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pulmonary lymphangitis carcinomatosis ofc lear cell renal cell carcinoma after angiogenesis inhibition
2018
1. Abstract 1.1. Background: Over eighty percent of renal
cell carcinomas of the clear cell type (ccRCC) constitutively secrete Vascular
Endothelial Growth Factor-A (VEGF-A), due to a defect in the von Hippel Lindau
(VHL) gene. These tumors are therefore highly angiogenic, making metastasized
ccRCC (m-ccRCC) patients the prime candidates for anti-angiogenic therapy.
Angiogenesis inhibition nowadays forms the backbone of first-line treatment of
m-ccRCC patients. Despite prolongation of disease-free and overall survival, common
experience is that resistance develops. 1.2. Objective: To get more insight in the
pathophysiological mechanisms that underlie disease progression under
anti-angiogenic therapy. 1.3. Methods: We extensively analyzed from a 68-year-old male
m-ccRCC patient the primary tumor and the corresponding pulmonary metastasis
that initially responded well to anti-angiogenic treatment, but ultimately
progressed. 1.4. Results: We show that anti-angiogenic treatment induced a
phenotypic adaptation in the lung lesion, characterized by infiltration of
tumor cells along and even in the pulmonary vasculature, resembling pulmonary
lymphangitis carcinomatosis. This phenotype was radiologically reflected by a
cloudy pattern on CT. 1.5. Conclusions: These observations suggest that
pulmonary metastases of renal cell carcinoma can respond to anti-angiogenic
therapies by adopting a diffuse phenotype that allows progression in an
angiogenesis-independent fashion through co-option. 2. Keywords: Angiogenesis; Cediranib;
Pulmonary metastases; Renal cell cancer
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