Research Letter |

Vismodegib as Eye-Sparing Adjuvant Treatment for Orbital Basal Cell Carcinoma

Alon Kahana, MD, PhD1; Francis P. Worden, MD2; Victor M. Elner, MD, PhD1
[+] Author Affiliations
1Eye Plastic and Orbital Surgery Service, Department of Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, Ann Arbor
2Hematology and Oncology Section, Department of Internal Medicine, University of Michigan, Ann Arbor
JAMA Ophthalmol. 2013;131(10):1364-1366. doi:10.1001/jamaophthalmol.2013.4430.
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Orbital invasion of basal cell carcinoma (BCC) may lead to disfigurement, blindness, or even death.1 Orbital exenteration, although disfiguring and blinding, is often the only option for cure when incompletely excised medial canthal tumors extend into the orbit.2 The US Food and Drug Administration has recently approved a hedgehog pathway inhibitor3 with an adequate safety profile,4 vismodegib (Erivedge), for oral treatment of basal cell nevus syndrome5 and locally advanced or metastatic BCC.6 We describe a patient with BCC invading the medial orbit who was treated with oral vismodegib, resulting in near-total tumor shrinkage that permitted complete excision with clear surgical margins. Histopathologically, the excised tissue contained scattered residual tumor cells exhibiting squamous differentiation and low proliferative capacity.

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Figure 1.
Treatment With Vismodegib Results in Reduction in the Size of a Left Medial Orbital Basal Cell Carcinoma

Before vismodegib treatment, magnetic resonance imaging shows a left medial orbital basal cell carcinoma (arrows) (A and inset of A), and hematoxylin-eosin staining (original magnification ×40) (B) and immunohistochemistry with K903 antibody staining (original magnification ×40) (C) for high-molecular-weight keratin show tumor cell content. Following vismodegib treatment, magnetic resonance imaging reveals a reduction in size (D), while hematoxylin-eosin staining (original magnification ×40) (E) and immunohistochemistry with K903 antibody staining (original magnification ×40) (F) reveal reduction in tumor cell content.

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Figure 2.
Histologic and Immunohistochemical Analysis of the Excised Residual Tumor

Histologic analysis of the excised residual tumor with hematoxylin-eosin staining reveals predominant pattern fibrosis (original magnification ×40 [A] and ×100 [B]) and degenerative nests (original magnification ×200) (C) with a lymphocytic infiltrate (original magnification ×200) (D). Leukocyte phagocytosis of degenerated cells is noted on hematoxylin-eosin staining (original magnification ×100) (E) and CD68 immunohistochemistry (original magnification ×100) (F). In contrast to a high pretreatment proliferative index as indicated by extensive nuclear immunostaining for Ki67 (original magnification ×100) (G), posttreatment tumor shows virtual absence of immunoreactivity (original magnification ×100) (I, representing the only area of the excised tumor with any hint of Ki67 staining). Histologic analysis of corresponding adjacent sections was performed with hematoxylin-eosin staining (original magnification ×100) (H and J).

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