Mouse model for endometriosis is characterized by proliferation and inflammation but not epithelial-to-mesenchymal transition and fibrosis

Endometriosis is a common disorder of unknown etiology, and non-surgical therapies are still a challenge. Tounderstand the pathogenesis and preclinical testing of drugs for endometriosis, animal models are highlydesirous. Herein, we carried out longitudinal characterization of a mouse model for endometriosis whereuterine tissue was transplanted onto the intestinal mesentery. During the course of lesion development from day15 to 60 post-induction, the ectopic endometrium became pale, fluid-filled and the animals developed peritoneal adhesions. Most lesions resembled a well-differentiated type of endometriosis and * 13% of animalshad mixed type of lesions. There was extensive stromal compaction in the ectopic tissue. During the progression of endometriosis, there was increased proliferation of epithelial and stromal cells as evident by PCNAstaining. Cyp19a1 (aromatase) mRNA was detected in the ectopic lesions on day 15 and 30 post-induction ofendometriosis, by day 60 the expression was reduced. As compared to the control endometrium, the mRNAlevels of Esr1 progressively reduced while the levels of inflammation associated genes (Esr2, Ifng, Tnf andIl1b) increased in the ectopic lesions. Infiltration of macrophages and polymorphonuclear leucocytes was alsoobserved in the ectopic lesions indicative of inflammation. As compared to control, there was no change inlevels of Cytokeratin and E-cadherin in the epithelial cells of ectopic endometrium. We did not observeexcessive collagen deposition or a-SMA positive myofibroblasts in the stroma of the ectopic endometrium.Thus, epithelial-to-mesenchymal transition and fibrosis are not detected in the mouse model of endometriosis.Our results show that the mouse model of endometriosis mimics some but not all the features of humanendometriosis.

Deletion of ABL/BCR on der(9) associated with severe basophilia.

Chronic basophilic leukemia is a rare form in chronic myeloid leukemia patients. Only limited number of reports are available. Herein, we describe a patient who presented with fatigue, weight loss, leucocytosis, prominent basophilia, and mild eosinophilia. On biopsy, bone marrow was hypercellular with marked basophils. The immunophenotype showed abnormal expression of CD7, which is suggestive of basophilic maturation. Chromosomal analysis from GTG-banded metaphases revealed Ph positivity, and fluorescence in situ hybridization (FISH) with BCR/ABL dual color, dual fusion probe showed single fusion on the der(22) chromosome and ABL/BCR fusion was deleted on the der(9) chromosome. The deletion (ABL/BCR) on der(9) may be associated with basophilia which may be also indicative of the transformation of CML to acute myeloid leukemia.