Background: Hemoglobin A1c levels and blood sugar is a diagnostic tests used for diabetes and to determine the developing of diabetic complications. The level of HbA1c is affected by factors such as the Haemoglobin, the age of RBCs in the blood circulation and the Hb glycation rate. The aim of this retrospective study is to assess the relationship of HbA1c levels and blood sugar with haemoglobin concentration, and RBC parameter during female clinic follow-up. Material and Method: The HbA1c levels of 202 patients was measured by NycoCard reader II analyzer and RBC, Haemoglobin concentration (Hb), hematocrit (Hct), Mean Corpuscular Volume (MCV), Mean Corpuscular Haemoglobin (MCH) and Mean Corpuscular Hemoglobin Concentration (MCHC) was measured by mindray BC-3000 Plus auto haematology analyzer, the statistical analyses were performed with SPSS software version 16.0. The Spearman correlation coefficient was used for the relationship of HbA1c, blood sugar with RBC parameters and Kruskal Wallis test for the comparison of HbA1c and RBC parameters between the Diabetics, pre-diabetic and non-diabetic patients. Results: The correlation of HbA1c and blood sugar levels with RBC parameter indicates positive correlation with RBC count and negative correlation with MCV and MCH, and the comparison among diabetic, pre-diabetic and non-diabetic patients, the results showed significantly higher mean of RBC count, Hb concentration and Hct in diabetic patients, and the mean MCV and MCH were significantly higher in non-diabetic compared with pre-diabetic and diabetic. Conclusion: The low level of HbA1c has been found in shorten RBCs lifespan, which is affected by RBC parameters and decrease of RBC lifespan in hyperglycaemia patients. Therefore, this study concludes that the RBC parameters are an excellent tool parallel with HbA1c and blood sugar for the assessment of diabetes patients.
Toll-like receptor 3 (TLR3)-mediated apoptotic changes in cancer cells are well-documented, and hence, several synthetic ligands of TLR3 are being used for adjuvant therapy, but there are reports showing a contradictory effect of TLR3 signaling, which include our previous report that had shown cell proliferation following surface localization of TLR 3. However, the underlying mechanism of cell surface localization of TLR3 and subsequent cell proliferation lacks clarity. This study addresses the TLR3 ligand-mediated signaling cascade that regulates a proliferative effect in breast cancer cells (MDA-MB-231 and T47D) challenged with TLR3 ligand in the presence of myeloid differentiation primary response 88 (MyD88) inhibitor. Evidences were obtained using immunoblotting, coimmunoprecipitation, confocal microscopy, immunocytochemistry, ELISA, and flow cytometry. Results had revealed that TLR3 ligand treatment significantly enhanced breast cancer cell proliferation marked by an upregulated expression of cyclinD1, but the same was suppressed by the addition of MyD88 inhibitor. Also, expression of interleukin 1 receptor-associated kinase 1 (IRAK1)-TNF receptor-associated factor 6 (TRAF6)-transforming growth factor beta-activated kinase 1 (TAK1) was altered in the given TLR3-signaling pathway. Inhibition of MyD88 disrupted the downstream adaptor complex and mediated signaling through the TLR3-MyD88-NF-κB (p65)-IL-6-cyclin D1 pathway. TLR3-mediated alternative signaling of the TLR3-MyD88-IRAK1-TRAF6-TAK1-TAB1-NF-κB axis leads to upregulation of IL6 and cyclin D1. This response is hypothesized to be via the MyD88 gateway that culminates in the proliferation of breast cancer cells. Overall, this study provides first comprehensive evidence on the involvement of canonical signaling of TLR3 using MyD88-cyclin D1-mediated breast cancer cell proliferation. The findings elucidated herein will provide valuable insights into understanding the TLR3-mediated adjuvant therapy in cancer.
Background: B-Cell lymphoma (BCL-2) is a antiapoptotic protein and an important clinical breast cancer prognostic marker but however its expression differs according to the molecular subtype and is reported to be a good marker only in Luminal A type. We aimed to assess its prognostic significance in patients with basal and non-basal TNBC. Methods: This study was a single centre, non-randomized, retrospective study with a prospective arm done on TNBC patients, diagnosed at Amrita Institute of Medical Sciences, Kochi between Jan 2009 and Nov 2014. A total of 113 patients were included in the study based on the ER, PR and HER2 results. The tumor paraffin blocks used for ER, PR and HER 2 studies at the time of diagnosis were obtained. All samples were tested for Bcl-2, CK 5/6 and CK 14 by IHC. Clinicopathological parameters including age, size of tumor, nodal status, histology, MBR grade, presence of lymphovascular invasion and survival anaylysis were compared. Results: In our study Bcl-2 was positive in 23.9% of TNBC. The 6 yr DFS and OS was 75.9% and 85%, 77.5% and 81.6% in Non-basal and Basal-like subgroups respectively. We found no statistically significance between patient survival and Bcl-2 expression in the Non-basal group. The 6 yr DFS for Bcl-2 positive was 82.5 % as compared to 73.9 % for Bcl-2 negative patients (p ¼ 0.650) among Non-basal TNBC. The 6 yr DFS for patients with Bcl-2 positivity was 92.4 % as compared to 76% for Bcl-2 negative among TNBC (p ¼ 0.080). A statistically significant association between Bcl-2 expression and DFS among Basal-like subgroup of TNBC was noted. The DFS at 6 yrs for Basal-like TNBC with Bcl-2 positivity was 100 % as compared to 80% for Bcl-2 negative which was statistically significant (p ¼ 0.040). A trend towards better survival was seen in Basal-like TNBC than in the Non-Basal subgroup and that histopathological characteristic like Pathological stage, LVI and LN ratio showed significant correlation with survival but not significantly associated with Bcl-2 expression. Conclusions: Our study revealed that Bcl-2 expression is not an independent predictor of outcome in the Non-Basal subgroup, but Bcl-2 negativity predicts poor outcomes in TNBC and Basal-like subgroup. Improved survival rates were seen in our TNBC's compared to the western population.Legal entity responsible for the study: Amrita Institute of Medical Sciences. Funding: Has not received any funding. Disclosure: All authors have declared no conflicts of interest.148P Investigation on the MyD88 mediated TLR3 signaling via cell surface in breast cancer
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