Chromogranin A, despite a number of limitations, is still the most valuable marker of neuroendocrine tumors (NETs). Granins belong to the family of acidic proteins that constitute a major component of secretory granules of various endocrine and neuroendocrine cells, which are components of both the classical endocrine glands and the diffuse neuroendocrine system. These cells are a potential source of transformation into neuroendocrine tumors. The awareness of potential causes influencing the false results of its concentrations simplifies diagnosis and treatment. One of the disadvantages of this marker is its non-specificity and the existence of a number of pathological processes leading to an increase in its concentration, which often results in confusion and diagnostic difficulties. The molecular structure is characterized by a number of sites susceptible to the proteolytic activity of enzymes, resulting in the formation of a number of biologically active peptides. Presumably they act as precursors of active proteins. Chromogranin expression correlates with the amount of secretory vesicles in neuroendocrine cells. The peptide chain during biochemical changes becomes a precursor of biologically active proteins with a wide range of activities. There are a number of commercially available kits for the determination of chromogranin A, which differ in methodology. We present the evaluation of chromogranin A as a marker of neuroendocrine tumors in clinical practice and the possible factors that may affect the outcome of its concentration.

In recent years, thyroid malignances have become more prevalent, especially among women. The most common sporadic types of thyroid tumors of follicular origin include papillary, follicular and anaplastic thyroid carcinomas. Although modern diagnosis methods enable the identification of tumors of small diameter, tumor subtype differentiation, which is imperative for the correct choice of treatment, is still troublesome. This review discusses the recent advances in the field of molecular marker identification via next-generation sequencing and microarrays. The potential use of these biomarkers to distinguish among the most commonly occurring sporadic thyroid cancers is presented and compared. Geographical heterogeneity might be a differentiator, although not necessarily a limiting factor, in biomarker selection. The available data advocate for a subset of mutations common for the three subtypes as well as mutations that are unique for a particular tumor subtype. Tumor heterogeneity, a known issue occurring within solid malignancies, is also discussed where applicable. Public databases with datasets derived from high-throughput experiments are a valuable source of information that aid biomarker research in general, including the identification of molecular hallmarks of thyroid cancer.

In acute stroke patients lower free T3 levels are an important factor related to unfavorable outcome, i. e., severe disability and death.

White blood cell counts (WBC), lymphocyte-to-monocyte ratio (LMR), and monocyte-to-high-density lipoprotein cholesterol ratio (MHR) are used as chronic inflammation markers. Polycystic ovary syndrome (PCOS) is a constellation of systemic inflammation linked to central obesity (CO), hyperandrogenism, insulin resistance, and metabolic syndrome. The waist-to-height ratio (WHtR) constitutes a highest-concordance anthropometric CO measure. This study aims to access WBC, LMR, and MHR in PCOS and healthy subjects, with or without CO. Establishing relationships between complete blood count parameters, high-sensitivity C-reactive protein (hsCRP), and hormonal, lipid and glucose metabolism in PCOS. To do this, WBC, LMR, MHR, hsCRP, anthropometric, metabolic, and hormonal data were analyzed from 395 women of reproductive age, with and without, PCOS. Correlations between MHR, and dysmetabolism, hyperandrogenism, and inflammation variables were examined. No differences were found in WBC, LMR, MHR, and hsCRP between PCOS and controls (p > 0.05). PCOS subjects with CO had higher hsCRP, MHR, and WBC, and lower LMR vs. those without CO (p < 0.05). WBC and MHR were also higher in controls with CO vs. without CO (p < 0.001). MHR correlated with anthropometric, metabolic, and endocrine parameters in PCOS. WHtR appeared to strongly predict MHR in PCOS. We conclude that PCOS does not independently influence WBC or MHR when matched for CO. CO and dysmetabolism may modify MHR in PCOS and control groups.

BackgroundDifferentiated thyroid carcinoma (DTC) originates from thyroid follicular epithelial cells and belongs to a group of slowly progressing tumors with a relatively good prognosis. However, recurrences and metastases are a serious problem in advanced stages. Furthermore, progression from a well differentiated thyroid carcinoma to an aggressive anaplastic one is possible.The majority of differentiated thyroid carcinomas are sporadic but a few alleles increasing the cancer risk are known. One of them is the c.470 T > C (p.I157T, rs17879961) missense substitution in the CHEK2 gene.Aim of the studyThe aim of this study was to investigate whether this specific CHEK2 alteration, c.470 T > C, predisposes the Great Poland (Wielkopolska) population to thyroid cancer.Methods602 differentiated thyroid carcinoma patients and 829 controls randomly selected from population were genotyped for the presence of the c.470C allele using pyrosequencing. Hardy-Weinberg Equilibrium (HWE) was tested for both groups by chi-square distribution and Fisher’s exact test. The odds ratios (ORs), 95% confidence intervals (CIs), and p-values were calculated using the R software.ResultsThe results of genotyping showed the presence of the c.470C allele in 51 patients with a frequency of 4.49%, while in a controls in 42 patients with a frequency of 2.53%. We demonstrated that in the Great Poland population the c.470C CHEK2 variant increases the risk of developing differentiated thyroid cancer almost twice (OR = 1.81, p = 0.004). The risk of papillary thyroid carcinoma in female patients homozygous for the c.470C allele was shown to increase almost 13-fold (OR = 12.81, p = 0.019).ConclusionsIdentification of c.470C CHEK2 gene variant ought to be taken into account by healthcare policymakers. Future well-designed and larger population studies are of great value in confirming these findings. Moreover, a combination of genetic factors together with environmental exposures should also be considered.Electronic supplementary materialThe online version of this article (doi:10.1186/s13053-015-0030-5) contains supplementary material, which is available to authorized users.