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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Medicine+(Baltimore)
2014 ; 93
(15
): e81
Nephropedia Template TP
gab.com Text
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English Wikipedia
Oncocytoma-like renal tumor with transformation toward high-grade oncocytic
carcinoma: a unique case with morphologic, immunohistochemical, and genomic
characterization
#MMPMID25275525
Sirintrapun SJ
; Geisinger KR
; Cimic A
; Snow A
; Hagenkord J
; Monzon F
; Legendre BL Jr
; Ghazalpour A
; Bender RP
; Gatalica Z
Medicine (Baltimore)
2014[Oct]; 93
(15
): e81
PMID25275525
show ga
Renal oncocytoma is a benign tumor with characteristic histologic findings. We
describe an oncocytoma-like renal tumor with progression to high-grade oncocytic
carcinoma and metastasis. A 74-year-old man with no family history of cancer
presented with hematuria. Computed tomography showed an 11?cm heterogeneous
multilobulated mass in the right kidney lower pole, enlarged aortocaval lymph
nodes, and multiple lung nodules. In the nephrectomy specimen, approximately one
third of the renal tumor histologically showed regions classic for benign
oncocytoma transitioning to regions of high-grade carcinoma without sharp
demarcation. With extensive genomic investigation using single nucleotide
polymorphism-based array virtual karyotyping, multiregion sequencing, and
expression array analysis, we were able to show a common lineage between the
benign oncocytoma and high-grade oncocytic carcinoma regions in the tumor. We
were also able to show karyotypic differences underlying this progression. The
benign oncocytoma showed no chromosomal aberrations, whereas the high-grade
oncocytic carcinoma showed loss of the 17p region housing FLCN (folliculin
[Birt-Hogg-Dubé protein]), loss of 8p, and gain of 8q. Gene expression patterns
supported dysregulation and activation of phosphoinositide 3-kinase (PI3K)/v-akt
murine thymoma viral oncogene homolog (Akt), mitogen-activated protein kinase
(MAPK)/extracellular-signal-regulated kinase (ERK), and mechanistic target of
rapamycin (serine/threonine kinase) (mTOR) pathways in the high-grade oncocytic
carcinoma regions. This was partly attributable to FLCN underexpression but
further accentuated by overexpression of numerous genes on 8q. In the high-grade
oncocytic carcinoma region, vascular endothelial growth factor A along with
metalloproteinases matrix metallopeptidase 9 and matrix metallopeptidase 12 were
overexpressed, facilitating angiogenesis and invasiveness. Genetic molecular
testing provided evidence for the development of an aggressive oncocytic
carcinoma from an oncocytoma, leading to aggressive targeted treatment but
eventual death 39 months after the diagnosis.