Heparanase (HPSE) gene polymorphism (rs12503843) contributes as a risk factor for hepatocellular carcinoma (HCC): a pilot study among Egyptian patients.

Background: Heparanase activity was found to be included in human cancer development and growth. Heparanase (HPSE) gene single nucleotide polymorphisms (SNPs) have been found to be correlated with different human cancers. In the current study, we investigated whether HPSE SNPs were a hepatocellular carcinoma (HCC) risk factor by carrying out a comprehensive case-control pilot study.

Efficient role of IgH 3' regulatory region deficient B-cells in the development of oil granulomas.

Functional B-cells are essential for the formation of oil granulomas. The IgH 3' regulatory region (3'RR) activates important check-points during B-cell maturation. We investigated if 3'RR-deficient B-cells remain efficient to develop oil granulomas in response to pristine.

The IgH 3' regulatory region influences lymphomagenesis in Igλ-Myc mice.

The IgH 3'regulatory region (3'RR), encompassing the four transcriptional enhancers hs3a-hs1,2-hs3b-hs4, has a key role on class switch recombination, somatic hypermutation, IgH transcription and B-cell fate. In plasma cells, transcribed IgH and IgL loci often colocalized in transcription factories and an IgL transcription defect might translate into lowered IgH transcription. We explored whether the 3'RR would affect lymphomagenesis in Igλ-Myc transgenic mice prone to lymphoproliferations.

Elucidation of IgH 3' region regulatory role during class switch recombination via germline deletion.

In mature B cells, class switch recombination (CSR) replaces the expressed constant Cμ gene with a downstream C(H) gene. How the four transcriptional enhancers of the IgH 3' regulatory region (3'RR) control CSR remains an open question. We have investigated IgG1 CSR in 3'RR-deficient mice.

The IgH 3' regulatory region governs μ chain transcription in mature B lymphocytes and the B cell fate.

We report that the IgH 3' regulatory region (3'RR) has no role on μ chain transcription and pre-BCR expression in B cell progenitors. In contrast, analysis of heterozygous IgH aΔ3'RR/bwt mice indicated that the 3'RR controls μ chain transcripts in mature splenocytes and impacts membrane IgM density without obvious effect on BCR signals (colocalisation with lipid rafts and phosphorylation of Erk and Akt after BCR crosslinking). Deletion of the 3'RR modulates the B cell fate to less marginal zone B cells.

Targeting the oncogene B lymphoma deregulator IgH 3' regulatory region does not impede the in vivo inflammatory response in mice.

The IgH 3' regulatory region (3'RR), encompassing the four transcriptional enhancers hs3a-hs1,2-hs3b-hs4, is a potent lymphoma oncogene deregulator but its role in B cell-mediated inflammatory responses is unknown. We investigated the 3'RR involvement in the in vivo pristane-induced inflammatory response in BALB/c mice. The lack of the 3'RR in BALB/c mice had no wide effect on the incidence, the kinetic of development and the cellular composition of peritoneal ascites.

Elucidation of the enigmatic IgD class-switch recombination via germline deletion of the IgH 3' regulatory region.

Classical class-switch recombination (cCSR) substitutes the Cμ gene with Cγ, Cε, or Cα, thereby generating IgG, IgE, or IgA classes, respectively. This activation-induced deaminase (AID)-driven process is controlled by the IgH 3' regulatory region (3'RR). Regulation of rare IgD CSR events has been enigmatic.