RENAL MEDULLARY CARCINOMA AND
            <i>ABL</i>
            GENE AMPLIFICATION

Simpson, Lijo; He, Xiang; Pins, Michael; Huang, Xiaoke; Campbell, Steven C.; Yang, Ximing J.; Perlman, Elizabeth J.; Bergan, Raymond C.

doi:10.1097/01.ju.0000158448.56888.09

Cited by 72 publications

(58 citation statements)

References 15 publications

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“…Changes in the activation of the Abl kinases also may modulate cell-cell adhesion during tumor progression and metastasis. In this regard, enhanced expression of Abl or Arg has been reported in a subset of metastatic colon carcinomas, pancreatic ductal carcinoma, and renal medullary carcinoma (40)(41)(42). Excessive Abl/Arg kinase activity may disturb the proper balance of Rho and Rac activation and induce altered cytoskeletal reorganization, thereby affecting cell-cell adhesion.…”

Section: Discussionmentioning

confidence: 99%

Abl tyrosine kinases regulate cell–cell adhesion through Rho GTPases

Zandy

Playford

Pendergast

2007

Proc. Natl. Acad. Sci. U.S.A.

119

132

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Section: Discussionmentioning

confidence: 99%

Abl tyrosine kinases regulate cell–cell adhesion through Rho GTPases

Zandy

Playford

Pendergast

2007

Proc. Natl. Acad. Sci. U.S.A.

119

132

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“…Chromosomal translocation events in human leukemias give rise to structurally altered oncogenic Abl fusion proteins such as Bcr-Abl, Tel-Abl, and Tel-Arg (17). Furthermore, enhanced expression of Abl kinases is observed in a subset of primary colon carcinomas and metastatic tumors (23), as well as in pancreatic ductal carcinomas and renal medullary carcinoma (24,25). Also, Abl kinases are constitutively activated downstream of ErbB receptors and Src kinases in breast cancer cell lines (20).…”

Section: Ligand-induced Endocytosis Of the Epidermal Growth Factor Rementioning

confidence: 99%

Abl Tyrosine Kinase Regulates Endocytosis of the Epidermal Growth Factor Receptor

Tanos

Pendergast

2006

Journal of Biological Chemistry

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Signal attenuation from ligand-activated epidermal growth factor receptor (EGFR) is mediated in part by receptor endocytosis and trafficking to the lysosomal degradative compartment. Uncoupling the activated EGFR from endocytosis and degradation has emerged as a mechanism for oncogenic activation of the EGFR. The Abl nonreceptor tyrosine kinase is activated by ligand-stimulated EGFR, but the role of Abl in EGFR signaling has not been defined. Here we uncovered a novel role for the activated Abl kinase in the regulation of EGFR endocytosis. We show that activated Abl impairs EGFR internalization. Moreover, we show that activated Abl phosphorylates the EGFR primarily on tyrosine 1173, and that mutation of this site to phenylalanine restores ligand-dependent endocytosis of the EGFR in the presence of activated Abl. Furthermore, we show that activated Abl allows the ligand-activated EGFR to escape Cbl-dependent down-regulation by inhibiting the accumulation of Cbl at the plasma membrane in response to epidermal growth factor stimulation and disrupting the formation of the EGFR⅐Cbl complex without affecting Cbl protein stability. These findings reveal a novel role for Abl in promoting increased cell-surface expression of the EGFR and suggest that Abl/EGFR signaling may cooperate in human tumors.

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“…There is a male predominance with a male/female ratio of 2:1, although for patients o10 years the male/female ratio is 5:1. 26 Where ethnicity was reported the overwhelming majority of patients were African American, whereas 15 patients were Hispanic/ Brazilian. Medullary carcinoma has only rarely (o10 cases) been reported in Caucasians.…”

Section: Renal Medullary Carcinomamentioning

confidence: 99%

“…On this basis the tumor, which was termed medullary carcinoma on morphologic grounds, was designated the seventh sickle cell nephropathy (the others being gross hematuria, papillary necrosis, nephrotic syndrome, renal infarction, inability to concentrate urine and pyelonephritis); 23 since the original study over 160 cases have been reported. [24][25][26][27][28][29][30][31][32][33] Patient age at diagnosis ranges from 5 to 69 years with a mean age of 19 years. There is a male predominance with a male/female ratio of 2:1, although for patients o10 years the male/female ratio is 5:1.…”

Section: Renal Medullary Carcinomamentioning

confidence: 99%

Uncommon and recently described renal carcinomas

2009

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Major consensus conferences held over a decade ago laid the foundations for the current (2004) WHO classification of renal carcinoma. Clear cell, papillary and chromophobe carcinomas account for 85-90% carcinomas seen in routine practice. The remaining 10-15% of carcinomas consist of rare sporadic and hereditary tumors, some of which had been long recognized, but many of which only emerged as distinct entities in the decade leading up to the WHO publication. Collecting-duct carcinoma is a rare, often lethal form of carcinoma. Medullary carcinoma associated with sickle cell trait, has emerged as a distinctive tumor showing some overlapping features with upper tract urothelial carcinoma. Mucinous tubular and spindle-cell carcinoma and tubulocystic carcinoma were earlier considered as patterns of low-grade collecting-duct carcinoma, but are now recognized as separate tumor entities. Carcinomas associated with somatic translocations of TFE3 and TFEB comprise a significant proportion of pediatric renal carcinomas. Oncocytoid renal carcinomas in neuroblastoma survivors was recognized as a unique tumor category in the WHO classification. Renal carcinoma associated with end-stage renal disease is now recognized as having distinct morphological patterns and behavior. In addition there is a group of rare recently described carcinomas, including clear cell papillary carcinoma, oncocytic papillary renal cell carcinoma, follicular renal carcinoma and leiomyomatous renal cell carcinoma. It behooves the surgical pathologist to not only be capable of diagnosing the common forms of renal cancer, but also to be aware of the rare types of renal carcinoma, many of which have emerged in recent years.

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RENAL MEDULLARY CARCINOMA AND ABL GENE AMPLIFICATION

Cited by 72 publications

References 15 publications

Abl tyrosine kinases regulate cell–cell adhesion through Rho GTPases

Abl tyrosine kinases regulate cell–cell adhesion through Rho GTPases

Abl Tyrosine Kinase Regulates Endocytosis of the Epidermal Growth Factor Receptor

Uncommon and recently described renal carcinomas

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