Embolization for acute gastrointestinal hemorrhage secondary to post-transplant lymphoproliferative disorder.

Gastrointestinal manifestations of post-transplant lymphoproliferative disorder (GI-PTLD) encompasses a spectrum of mucosal inflammation and ulceration that can present as severe acute gastrointestinal bleed. This case report describes a case of GI-PTLD in a 19-year-old female status postcardiac transplant. This patient presented with extensive gastrointestinal hemorrhage secondary to PTLD involving the duodenum.

Genetic mechanisms in Apc-mediated mammary tumorigenesis.

Many components of Wnt/beta-catenin signaling pathway also play critical roles in mammary tumor development, yet the role of the tumor suppressor gene APC (adenomatous polyposis coli) in breast oncongenesis is unclear. To better understand the role of Apc in mammary tumorigenesis, we introduced conditional Apc mutations specifically into two different mammary epithelial populations using K14-cre and WAP-cre transgenic mice that express Cre-recombinase in mammary progenitor cells and lactating luminal cells, respectively. Only the K14-cre-mediated Apc heterozygosity developed mammary adenocarcinomas demonstrating histological heterogeneity, suggesting the multilineage progenitor cell origin of these tumors.

Adenomatous polyposis coli (APC) is required for normal development of skin and thymus.

The tumor suppressor gene Apc (adenomatous polyposis coli) is a member of the Wnt signaling pathway that is involved in development and tumorigenesis. Heterozygous knockout mice for Apc have a tumor predisposition phenotype and homozygosity leads to embryonic lethality. To understand the role of Apc in development we generated a floxed allele.