Time trends in the incidence of oesophageal cancer in Asia: Variations across populations and histological types

Publication date: October 2016
Source:Cancer Epidemiology, Volume 44
Author(s): Shao-Hua Xie, Jesper Lagergren
ObjectiveWe aimed to assess temporal trends in incidence rates of oesophageal cancer in Asian countries.Materials and methodsUsing data from the Cancer Incidence in Five Continents series, we examined the temporal trends in incidence rates of oesophageal cancer by population and histological type in seven Asian countries in 1988–2007. Age-period-cohort analyses estimated the overall annual percentage changes (net drifts) and their 95% confidence intervals (CIs) in incidence rates.ResultsThe age-standardised incidence rate of oesophageal cancer declined in most Asian populations, but remained relatively unchanged in Japan and Israel. The rate of oesophageal squamous cell carcinoma decreased in Hong Kong, Singapore and Israel, but was stable in Japan. The net drifts were statistically significant in men in Hong Kong (−3.4%, 95% CI: −6.1%, −0.7%) and in women in Singapore (−10.1%, 95% CI: −14.4%, −5.5%). The age-standardised incidence rates of oesophageal adenocarcinoma were below 2 and 0.5 per 100 000 in men and women, respectively, across all periods in the all registers containing valid data on histological type. The age-standardised incidence rate of oesophageal adenocarcinoma slightly increased in Japan, Singapore, and Israel, although the net drift was statistically significant only in Israeli men (4.9%, 95% CI: 0.8%, 9.1%).ConclusionThe overall incidence rates of oesophageal cancer declined in most Asian countries, which is due to a decrease in oesophageal squamous cell carcinoma incidence. However, attention needs to be paid to a probable beginning of an increasing incidence of oesophageal adenocarcinoma in Asia.



from Cancer via ola Kala on Inoreader http://ift.tt/2aSaYnv
via IFTTT

Inflammatory biomarkers, aspirin, and risk of colorectal cancer: Findings from the physicians’ health study

Publication date: October 2016
Source:Cancer Epidemiology, Volume 44
Author(s): Chul Kim, Xuehong Zhang, Andrew T. Chan, Howard D. Sesso, Nader Rifai, Meir J. Stampfer, Jing Ma
BackgroundChronic inflammation has been implicated in colorectal carcinogenesis. However, the associations between plasma inflammatory markers and risk of colorectal cancer have been inconsistent.MethodsIn a nested case-control study in the Physicians' Health Study, we prospectively investigated the associations of plasma C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor receptor 2 (TNFR-2) with risk of colorectal cancer, and whether aspirin modified these associations among 268 colorectal cancer patients and 446 age- and smoking-matched controls.ResultsIn multivariate-adjusted models, plasma levels of CRP, IL-6 and TNFR-2 were not significantly associated with risk of colorectal cancer, although a positive trend was observed for TNFR-2 (RRhighestvs.lowestquartile=1.55; 95% CI=0.95-2.54; Ptrend=0.05). We observed a statistically significant association between elevated TNFR-2 levels and colorectal cancer risk in the placebo arm (RRhighestvs.lowesttertile=1.77; 95% CI=1.02-3.06; Ptrend=0.02), but not in the aspirin arm (Ptrend=0.72). However, the interaction between TNFR-2 and aspirin was not statistically significant (Pinteraction=0.34).ConclusionPlasma inflammatory markers were not significantly associated with colorectal cancer risk among men, though there was a statistically non-significant positive trend between TNFR-2 and colorectal cancer risk. More studies are required to understand the relationship between the role of TNFα pathway, aspirin, and colorectal cancer risk.



from Cancer via ola Kala on Inoreader http://ift.tt/2aEu0kl
via IFTTT

Inhibition of HIF-1α enhances anti-tumor effects of dendritic cell-based vaccination in a mouse model of breast cancer

Abstract

Considerable evidence shows that the tumor microenvironment is an active participant in preventing immunosurveillance and limiting the efficacy of anticancer therapies. Hypoxia is a prominent characteristic of the solid tumor microenvironment. The transcription factor hypoxia-inducible factor-1α (HIF-1α) is an important mediator of hypoxic response of tumor cells that modulates the expression of specific genes involved in tumor immunosuppression. Using a 4T1 breast cancer model, we show that in vivo administration of PX-478, an inhibitor of oxygen-sensitive HIF-1α, led to reduced expression of Foxp3 and VEGF transcript and/or protein, molecules that are directly controlled by HIF-1. When combined with dendritic cell (DC)-based vaccination, HIF-1α inhibition resulted in an augmented cytotoxic T lymphocyte effector function, improved proliferation status of T cells, increased production of inflammatory cytokine IFN-γ, as well as reduced regulatory function of T cells in association with slower tumor growth. Taken together, our findings indicate that the use of HIF-1α inhibition provides an immune adjuvant activity, thereby improves the efficacy of tumor antigen-based DC vaccine.

from Cancer via ola Kala on Inoreader http://ift.tt/2aR4mWt
via IFTTT

Inhibition of HIF-1α enhances anti-tumor effects of dendritic cell-based vaccination in a mouse model of breast cancer

Abstract

Considerable evidence shows that the tumor microenvironment is an active participant in preventing immunosurveillance and limiting the efficacy of anticancer therapies. Hypoxia is a prominent characteristic of the solid tumor microenvironment. The transcription factor hypoxia-inducible factor-1α (HIF-1α) is an important mediator of hypoxic response of tumor cells that modulates the expression of specific genes involved in tumor immunosuppression. Using a 4T1 breast cancer model, we show that in vivo administration of PX-478, an inhibitor of oxygen-sensitive HIF-1α, led to reduced expression of Foxp3 and VEGF transcript and/or protein, molecules that are directly controlled by HIF-1. When combined with dendritic cell (DC)-based vaccination, HIF-1α inhibition resulted in an augmented cytotoxic T lymphocyte effector function, improved proliferation status of T cells, increased production of inflammatory cytokine IFN-γ, as well as reduced regulatory function of T cells in association with slower tumor growth. Taken together, our findings indicate that the use of HIF-1α inhibition provides an immune adjuvant activity, thereby improves the efficacy of tumor antigen-based DC vaccine.

from Cancer via ola Kala on Inoreader http://ift.tt/2aR4mWt
via IFTTT

Inhibition of HIF-1α enhances anti-tumor effects of dendritic cell-based vaccination in a mouse model of breast cancer

Abstract

Considerable evidence shows that the tumor microenvironment is an active participant in preventing immunosurveillance and limiting the efficacy of anticancer therapies. Hypoxia is a prominent characteristic of the solid tumor microenvironment. The transcription factor hypoxia-inducible factor-1α (HIF-1α) is an important mediator of hypoxic response of tumor cells that modulates the expression of specific genes involved in tumor immunosuppression. Using a 4T1 breast cancer model, we show that in vivo administration of PX-478, an inhibitor of oxygen-sensitive HIF-1α, led to reduced expression of Foxp3 and VEGF transcript and/or protein, molecules that are directly controlled by HIF-1. When combined with dendritic cell (DC)-based vaccination, HIF-1α inhibition resulted in an augmented cytotoxic T lymphocyte effector function, improved proliferation status of T cells, increased production of inflammatory cytokine IFN-γ, as well as reduced regulatory function of T cells in association with slower tumor growth. Taken together, our findings indicate that the use of HIF-1α inhibition provides an immune adjuvant activity, thereby improves the efficacy of tumor antigen-based DC vaccine.

from Cancer via ola Kala on Inoreader http://ift.tt/2aR4mWt
via IFTTT

Rituximab to treat gemcitabine-induced hemolytic–uremic syndrome (HUS) in pancreatic adenocarcinoma: a case series and literature review

Abstract

Purpose

Hemolytic–uremic syndrome (HUS) is a rare side effect of gemcitabine, which is reported as having a high morbidity and mortality despite interventions with standard HUS therapies including plasmapheresis. The purpose of this report was to describe the successful treatment of gemcitabine-induced HUS (G-HUS) with rituximab. It also aims to summarize the literature regarding the morbidity and mortality of G-HUS in pancreatic adenocarcinoma depending on the treatment given, ultimately providing some guidance for beneficial therapies.

Methods

This is a retrospective report of three patients with pancreatic adenocarcinoma who developed G-HUS and were treated with a combination of therapies including rituximab.

Results

All three patients received a combination of therapies to treat their HUS. One patient appeared to have some benefit with plasmapheresis. Resolution occurred following one course of rituximab for all three patients. This resolution has been long lasting with a minimum of eighteen month's follow-up. Similarly, in our literature review a variety of therapies were utilized, but immune therapies appear to reverse HUS if other therapies are failing.

Conclusion

Rituximab can be an effective therapy for reversal of hemolysis and stabilization of renal function in G-HUS when other therapies fail.

from Cancer via ola Kala on Inoreader http://ift.tt/2b4o2pA
via IFTTT

Rituximab to treat gemcitabine-induced hemolytic–uremic syndrome (HUS) in pancreatic adenocarcinoma: a case series and literature review

Abstract

Purpose

Hemolytic–uremic syndrome (HUS) is a rare side effect of gemcitabine, which is reported as having a high morbidity and mortality despite interventions with standard HUS therapies including plasmapheresis. The purpose of this report was to describe the successful treatment of gemcitabine-induced HUS (G-HUS) with rituximab. It also aims to summarize the literature regarding the morbidity and mortality of G-HUS in pancreatic adenocarcinoma depending on the treatment given, ultimately providing some guidance for beneficial therapies.

Methods

This is a retrospective report of three patients with pancreatic adenocarcinoma who developed G-HUS and were treated with a combination of therapies including rituximab.

Results

All three patients received a combination of therapies to treat their HUS. One patient appeared to have some benefit with plasmapheresis. Resolution occurred following one course of rituximab for all three patients. This resolution has been long lasting with a minimum of eighteen month's follow-up. Similarly, in our literature review a variety of therapies were utilized, but immune therapies appear to reverse HUS if other therapies are failing.

Conclusion

Rituximab can be an effective therapy for reversal of hemolysis and stabilization of renal function in G-HUS when other therapies fail.

from Cancer via ola Kala on Inoreader http://ift.tt/2b4o2pA
via IFTTT