Rat Ocm (Oncomodulin) ELISA Kit

Background: The primary objective of this study was to assess the cumulative incidence of cause-specific mortality (CSM) and other causes of mortality (OCM) for patients with metastatic pancreatic duct adenocarcinoma (mPDAC). The secondary objective was to calculate the probability of CSM and build a competing risk nomogram to predict CSM for mPDAC. Material/Methods: We identified patients with mPDAC between 2010 and 2015 from the Surveillance, Epidemiology, and End Results (SEER) database. We assessed the cumulative incidence function (CIF) for cause-specific mortality and other causes of mortality. We used Gray's test to investigate the differences. The Fine and Gray proportional subdistribution hazard model was applied to model CIF. And a competing risk nomogram was built to predict the probability of CSM for mPDAC. Results: There were 10 527 eligible patients diagnosed with mPDAC from 2010 to 2015 who were included in our formal analysis. The 6-month cumulative incidence of CSM was 60.3% and 5.9% for other causes. Predictors of SCM for mPDAC included surgery, age, tumor size, chemotherapy, radiation therapy, bone metastasis, and liver metastasis. The nomogram was proven to be well calibrated, and had good model discriminative ability. Conclusions: We assessed the CIF of CSM and competing risk mortality in patients with mPDAC using the SEER database. The Fine and Gray proportional subdistribution hazard model performance was good, with a concordance index of 0.74, and the competing-risks nomogram was built, which can be a helpful predictive tool for cases with mPDAC. However, a validation sample data set and further verification are still needed to assess a profile for prognostic use in a prospective study.

Intraperitoneal metastasis is a common occurrence and is usually involved in the poor prognosis of ovarian cancer. Its specific metastatic pattern implies that certain indispensable microenvironmental factors secreted in the peritoneal cavity can direct metastatic ovarian cancer cells to permissive niches for secondary lesion formation. However, the underlying molecular mechanisms are ill defined. Herein, we report that GRO-alpha and IL-8 are predominately upregulated in culture media derived from either normal or cancerous omenta and are associated with increased ovarian cancer aggressiveness. Methods: OCM was established from culture medium of fresh human omental tissues. Primary and metastatic ovarian cancer cell lines were generated from human tumor tissues and verified by specific antibodies. The functional roles of GRO-alpha, IL-8, and their specific receptor CXCR2 were examined by neutralizing antibodies, shRNA gene knockdown, CRISPR/Cas9 gene knockout and pharmaceutical CXCR2 inhibitor SB225002. The oncogenic properties of ovarian cancer cells were examined by in vitro and in vivo mouse models. Results: Both GRO-alpha and IL-8 can activate TAK1/NF kappa B signaling via the CXCR2 receptor. Intriguingly, TAK1/NF kappa B signaling activity was higher in metastatic ovarian cancer cells; this higher activity makes them more susceptible to OCM-induced tumor aggressiveness. Treatment of ovarian cancer cells with GRO-alpha and IL-8 neutralizing antibodies or ablation of CXCR2 by shRNA gene knockdown, CRISPR/Cas9 gene knockout, or CXCR2 inhibitor SB225002 treatment significantly attenuated TAK1/NF kappa B signaling and decreased in vitro and in vivo oncogenic and metastatic potential, suggesting CXCR2 plays a key role in the GRO-alpha and IL-8-governed metastatic spreading of ovarian cancer cells in the intraperitoneal cavity. Conclusion: This study highlights the significance of GRO-alpha and IL-8 as the key chemokines in the peritoneal tumor microenvironment and suggests the utility of targeting their receptor CXCR2 as a potential target-based therapy for peritoneal metastases of ovarian cancer.