Similarities and disparities in cancer burden among Arab world females.

Introduction: Cancer is the leading cause of increased morbidity and mortality worldwide. This work aims to study the Arab-world females' cancers (AFCs), the similarities and disparities from epidemiological, economic and development-indices points of view.

Materials And Methods: Descriptive - Analytical review of the 2018 Global Cancer Observatory concerning AFCs.

PD-1 and CTLA-4 up regulation on donor T cells is insufficient to prevent GvHD in allo-HSCT recipients.

The expression of checkpoint blockade molecules PD-1, PD-L1, CTLA-4, and foxp3+CD25+CD4+ T cells (Tregs) regulate donor T cell activation and graft-vs-host disease (GvHD) in allogeneic hematopoietic stem cell transplant (allo-HSCT). Detailed kinetics of PD-1-, CTLA-4-, and PD-L1 expression on donor and host cells in GvHD target organs have not been well studied. Using an established GvHD model of allo-HSCT (B6 → CB6F1), we noted transient increases of PD-1- and CTLA-4-expressing donor CD4+ and CD8+ T cells on day 10 post transplant in spleens of allo-HSCT recipients compared with syngeneic HSCT (syn-HSCT) recipients.

A truncation mutant of Csf3r cooperates with PML-RARα to induce acute myeloid leukemia in mice.

Severe congenital neutropenia is associated with a marked propensity to develop myelodysplasia or acute myeloid leukemia (AML). Truncation mutations of CSF3R, encoding the granulocyte colony-stimulating factor receptor (G-CSFR), are associated with development of myelodysplasia/AML in severe congenital neutropenia. However, a causal relationship between CSF3R mutations and leukemic transformation has not been established.

Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5.

A fundamental property of leukemic stem cells is clonal dominance of the bone marrow microenvironment. Truncation mutations of CSF3R, which encodes the G-CSF receptor (G-CSFR), are implicated in leukemic progression in patients with severe congenital neutropenia. Here we show that expression of a truncated mutant Csf3r in mice confers a strong clonal advantage at the HSC level that is dependent upon exogenous G-CSF.

Distinct patterns of mutations occurring in de novo AML versus AML arising in the setting of severe congenital neutropenia.

Severe congenital neutropenia (SCN) is an inborn disorder of granulopoiesis. Like most other bone marrow failure syndromes, it is associated with a marked propensity to transform into a myelodysplastic syndrome (MDS) or acute leukemia, with a cumulative rate of transformation to MDS/leukemia that exceeds 20%. The genetic (and/or epigenetic) changes that contribute to malignant transformation in SCN are largely unknown.

Use of [18F]fluorodeoxyglucose positron emission tomography in evaluating locally recurrent and metastatic adrenocortical carcinoma.

Context: Adrenocortical carcinomas are uncommon, and their evaluation by [(18)F]fluorodeoxyglucose positron emission tomography (FDG PET) has not been well evaluated.

Objective: The purpose of this study was to examine the potential utility of FDG PET in the detection of recurrent or metastatic adrenocortical carcinoma.

Design: In patients with known adrenocortical carcinoma who underwent FDG-PET imaging for suspected recurrence or metastasis, FDG activity was compared with other imaging findings, clinical features, and the presence or absence of disease as confirmed by resection, biopsy, or clinical follow-up.