The objectives of this study were to estimate the prevalence of anemia and iron deficiency among schoolchildren in the Aral Sea region of Kazakhstan and to determine the various factors associated with anemia in this population. We conducted a cross-sectional study of randomly selected schoolchildren. Blood samples were collected for measuring hemoglobin (Hb), serum ferritin (SF), total iron binding capacity (TIBC), and other hematological indices, and subjects were screened for anemia and iron deficiency. Associations between Hb concentration and SF, TIBC, anthropometric, and socioeconomic data were evaluated using regression analysis. The prevalence of anemia was 49.8 per cent although levels were mostly mild. Twenty-two per cent of the children were iron depleted (SF < 12 microg/l). Of the anemic children, 32.4 per cent were found to have iron deficiency anemia (anemia with SF < 12 microg/l). There were significant positive correlations between the levels of Hb and SF, but a negative correlation with serum TIBC. Age, mean corpuscular volume (MCV) and SF were found to be significantly related to Hb by stepwise multiple regression analysis. Multiple logistic regression analysis revealed that anemia was independently related to living district, education of father, and child's age. The results suggest that iron deficiency is an important determinant of anemia in this population; however, whole anemia cannot be solely explained by iron deficiency. Further studies are needed for consideration of micronutrients status, parasite infestation, hereditary disorders, and exposure to environmental pollutants.

Background Colorectal adenocarcinoma with enteroblastic differentiation (CAED) is a rare subtype of colorectal malignancy with expression of enteroblastic markers (glypican 3, SALL4, AFP); however, the clinicopathological and epidemiological features are not fully elucidated. Aims The aims of this study were to elucidate and establish the molecular and clinicopathological characteristics of CAED. Materials and Methods In addition to three cases recently diagnosed as CAED, colorectal carcinoma (CRC) with expression of enteroblastic markers were selected by using immunohistochemistry (IHC) on tissue microarrays of 988 advanced CRC. We employed next‐generation sequencing (NGS) and Sanger sequencing for the detection of genetic alterations. IHC for p53 and HER2, HER2‐FISH and MSI status was also investigated. Survival analyses for clinicopathological parameters were performed using Kaplan–Meier methods. Results Thirty‐nine cases (4.0%) were positive for at least one enteroblastic marker. Histological evaluation of the total of 42 cases revealed that 10 contained tumour cells with clear cytoplasm. Enteroblastic marker‐positive cases had aggressive behaviour and poor prognosis. NGS revealed TP53 as the most frequently mutated gene. The rate of HER2‐positive cases and MSI‐H cases was 9.5% (four of 42) and 12.2% (five of 41), respectively. Among these 42 cases, there were no molecular and clinicopathological differences according to the presence of tumour cells with clear cytoplasm. Conclusions Enteroblastic marker‐positive CRC could be grouped together as CAED regardless of clear cell cytoplasm. Using this definition, the frequency of CAED is 4.0% and has a poorer prognosis than that for conventional CRCs. HER2 targeted therapy would be a meaningful treatment for CAED, and CAEDs contain both MSI‐H and MSI‐stable CRCs, although the MSS phenotype is dominant.

There were significant differences identified between the growth of breastfed infants and existing national references and WHO standards.

Aims Colorectal adenocarcinoma with enteroblastic differentiation (CAED) is a rare malignancy, and its clinicopathological characteristics have not yet been fully elucidated. This study aimed to elucidate the clinicopathological features of CAED through immunostaining of enteroblastic lineage markers alpha‐fetoprotein (AFP), glypican‐3 (GPC3), and spalt‐like transcription factor 4 (SALL4). Methods and results We identified five CAED cases (0.3%) from 1666 colorectal carcinomas, analysed the clinicopathological characteristics and performed immunostaining for AFP, GPC3 and SALL4. Three patients were male and two were female. All cases were located in the sigmoid colon or rectum. Histologically, all cases showed adenocarcinoma composed of cuboidal or columnar cells, with clear cytoplasm resembling the primitive gut; one case exhibited a partial hepatoid pattern. The depth of invasion was T2 and T3 in two and three cases, respectively. Lymphatic/venous invasion was found in all cases (100%), lymph node metastases in four of five cases (80%) and distant metastases in three of five cases (60%) (liver, two cases; lung, one case). Two patients died as a result of their disease during follow‐up. Immunohistochemically, SALL4 and GPC3 were each positive in four of five cases, whereas one case with a hepatoid component was positive for AFP. All three CAED cases with distant metastases were GPC3‐positive. Conclusions CAED was frequently located in the sigmoid colon or rectum, showed aggressive behaviour, such as lymph node metastasis and distant metastasis, and had a dismal prognosis. In addition, CAED was immunoreactive to AFP, GPC3 or SALL4, indicating that these markers may be characteristic of CAED.

NTRK fusion-positive tumors are known to be highly sensitive to TRK inhibitors, such as larotrectinib and entrectinib. Therefore, identification of patients who can potentially benefit from these inhibitors is important; however, the frequency of NTRK fusions in Japanese patients with colorectal cancer (CRC) is unknown. We performed pan-TRK staining using TMA-based immunohistochemistry (IHC) on samples from 971 consecutive Japanese CRC cases from a single institution. Positive cases were further analyzed using NanoString and subsequent targeted RNA sequencing. We found three positive cases using TRK-IHC. Furthermore, the Nanostring assay supported the presence of NTRK fusion in these cases. Subsequent targeted RNA-sequencing and RT-PCR revealed two cases with TPM3-NTRK1 and one with TPR-NTRK1. The TNM stages of these cases were stage I, stage IIA, and stage IIIB, and two showed microsatellite instability-high status. Next-generation sequencing analysis using Cancer hotspot panel revealed TP53 and SMAD4 mutations in separate cases. IHC of β-catenin did not show nuclear accumulation. We found three cases (0.31%) of CRC with NTRK1 fusion among 971 consecutive Japanese CRC cases. No potential driver alterations other than NTRK fusion were identified in these three patients.