX1, LIAS, MTF1 and related proteins play key roles in the tricarboxylic acid cycle and cuproptosis. Gene Expression Omnibus database validation showed that the expression levels of FDX1, LIAS, and MTF1 were consistent with those in the TCGA cohort. Top 10 perturbagens has been filtered by Connectivity Map.In conclusion, FDX1, LIAS, and MTF1 could serve as potential prognostic biomarkers for GC patients and provide novel targets for immunotarget therapy.
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