APOBEC3B (A3B) is aberrantly overexpressed in a subset of breast cancers, where it associates with advanced disease, poor prognosis, and treatment resistance, yet the causes of A3B dysregulation in breast cancer remain unclear. In the associated publication, A3B mRNA and protein expression levels were quantified in different cell lines and breast tumors and related to cell cycle markers using RT-qPCR and multiplex immunofluorescence imaging. The inducibility of A3B expression during the cell cycle was additionally addressed after cell cycle synchronization with multiple methods. First, we found that A3B protein levels within cell lines and tumors are heterogeneous and associate strongly with the proliferation marker Cyclin B1 characteristic of the G2/M phase of the cell cycle. Second, in multiple breast cancer cell lines with high A3B, expression levels were observed to oscillate throughout the cell cycle and again associate with Cyclin B1. Third, induction of A3B expression is potently repressed throughout G0/early G1, likely by RB/E2F pathway effector proteins. Fourth, in cells with low A3B, induction of A3B through the PKC/ncNF-κB pathway occurs predominantly in actively proliferating cells and is largely absent in cells arrested in G0. Altogether, these results support a model in which dysregulated A3B overexpression in breast cancer is the cumulative result of proliferation-associated relief from repression with concomitant pathway activation during the G2/M phase of the cell cycle. This repository contains all quantitative data pertaining to this paper PMID37190094.

This dataset corresponds to the article ‘Diurnal salivary androstenedione and 17-hydroxyprogesterone levels in healthy volunteers for monitoring treatment efficacy of patients with congenital adrenal hyperplasia’ (DOI: 10.1111/cen.14690) published in Clinical Endocrinology (Clin Endo). This study aimed to establish age-adjusted reference values for salivary androstenedione and 17-hydroxyrprogesterone. We wanted to get insight into the diurnal variation of these adrenal steroids in the heatlhy population and therefore measured these hormones in saliva that was collected in the morning, afternoon, and evening. For this dataset, we used saliva of healthy volunteers from schools in Nijmegen, the Netherlands and also asked (grand)parents / caregivers of these children to collected saliva at these times to enable inclusion of volunteers with a broad age range. With this data set, age-adjusted reference values for these three time points could be established. The attached file contains the raw data used for conducting this study. For each participant the sex, menstruation status, and age (in years) are given. Thereafter, the time of saliva collection is given in a 24-hour data notation for the morning, afternoon, and evening. Then, the androstenedione and 17-hydroxyprogesterone levels (in pmol/L) are given for the morning, afternoon, and evening samples. If the concentration of the measured steroid was below the lower limit of quantification (LLOQ) and the signal-to-noise ratio was <10, the value was assigned half of the LLOQ. The LLOQ for androstenedione is 7 pmol/L, and for 17-hydroxyprogesterone 20 pmol/L.

Supplementary material corresponding to the article ‘Free cortisol and free 21-deoxycortisol in the clinical evaluation of congenital adrenal hyperplasia’ (DOI: 10.1210/clinem/dgae591) published in The Journal of Clinical Endocrinology & Metabolism (JCEM).This study aimed to measure free cortisol and free 21-deoxycortisol concentrations in patients with congenital adrenal hyperplasia and compare this to levels in patients with non-classic congenital adrenal hyperplasia, patients with other forms of adrenal insufficiency, and controls.This collection includes the supplementary materials: - Table S1: Genetic analyses of included CAH patients (n=34) with predicted phenotype based on residual enzyme activity and literature. - Table S2: liquid chromatography tandem mass spectrometry setting for measuring total cortisol and 21-deoxycortisol - Table S3: liquid chromatography tandem mass spectrometry setting for measuring total cortisol and 21-deoxycortisol - Figure S1: Flowchart of included patients for this research- Figure S2: Percentage of free cortisol before (T0) and after (T60) administration of Synacthen® in patients with classic congenital adrenal hyperplasia (CAH), non-classic congenital adrenal hyperplasia (NCCAH), adrenal insufficiency but not CAH (AI), and controls. (S2A) Free cortisol percentage at T0; (S2B) Change in free cortisol percentages between T0 and T60; (S2C) Free cortisol percentage at T60. - Reference list of the references used in this document.

This dataset corresponds to the article ‘Reference intervals for serum 11-oxygenated androgens in children’ (DOI: 10.1093/ejendo/lvae008.) published in the European Journal of Endocrinology (EJE).This study aimed to establish pediatric reference values for eight androgens, including four 11-oxygenated androgens. For this purpose, a liquid-chromatography tandem mass spectrometry (LC-MS/MS) assay was developed and validated for clinical use. To establish pediatric reference values, we measured these androgens in 256 children. Blood was taken from these children before minor surgery or medical procedure. This group of children was previously described in ‘Standardized serum hepcidin values in Dutch children: Set point relative to body iron changes during childhood’ (DOI: 10.1002/pbc.28038). Data on demographics of the included patients can be requested by contacting the corresponding author of that article.This dataset only comprises the patient number, the age (in years), and the concentrations (in nmol/L) of eight androgens: dehydroepiandrosterone (DHEA), androstenedione (A4), testosterone (TES), dihydrotestosterone (DHT), 11-hydroxyandrostenedione (11OHA4), 11-ketoandrostenedione (11KA4), 11-hydroxytestosterone (11OHT), and 11-ketotestosterone (11KT). Concentration below the lower limit of quantification (LLOQ) with a signal-to-noise (S/N) ratio ≤5 are given as half the LLOQ-value. Concentrations <LLOQ with a S/N-ratio >5 are given as absolute measured value.

These data pertain to 2 publications on the effect of tamoxifen and irradiation on ROS and antioxidants. Earlier, we reported that tamoxifen-resistant (TAM-R) breast cancer cells are cross-resistant to irradiation. In PMID: 36755288, we investigated the mechanisms associated with tamoxifen-induced radioresistance, aiming to prevent or reverse resistance and improve breast cancer treatment. Wild-type ERα-positive MCF7 and ERα-negative MDA-MB-231 breast cancer cells and their TAM-R counterparts were analyzed for cellular metabolism using the Seahorse metabolic analyzer. Real-time ROS production, toxicity, and antioxidant capacity in response to H2O2, tamoxifen, and irradiation were determined. Real-time measurement of ROS after tamoxifen and H2O2 exposure indicated lower ROS levels and toxicity in TAM-R cells. Consistently, higher antioxidant levels were found in TAM-R cells, providing protection from irradiation-induced ROS.In PMID: 38292333, total antioxidant capacity (TAC) was analyzed in head and neck cancer (HNSCC) tumor cells in vitro and in serum of HNSCC patients before, during, and after radiotherapie. We found that irradiation induced NRF2 expression and upregulated TAC, which may compromise the effect of RT-induced ROS.