Orbital Metastasis as the Initial Presentation of Invasive Lobular Carcinoma of Breast
Department of Medicine, University of Pittsburgh Medical Center, USA.Internal Medicine (Impact Factor: 0.9). 06/2012; 51(12):1635-8. DOI: 10.2169/internalmedicine.51.7641
This is an unusual case of invasive lobular carcinoma of the breast presenting as an orbital metastasis. A 70 year-old female presented with a gradually worsening blurred vision, periorbital swelling and ascites. The biopsy of the eyelid demonstrated dense fibrosis with neoplastic cells and the diagnosis of carcinoma was made; however, the site of origin of carcinoma was difficult to determine. The histopathologic characteristics of the carcinoma in the orbit and ascites fluid combined with the immunophenotypic features helped determine the primary site of the malignancy. Subsequently, the primary malignancy was identified by examination of the patient's breast.
- Ophthalmic plastic and reconstructive surgery 05/2013; 30(2). DOI:10.1097/IOP.0b013e3182916537 · 0.88 Impact Factor
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ABSTRACT: Objective: This article reviews unusual distant metastatic patterns of infiltrating lobular carcinoma (ILC) of the breast. Conclusion: ILC of the breast tends to spread to the gastrointestinal tract, genitourinary tract, peritoneum, retroperitoneum, and leptomeninges in addition to common visceral sites such as the liver, bone, and lung. Knowledge of these unusual metastatic manifestations and disease patterns may aid in differentiating distant metastatic disease from secondary primary cancers and help plan appropriate therapy.American Journal of Roentgenology 05/2014; 202(5):1140-8. DOI:10.2214/AJR.13.11156 · 2.73 Impact Factor
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ABSTRACT: E-cadherin inactivation underpins the progression of invasive lobular breast carcinoma (ILC). In ILC, p120-catenin (p120) translocates to the cytosol where it controls anchorage independence through the Rho-Rock signaling pathway, a key mechanism driving tumor growth and metastasis. We now demonstrate that anchorage-independent ILC cells show an increase in nuclear p120, which results in relief of transcriptional repression by Kaiso. To identify the Kaiso target genes that control anchorage independence we performed genome-wide mRNA profiling on anoikis resistant mouse ILC cells, and identified 29 candidate target genes including the established Kaiso target Wnt11. Our data indicate that anchorage-independent upregulation of Wnt11 in ILC cells is controlled by nuclear p120 through inhibition of Kaiso-mediated transcriptional repression. Finally, we show that Wnt11 promotes activation of RhoA, which causes ILC anoikis resistance. Our findings thereby establish a mechanistic link between E-cadherin loss and subsequent control of Rho-driven anoikis resistance through p120/Kaiso-dependent expression of Wnt11.Disease Models and Mechanisms 02/2015; 8(4). DOI:10.1242/dmm.018648 · 4.97 Impact Factor
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