Characteristics of Colorectal Cancer in Young Patients at an Urban County Hospital

2008 ◽  
Vol 74 (10) ◽  
pp. 973-976 ◽  
Author(s):  
Benjamin Karsten ◽  
Justin Kim ◽  
Justin King ◽  
Ravin R. Kumar
Keyword(s):  
Colorectal Cancer ◽  
Young Patients ◽  
Ethnically Diverse ◽  
Tumor Grade ◽  
Tumor Stage ◽  
Young Group ◽  
Advanced Tumor Stage ◽  
Young Population ◽  
Aggressive Approach ◽  
Advanced Tumor

Colorectal cancer (CRC) is a disease primarily affecting an older population. The incidence of CRC in young patients has been rising. The purpose of this study was to evaluate the characteristics of CRC in an ethnically diverse, young population. Two groups of patients with CRC (40 years old or younger and 60 years old or older) treated from 1998 to 2005 were retrospectively evaluated. Forty-one young patients with CRC were identified. Hispanics constituted 51 per cent of the young population. Forty-four per cent of the lesions were right-sided in the young group compared with 21 per cent in the older group (P = 0.004). Advanced tumor stage (T3 and T4) was noted in 87.8 per cent of the young and 63 per cent of the older patients (P = 0.002; OR, 4.08). Poorly differentiated tumor grade was more common in young patients (P = 0.003) as well as mucinous/signet ring characteristics (P = 0.005). Young patients had an increased likelihood of a family history (P = 0.0001). Operative intervention and survival were similar for the two groups. Our study confirms, in an ethnically diverse young population, that CRC tends to be advanced stage, aggressive, and frequently nonoperable at the time of diagnosis. It is important for physicians to recognize the poor outcome of CRC in a younger population and consider an aggressive approach to diagnosis and early treatment.

scholarly journals HSD17B6 downregulation predicts poor prognosis and drives tumor progression via activating Akt signaling pathway in lung adenocarcinoma

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Tian Tian ◽  
Fu Hong ◽  
Zhiwen Wang ◽  
Jiaru Hu ◽  
Ni Chen ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Lung Adenocarcinoma ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Tumor Grade ◽  
Tumor Stage ◽  
Advanced Tumor Stage ◽  
Large Tumor ◽  
Mesenchymal Transition ◽  
Advanced Tumor

AbstractLung adenocarcinoma is one of the most frequent tumor subtypes, involving changes in a variety of oncogenes and tumor suppressor genes. Hydroxysteroid 17-Beta Dehydrogenase 6 (HSD17B6) could synthetize dihydrotestosterone, abnormal levels of which are associated with progression of multiple tumors. Previously, we showed that HSD17B6 inhibits malignant progression of hepatocellular carcinoma. However, the mechanisms underlying inhibiting tumor development by HSD17B6 are not clear. Moreover, its role in lung adenocarcinoma (LUAD) is yet unknown. Here, we investigated its expression profile and biological functions in LUAD. Analysis of data from the LUAD datasets of TCGA, CPTAC, Oncomine, and GEO revealed that HSD17B6 mRNA and protein expression was frequently lower in LUAD than in non-neoplastic lung tissues, and its low expression correlated significantly with advanced tumor stage, large tumor size, poor tumor differentiation, high tumor grade, smoking, and poor prognosis in LUAD. In addition, its expression was negatively regulated by miR-31-5p in LUAD. HSD17B6 suppressed LUAD cell proliferation, migration, invasion, epithelial–mesenchymal transition (EMT), and radioresistance. Furthermore, HSD17B6 overexpression in LUAD cell lines enhanced PTEN expression and inhibited AKT phosphorylation, inactivating downstream oncogenes like GSK3β, β-catenin, and Cyclin-D independent of dihydrotestosterone, revealing an underlying antitumor mechanism of HSD17B6 in LUAD. Our findings indicate that HSD17B6 may function as a tumor suppressor in LUAD and could be a promising prognostic indicator for LUAD patients, especially for those receiving radiotherapy.

scholarly journals FOXM1 and β-catenin are potential prognostic markers in muscle-invasive bladder carcinoma

2020 ◽  
Author(s):  
Huiming Gui ◽  
Yutong Song ◽  
Yongsheng Yin ◽  
Ronald Rodriguez ◽  
Zhiping Wang
Keyword(s):  
Lymph Node ◽  
Lymph Node Metastases ◽  
Univariate Analysis ◽  
Tumor Grade ◽  
Tumor Stage ◽  
Study Cohort ◽  
Advanced Tumor Stage ◽  
Advanced Tumor ◽  
Node Metastases ◽  
Muscle Invasive

Abstract BackgroundForkhead box protein M1 (FOXM1) and β-catenin were confirmed to associate with numerous cancers, which attracted more attention in recent years. Our research investigated the expression of FOXM1 and β-catenin and their effects on prognosis of patients with muscle-invasive bladder cancer (MIBC). MethodsIn this study, FOXM1 and β-catenin expression was detected by immunohistochemistry in a study cohort including 121 MIBC patients. Results The results showed significant correlations of FOXM1 and β-catenin expression with tumor stage, tumor grade, and lymph node metastases in MIBC patients. Univariate analysis showed that patients with high FOXM1 (HR = 2.986; P = 0.011) and low β-catenin (HR = 2.623; P = 0.001) expression levels, advanced tumor stage (HR = 2.325; P = 0.002), advanced tumor grade (HR = 2.790; P < 0.001), tumor size (HR = 2.080; P = 0.020), lymph node metastases (HR = 3.392; P < 0.001), or recurrence status (HR = 2.016; P = 0.011) had a significantly higher risk of worse overall survival (OS). In the multivariate analysis, tumor stage (HR = 2.095; P = 0.009), tumor grade (HR = 1.962; P = 0.019), FOXM1 expression (HR = 2.196; P = 0.017) and lymph node metastases (HR = 2.136; P = 0.015) predicted worse OS. ConclusionTherefore, FOXM1 and β-catenin expression was relevant to MIBC incidence, tumor stage, tumor grade, metastasis, and survival and might be a reliable index to judge the prognosis of patients with MIBC.

scholarly journals Hsa_circ_0062682 Promotes Serine Metabolism and Tumor Growth in Colorectal Cancer by Regulating the miR-940/PHGDH Axis

2021 ◽  
Vol 9 ◽  
Author(s):  
Shengbai Sun ◽  
Chaoqun Li ◽  
Kaisa Cui ◽  
Bingxin Liu ◽  
Mingyue Zhou ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Tumor Stage ◽  
Inhibitory Effect ◽  
Circular Rnas ◽  
Advanced Tumor Stage ◽  
Advanced Tumor ◽  
Serine Metabolism

Colorectal cancer (CRC) is one of the most common malignancies globally. Increasing evidence indicates that circular RNAs (circRNAs) play a pivotal role in various cancers. The present study focused on exploring the role of a functionally unknown circRNA, hsa_circ_0062682 (circ_0062682), in CRC. By online analyses and experimental validations, we showed that circ_0062682 expression was aberrantly increased in CRC tissues compared with paired normal tissues. Increased expression of circ_0062682 in CRC notably correlated with a poor prognosis and advanced tumor stage. Functional experiments showed that circ_0062682 knockdown reduced CRC growth both in vitro and in vivo. Mechanistically, we revealed that circ_0062682 could sponge miR-940 and identified D-3-phosphoglycerate dehydrogenase (PHGDH), a key oxidoreductase involved in serine biosynthesis, as a novel target of miR-940. Silencing miR-940 expression could mimic the inhibitory effect of circ_0062682 knockdown on CRC proliferation. The expression of PHGDH was downregulated in circ_0062682-depleted or miR-940 overexpressing CRC cells at both the mRNA and protein levels. Circ_0062682 knockdown suppressed CRC growth by decreasing PHGDH expression and serine production via miR-940. Taken together, these data demonstrate, for the first time, that circ_0062682 promotes serine metabolism and tumor growth in CRC by regulating the miR-940/PHGDH axis, suggesting circ_0062682 as a potential novel therapeutic target for CRC.

scholarly journals Clinicopathological features and survival of colorectal cancer patients younger than 50 years: a retrospective comparative study

2019 ◽  
Vol 31 (1) ◽  
Author(s):  
Robabeh Ghodssi-Ghassemabadi ◽  
Ebrahim Hajizadeh ◽  
Shaghayegh Kamian ◽  
Mahmood Mahmoudi
Keyword(s):  
Colorectal Cancer ◽  
Cox Regression ◽  
Disease Free Survival ◽  
Tumor Stage ◽  
Clinicopathological Features ◽  
Advanced Tumor Stage ◽  
Cancer Specific Survival ◽  
Younger Patients ◽  
Advanced Tumor ◽  
Poorly Differentiated

Abstract Background Colorectal cancer (CRC) is a disease of old age, but its incidence has been rising among younger population compared to older ones. Nevertheless, there is a controversy over survival of younger patients compared to the older ones. Therefore, in the current study, we investigated the clinicopathological features and survival of the younger (< 50 years) versus older (≥ 50 years) CRC patients. Results The younger and older groups consisted of 39.4% and 60.6% of patients, respectively. Both age groups were comparable regarding the symptom presentation and duration, and pre-operative carcinoembryonic antigen (CEA). The younger patients were diagnosed with a higher proportion of poorly differentiated (14.7% vs. 8.3%; p < 0.001) and more advanced tumors (53.2% vs. 45.9%; p = 0.266). The rectum tumor site was significantly more common among the younger patients (p = 0.021). The overall survival (OS) (p = 0.278), the cancer-specific survival (CSS) (p = 0.233), and the disease-free survival (DFS) (p = 0.497) did not differ significantly between the two groups. Based on Cox regression model, elevated pre-operative CEA level (HR = 1.41; 95%CI of 1.01–1.97), advanced tumor stage (6.06; 95%CI of 3.03–12.15), and poorly differentiated tumor (HR = 1.69; 95%CI of 1.05–2.71) were associated with decreased survival. Conclusions The younger patients did not have poor prognosis compared to the older ones despite having an advanced tumor stage and a poor tumor differentiation.

scholarly journals Genetic Variants of lncRNA GAS5 Are Associated with the Clinicopathologic Development of Oral Cancer

2021 ◽  
Vol 11 (5) ◽  
pp. 348
Author(s):  
Ming-Hong Hsieh ◽  
Hsueh-Ju Lu ◽  
Chiao-Wen Lin ◽  
Chia-Yi Lee ◽  
Shang-Jung Yang ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Oral Cancer ◽  
Cancer Patients ◽  
Alcohol Drinking ◽  
Tumor Size ◽  
Genetic Variants ◽  
Tumor Stage ◽  
Advanced Tumor Stage ◽  
Advanced Tumor ◽  
Oral Cancer Patients

The long noncoding RNA, Growth arrest-specific 5 (GAS5) plays a crucial role in the development of oral cancer. However, potential genetic variants in GAS5 that affect the susceptibility and progression of oral cancer have rarely been explored. In this study, two loci of GAS5 single nucleotide polymorphisms (SNPs) (rs145204276 and rs55829688) were genotyped by using the TaqMan allelic discrimination in 1125 oral cancer patients and 1195 non-oral-cancer individuals. After statistical analyses, the distribution of both the GAS5 SNP rs145204276 and GAS5 SNP rs55829688 frequencies were similar between the study and control groups. However, the patients with GAS5 SNP rs145204276 variants (Ins/Del or Del/Del) showed a higher tendency of moderate to poor cell differentiation of oral cancer (OR: 1.454, 95% CI: 1.041–2.031, p = 0.028). Moreover, the GAS5 SNP rs145204276 variants (Ins/Del or Del/Del) in the non-alcohol-drinking population were associated with significantly advanced tumor stage (OR: 1.500, 95% CI: 1.081–2.081, p = 0.015) and larger tumor size (OR: 1.494, 95% CI: 1.076–2.074, p = 0.016). Furthermore, individuals with the GAS5 SNP rs145204276 variant were associated with a higher expression of GAS5 in the GTEx database (p = 0.002), and the higher GAS5 level was associated with poor cell differentiation, advanced tumor stage and larger tumor size in head and neck squamous cell carcinoma from the TCGA database (all p < 0.05). In conclusion, the GAS5 SNP rs145204276 variant is related to poor-differentiation cell status in oral cancer. Besides, the presence of the GAS5 SNP rs145204276 variant is associated with a worse tumor stage and tumor size in oral cancer patients without alcohol drinking.

scholarly journals EPDR1 is related to stages and metastasize in bladder cancer and can be used as a prognostic biomarker

BMC Urology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yue Yang ◽  
Hanchao Zhang ◽  
Zhengdao Liu ◽  
Faliang Zhao ◽  
Guobiao Liang
Keyword(s):  
Bladder Cancer ◽  
T Cells ◽  
Prognostic Biomarker ◽  
Transmembrane Protein ◽  
Tumor Stage ◽  
Receptor Interaction ◽  
Advanced Tumor Stage ◽  
Normal Bladder ◽  
Advanced Tumor ◽  
Significant Difference

AbstractBackgroundBladder cancer (BLCA) is a malignant urothelial carcinoma and has a high mortality rate. EPDR1 (ependymin related 1) is a type II transmembrane protein and related to calcium-dependent cell adhesion.MethodsWe explored the potential oncogenic roles of EPDR1 in BLCA basing on the multiple public datasets.ResultsWe found that EPDR1 expression had a significant difference in BLCA and adjacent normal bladder tissues, and the level of EPDR1was up-regulated with advanced tumor stage and metastasis in BLCA. Meanwhile, the high expression group of EPDR1 had a shorter OS compared to the low or medium expression-group. Furthermore, EPDR1 expression was associated with tumor-infiltrating immune cells (TIICs), including NK cells, CD8 + T cells, CD4 + T cells, Macrophages cells, and so on. Moreover, EPDR1 also involved in several signaling pathways as well as PI3K/AKT pathway, Cytokine receptor interaction, and apoptosis.ConclusionEPDR1 can be used as a novel prognostic biomarker as well as an effective target for diagnosis and treatment in BLCA.

scholarly journals E-Cadherin expression in human tumors: a tissue microarray study on 10,851 tumors

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Eike Burandt ◽  
Felix Lübbersmeyer ◽  
Natalia Gorbokon ◽  
Franziska Büscheck ◽  
Andreas M. Luebke ◽  
...  
Keyword(s):  
Tissue Microarray ◽  
Poor Prognosis ◽  
Triple Negative ◽  
Lobular Carcinoma ◽  
Tumor Stage ◽  
Advanced Tumor Stage ◽  
Carcinoma Of The Breast ◽  
Advanced Tumor ◽  
Tumor Entities ◽  
E Cadherin

Abstract Background The E-Cadherin gene (CDH1, Cadherin 1), located at 16q22.1 encodes for a calcium-dependent membranous glycoprotein with an important role in cellular adhesion and polarity maintenance. Methods To systematically determine E-Cadherin protein expression in normal and cancerous tissues, 14,637 tumor samples from 112 different tumor types and subtypes as well as 608 samples of 76 different normal tissue types were analyzed by immunohistochemistry in a tissue microarray format. Results E-Cadherin was strongly expressed in normal epithelial cells of most organs. From 77 tumor entities derived from cell types normally positive for E-Cadherin, 35 (45.5%) retained at least a weak E-Cadherin immunostaining in ≥99% of cases and 61 (79.2%) in ≥90% of cases. Tumors with the highest rates of E-Cadherin loss included Merkel cell carcinoma, anaplastic thyroid carcinoma, lobular carcinoma of the breast, and sarcomatoid and small cell neuroendocrine carcinomas of the urinary bladder. Reduced E-Cadherin expression was linked to higher grade (p = 0.0009), triple negative receptor status (p = 0.0336), and poor prognosis (p = 0.0466) in invasive breast carcinoma of no special type, triple negative receptor status in lobular carcinoma of the breast (p = 0.0454), advanced pT stage (p = 0.0047) and lymph node metastasis in colorectal cancer (p < 0.0001), and was more common in recurrent than in primary prostate cancer (p < 0.0001). Of 29 tumor entities derived from E-Cadherin negative normal tissues, a weak to strong E-Cadherin staining could be detected in at least 10% of cases in 15 different tumor entities (51.7%). Tumors with the highest frequency of E-Cadherin upregulation included various subtypes of testicular germ cell tumors and renal cell carcinomas (RCC). E-Cadherin upregulation was more commonly seen in malignant than in benign soft tissue tumors (p = 0.0104) and was associated with advanced tumor stage (p = 0.0276) and higher grade (p = 0.0035) in clear cell RCC, and linked to advanced tumor stage (p = 0.0424) and poor prognosis in papillary RCC (p ≤ 0.05). Conclusion E-Cadherin is consistently expressed in various epithelial cancers. Down-regulation or loss of E-Cadherin expression in cancers arising from E-Cadherin positive tissues as well as E-Cadherin neo-expression in cancers arising from E-Cadherin negative tissues is linked to cancer progression and may reflect tumor dedifferentiation.

scholarly journals Type III TGF-β Receptor Down-Regulation Promoted Tumor Progression via Complement Component C5a Induction in Hepatocellular Carcinoma

Cancers ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1503
Author(s):  
Oscar Wai Ho Yeung ◽  
Xiang Qi ◽  
Li Pang ◽  
Hui Liu ◽  
Kevin Tak Pan Ng ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Progression ◽  
Tumor Stage ◽  
Complement Component ◽  
Soluble Form ◽  
Advanced Tumor Stage ◽  
Down Regulation ◽  
Type Iii ◽  
Advanced Tumor ◽  
Β Receptor

Background and Aims—Transforming growth factor-beta (TGF-β) signaling orchestrates tumorigenesis and one of the family members, TGF-β receptor type III (TGFβR3), are distinctively under-expressed in numerous malignancies. Currently, the clinical impact of TGFβR3 down-regulation and the underlying mechanism remains unclear in hepatocellular carcinoma (HCC). Here, we aimed to identify the tumor-promoting roles of decreased TGFβR3 expression in HCC progression. Materials and Methods—For clinical analysis, plasma and liver specimens were collected from 100 HCC patients who underwent curative resection for the quantification of TGFβR3 by q-PCR and ELISA. To study the tumor-promoting mechanism of TGFβR3 downregulation, HCC mouse models and TGFβR3 knockout cell lines were applied. Results—Significant downregulation of TGFβR3 and its soluble form (sTGFβR3) were found in HCC tissues and plasma compared to healthy individuals (p < 0.01). Patients with <9.4 ng/mL sTGFβR3 exhibited advanced tumor stage, higher recurrence rate and shorter disease-free survival (p < 0.05). The tumor-suppressive function of sTGFβR3 was further revealed in an orthotopic mouse HCC model, resulting in 2-fold tumor volume reduction. In TGFβR3 knockout hepatocyte and HCC cells, increased complement component C5a was observed and strongly correlated with shorter survival and advanced tumor stage (p < 0.01). Interestingly, C5a activated the tumor-promoting Th-17 response in tumor associated macrophages. Conclusion—TGFβR3 suppressed tumor progression, and decreased expression resulted in poor prognosis in HCC patients through upregulation of tumor-promoting complement C5a.

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