scholarly journals Metastases of Renal Cell Carcinoma to the Thyroid Gland with Synchronous Benign and Malignant Follicular Cell-Derived Neoplasms

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Carlos Zamarrón ◽  
Ihab Abdulkader ◽  
María C. Areses ◽  
Vanesa García-Paz ◽  
Luís León ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Growth Factor ◽  
Thyroid Gland ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Growth Factor Receptor ◽  
Follicular Adenoma ◽  
Distant Metastases ◽  
Whole Body ◽  
Cell Renal Cell Carcinoma

Clear cell renal cell carcinoma (CCRCC) is the most common origin for metastasis in the thyroid. A 51-year-old woman was referred to our hospital for a subcarinal lesion. Ten years before, the patient had undergone a nephrectomy for CCRCC. Whole-body fluorodeoxyglucose positron emission tomography revealed elevated values in the thyroid gland, while the mediastinum was normal. An endoscopic ultrasonography-guided fine-needle aspiration biopsy of the mediastinal mass was consistent with CCRCC, and this was confirmed after resection. The thyroidectomy specimen also revealed lymphocytic thyroiditis, nodular hyperplasia, one follicular adenoma, two papillary microcarcinomas, and six foci of metastatic CCRCC involving both thyroid lobes. Curiously two of the six metastatic foci were located inside two adenomatoid nodules (tumor-in-tumor). The metastatic cells were positive for cytokeratins, CD10, epidermal growth factor receptor, and vascular endothelial growth factor receptor 2. NoBRAFgene mutations were found in any of the primary and metastatic lesions. The patient was treated with sunitinib and finally died due to CCRCC distant metastases 6 years after the thyroidectomy. In CCRCC patients, a particularly prolonged survival rate may be achieved with the appropriate therapy, in contrast to the ominous prognosis typically found in patients with thyroid metastases from other origins.

scholarly journals Case: Secondary polycythemia due to pazopanib in patients with metastatic renal cell carcinoma

2017 ◽  
Vol 11 (11) ◽  
pp. E449-50 ◽  
Author(s):  
Nedal Bukhari ◽  
Eric Winquist
Keyword(s):  
Renal Cell Carcinoma ◽  
Growth Factor ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Growth Factor Receptor ◽  
Cell Receptor ◽  
Renal Neoplasm ◽  
Vascular Endothelial ◽  
Cell Renal Cell Carcinoma ◽  
Endothelial Growth Factor

Clear-cell renal cell carcinoma (RCC) is the most common primary malignant renal neoplasm. Up to 30% of patients have metastatic disease at the time of initial diagnosis.1 Small molecule inhibitors of vascular endothelial growth factor receptor tyrosine kinase (VEGFR TKIs) are used as first-line treatment for most patients with incurable RCC. Pazopanib is a TKI inhibiting VEGFR,1-3 as well as plateletderived growth factor receptors (PDGFRs) α and β and stem cell receptor c-kit. The most common side effects of pazopanib are diarrhea, hypertension, changes in hair colour, anorexia, nausea, and vomiting. Severe hepatic toxicity is the adverse effect of greatest concern,but is uncommon. Myelosuppressive effects are also noted, such as anemia, thrombocytopenia, and leukopenia, and are presumably mediated through c-kit inhibition. Erythrocytosis is a wellrecognized paraneoplastic syndrome associated with RCC; however, erythrocytosis due to pazopanib therapy has only recently been described. We report two cases and review of the literature related to this phenomenon.

scholarly journals Chromosome 3p Loss–Orchestrated VHL, HIF, and Epigenetic Deregulation in Clear Cell Renal Cell Carcinoma

2018 ◽  
Vol 36 (36) ◽  
pp. 3533-3539 ◽  
Author(s):  
James J. Hsieh ◽  
Valerie H. Le ◽  
Toshinao Oyama ◽  
Christopher J. Ricketts ◽  
Thai Huu Ho ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Growth Factor ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Cell Renal Cell Carcinoma ◽  
Genetic Event ◽  
Chromosome 3P ◽  
Endothelial Growth Factor

Clear cell renal cell carcinoma (ccRCC) is the most common renal cell carcinoma subtype, and metastatic ccRCC is associated with 5-year survival rates of 10% to 20%. Genetically, ccRCC originates from sequential losses of multiple tumor suppressor genes. Remarkably, chromosome 3p loss occurs in more than 90% of sporadic ccRCCs. This results in concurrent one-copy loss of four tumor suppressor genes that are also mutated individually at high frequency in ccRCC (ie, VHL, 80%; PBRM1, 29% to 46%; BAP1, 6% to 19%; and SETD2, 8% to 30%). Pathogenically, 3p loss probably represents the first genetic event that occurs in sporadic ccRCC and the second genetic event in VHL-mutated hereditary ccRCC. VHL constitutes the substrate recognition module of the VCB-Cul2 E3 ligase that degrades HIF1/2α, whereas PBRM1, BAP1, and SETD2 are epigenetic modulators that regulate gene transcription. Because 3p loss and VHL inactivation are nearly universal truncal events in ccRCC, the resulting HIF1/2 signaling overdrive and accompanied tumor hypervascularization probably underlie the therapeutic benefits observed with vascular endothelial growth factor receptor inhibitors, including sorafenib, sunitinib, pazopanib, axitinib, bevacizumab, cabozantinib, and lenvatinib. Furthermore, recent marked advances in ccRCC genomics, transcriptomics, proteomics, metabolomics, molecular mechanisms, mouse models, prognostic and predictive biomarkers, and clinical trials have rendered invaluable translational insights concerning precision kidney cancer therapeutics. With an armamentarium encompassing 13 drugs that exploit seven unique therapeutic mechanisms (ie, cytokines, vascular endothelial growth factor receptor, mTORC1, cMET/AXL, fibroblast growth factor receptor, programmed cell death-1 and programmed death-ligand 1, and cytotoxic T-cell lymphocyte associated-4) to treat metastatic renal cell carcinoma, one of the imminent clinical questions concerning care of patients with metastatic ccRCC is how a personalized treatment strategy, through rationally combining and sequencing different therapeutic modalities, can be formulated to offer the best clinical outcome for individual patients. Here, we attempt to integrate recent discoveries of immediate translational impacts and discuss future translational challenges and opportunities.

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