175 Background: Colorectal adenocarcinoma (COAD) is a common cancer in gastrointestinal tract. Endonuclease V (ENDOV), an enzyme with specificity for deaminated adenosine (inosine) in nucleic acids, was found to be involved in the development of certain cancers. Thus, this study was performed to explore the effects of ENDOV on the prognosis of COAD. Methods: RNA-sequencing FPKM data and corresponding clinical information of 41 normal tissues and 480 tumor tissues of COAD were acquired from The Cancer Genome Atlas (TCGA). Then ENDOV expression differences between the normal and cancer tissues were compared with Wilcoxon rank-sum test via ‘limma’ package. Overall survival (OS) and disease specific survival (DSS) analyses were conducted by Kaplan–Meier (K–M) method via ‘survminer’ package. Subgroup analyses of different genders were also performed. Results: The expression of ENDOV was downregulated in tumors compared with normal tissues (p < 0.001). However, higher expression of ENDOV is associated with worse OS (HR: 1.83, 95%CI: 1.23-2.73, P = 0.003) and DSS (HR: 1.75, 95%CI 1.06-2.91, P = 0.03). Subgroup analysis found that higher expression of ENDOV was associated with worse OS (HR: 2.17, 95%CI 1.18-3.98, P = 0.012) in females, but not in males (HR: 1.48, 95%CI 0.86-2.53, P = 0.158). As for DSS, higher expression of ENDOV was also correlated with worse outcome (HR: 2.36, 95%CI 1.07-5.19, P = 0.033) in females, but not in males (HR: 1.45, 95%CI 0.73-2.86, P = 0.287). Conclusions: ENDOV is overall downregulated in COAD tumor samples. However, higher expression of ENDOV in certain COAD patients is associated worse OS and DSS in females but not in males. This indicates the potential role of ENDOV in predicating the prognosis of COAD in female patients.
332 Background: Gastric cancer (GC) is a common cancer worldwide. The integrin α (ITGA) family members play essential roles in various cancers and variants of ITGA are involved in metastatic process in gastric cancer. Thus, this study was conducted to explore the roles of ITGA family members in stomach adenocarcinoma (STAD). Methods: RNA-sequencing FPKM data and corresponding clinical information of 375 STAD tumor tissues and 32 normal tissues were retrieved from The Cancer Genome Atlas (TCGA). The ‘limma’ package was used to compare the expression differences between the normal and cancer tissues using Wilcoxon rank-sum test. Analysis of overall survival (OS) was conducted by Kaplan–Meier (K–M) method via ‘survminer’ package. Univariate Cox hazard regression analysis was applied to seven clinicopathological variables from T stage, N stage, M stage, pathologic stage, histologic grade, gender, age, and expression level of selected ITGA family members, by using ‘survival’ package. Furthermore, a nomogram was also visualized by the R ‘rms’ package and ‘survival’ package to predict the 1-, 3-, and 5-year OS and individual predictors. Results: The expression of ITGA2, ITGA3, ITGA4, ITGA5, ITGA6, ITGA11, and ITGAV were upregulated in STAD tissues compared with normal tissues (P<0.05), whereas ITGA7, ITGA8, and ITGA9 were downregulated in tumor tissues (P<0.05). In addition, no statistically significant difference was found for TGA1 and ITGA10 between tumor and normal tissues ((P>0.05). Further survival analysis found that higher expression of ITGA 11 (HR=1.46, 95%CI 1.05-2.03, P<0.026) and ITGAV (HR=1.92, 95%CI 1.37-2.70, P<0.001) were associate with worse OS. Univariate Cox hazard regression analysis showed that T3, T4, N1, N3, M1, pathologic stage III and IV, age>65, and high expression level of ITGA11 and ITGAV were associated with worse OS (all P < 0.05). The nomogram based on six clinicopathological variables (T stage, N stage, M stage, pathologic stage, age, and expression levels of ITGA11 and ITGAV) and 1-, 3-, 5-year OS probabilities were developed. The concordance index (C-index) of the nomograms was 0.673(0.647-0.700), indicating that the potential predicting role and sufficient discrimination ability of the nomogram as C-index was more than 0.5. The calibration curves of 1-, 3-, and 5-year indicated the consistency of our results and the predictive values, indicating satisfactory performance for this nomogram. However, 1-, 3-, 5-year AUCs of ITGA11- and ITGAV-based nomogram were 0.687, 0.691, and 0.687, showing a relatively acceptable accuracy as they were great than 0.5. Conclusions: ITGA2, ITGA3, ITGA4, ITGA5, ITGA6, ITGA11, and ITGAV are upregulated, while ITGA7, ITGA8, and ITGA9 are down regulated in STAD tumor samples. High expression levels of ITGA11 and ITGAV are associated with worse OS. The ITGA11- and ITGAV-based monogram developed by this study might be useful in predicting the OS outcome for STAD patients.
158 Background: Colon adenocarcinoma (COAD) is one of the most common gastrointestinal cancers worldwide. Previous studies found that Ladybird homeobox 1 (LBX1) and Ladybird homeobox 2 (LBX2), were involved in the progress of several types of cancer. However, studies on their roles in cancers, such as COAD, are very limited. Thus, this study was performed to explore their roles in COAD. Methods: RNA-sequencing FPKM data and corresponding clinical information of 480 tumor tissues of COAD and 41 normal tissues were obtained from The Cancer Genome Atlas (TCGA). The ‘limma’ package was used to compare the expression differences of LBX1 and LBX2 between the normal and cancer tissues using Wilcoxon rank-sum test. Analysis of overall survival (OS), disease specific survival (DSS), and progression free interval (PFI) were conducted by Kaplan–Meier (K–M) method via ‘survminer’ package. Univariate Cox hazard regression analysis of OS was applied to five clinicopathological variables from T stage, N stage, M stage, pathologic stage, CEA level, as well as the expression level of family members of LBX that are overexpressed and associated with worsening survival outcomes, by using ‘survival’ package. Furthermore, a nomogram was also visualized by the R ‘rms’ package and ‘survival’ package to predict the 1-, 3-, and 5-year OS and individual predictors. Results: The expression of LBX2 (p = 8.1e-20) was upregulated in COAD tissues compared with normal tissues, while no statistically significant difference of expression between normal tissues and tumor was found for LBX1 (p = 0.06). Further survival analysis found that higher expression of LBX2 was associate with worse OS (HR = 2.45, 95%CI 1.62-3.71, p < 0.001), DSS (HR = 2.34, 95%CI 1.39-3.96, p = 0.001), and PFI (HR = 1.48, 95%CI 1.04-2.10, p = 0.03). Univariate Cox hazard regression analysis showed that N1, N2, N3, M1, pathologic stage III and IV, CEA level>5, and high expression level of LBX2 were associated with worse OS (all p < 0.05). The nomogram based on six clinicopathological variables (T stage, N stage, M stage, pathologic stage, CEA level, and LBX2 expression level) and 1-, 3-, 5-year OS probabilities were developed, with concordance index (C-index) of 0.795(0.755-0.834), indicating its prediction value and sufficient discrimination ability, as C-index was more than 0.7. The calibration curves of 1-, 3-, and 5-year demonstrated the consistency of our results and the predictive values, indicating satisfactory performance for this nomogram. Moreover1-, 3-, 5-year AUCs of LBX2-based nomogram were 0.805, 0.831, and 0.774, showing a moderate accuracy. Conclusions: LBX2 are upregulated in COAD tumor samples, and its higher expression is associated with worsening OS, DSS, and PFI. The LBX2-based monogram developed by this study might help predict the OS possibilities for COAD patients. LBX2 can be a potential diagnostic and prognostic marker, and therapeutic marker in COAD.
We present a case of 30-year-old female with past medical history of Type 2 DM, Thyroid nodule and asymptomatic cholelithiasis who presented to ED with abdominal pain, vomiting and sinus tachycardia of 120’s for past one day. She had generalized abdominal pain, not relieved by pain killers. Her lab test includes normal blood count, glucose 150mg/dl, anion gap of 20, metabolic acidosis. Her ultrasound abdomen showed cholelithiasis with no biliary sludge formation. Given her acidosis and severe abdominal pain she was started on Zosyn and underwent cholecystectomy. Her abdominal pain and sinus tachycardia did not resolve till day 3 of admission. Urine was positive for ketones. On chart review, it was found that she started taking sodium glucose transporter 2 inhibitor (SGLT-2 inhibitor), Canagliflozin. She was given IV fluids and insulin. She improved and her tachycardia resolved. Euglycemic acidosis is a rare phenomenon but frequently misdiagnosed. This case emphasizes on importance of side effects of oral glucose lowering agents. SGLT-2 inhibitors can cause lipolysis and ketosis while maintaining euglycemia. Prompt clinical judgement is needed to prevent misdiagnosis. Also, patients should be educated about aggravating factors like stress, dehydration or other severe illnesses.
Colorectal carcinoma metastases to the head and neck are exceedingly rare. Patients may present with vague symptoms that may lead to a delay in diagnosis. We report the case of a 51-year-old man with a known history of stage IIIB colorectal adenocarcinoma who presented with right-sided molar tooth bleeding and right-sided palate swelling that led to difficulty speaking, eating and weight-loss of 15 pounds. Imaging studies revealed a 3.1×4.8×3 cm mass that was centred around the posterior aspect of the maxilla. Pathology revealed moderately differentiated intestinal type adenocarcinoma of colonic subtype, immune histochemistry was positive for CDX2, CK20 and MUC2, thus confirming metastatic disease to the maxilla. The patient is undergoing chemoradiation therapy for palliation of his symptoms. Clinicians should be aware of this potentional site of metastatic disease and suspect the diagnosis in a timely manner to avoid delays in making a diagnosis.
159 Background: Colorectal adenocarcinoma (COAD) is a common cancer in gastrointestinal tract. CDC-like kinase (CLK) family, containing four characterized isoforms (CLK1-4), have been reported for their roles in precursor-mRNA splicing. However, studies on their roles in COAD are limited. Thus, this study was performed to explore the roles of CLK family members in COAD. Methods: RNA-sequencing FPKM data and corresponding clinical information of 41 normal tissues and 480 tumor tissues of COAD were obtained from The Cancer Genome Atlas (TCGA). Then expression differences of CLK family between the normal tissues and COAD cancer tissues were compared with Wilcoxon rank-sum test via ‘limma’ package. Overall survival (OS) of upregulated CLK family members was analyzed by Kaplan–Meier (K–M) method via ‘survminer’ package. Subgroup analyses of different genders were also conducted. The best discriminate cut-off point between the high and low expression groups was assessed by the receiver operating characteristic (ROC) curve and area under the curve (AUC) values for upregulated CLK family members via ‘pROC’ package to assess their diagnostic values. Results: The expression of CLK1 and CLK2 were upregulated in tumors compared with normal tissues (p < 0.001), while CLK3 were downregulated in tumor tissues (p = 0.02) and no statically significant difference was found regarding CLK4 (p = 0.25). Higher expression of CLK1 was not associated with a change of OS (HR: 1.24, 95%CI: 0.84-1.83, p = 0.279), while higher expression of CLK2 is associated with worse OS (HR: 2.03, 95%CI: 1.34-3.06, p = 0.001). Subgroup analysis found that higher expression of CLK2 was associated with worse OS (HR: 2.28, 95%CI 1.27-4.08, p = 0.006) in males, but not in females (HR: 1.72, 95%CI 0.95-3.10, P = 0.072). Further analysis of ROC curve shown that AUC of CLK1 and CLK2 were 0.748 (0.687-0.809) and 0.884 (0.840-0.928), respectively. Conclusions: CLK1 and CLK2 are upregulated in COAD tumor samples, and higher expression of CLK2 in male COAD patients is associated worse OS. This demonstrated the potential therapeutic value of CLK2 in male patients with COAD. ROC curve indicated the potential diagnostic value of CLK1 and CLK2.
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