Sarcomatoid renal-cell carcinoma: treatment strategy, review of the literature and a case report

Oncoreview ◽  
2016 ◽  
Vol 6 (4) ◽  
pp. 0-0 ◽  
Author(s):  
Agnieszka Gębara-Puchniarz ◽  
Beata Hryciuk ◽  
Rafał Stec ◽  
Cezary Szczylik ◽  
Bartłomiej Grala ◽  
...  

Introduction: Sarcomatoid renal-cell carcinoma is a very rare cancer characterised with aggressive course of disease and poor prognosis. At present there are no standards of care for this histologic subtype of renal cell carcinoma resistant to various forms of systemic treatment. Methods: The study describes a case of 58 year old woman after left nephrectomy for clear cell carcinoma with sarcomatoid component and after resection of right-kidney tumour for synchronous clear cell carcinoma who received first-line bevacizumab and temsirolimus under the clinical trial, and then second-line chemotherapy based on gemcitabine and doxorubicin and ifosfamide-based third-line chemotherapy. The patient underwent pulmonary metastasectomy twice, and once a metastasectomy for liver metastases. Conclusions: Surgery (including metastases treatment) followed by the systemic chemotherapy seems to be correct option of treatment in patients with renal cell carcinoma with sarcomatoid features. The development of optimum method of systemic treatment requires further prospective randomised trials.

2000 ◽  
Vol 124 (12) ◽  
pp. 1830-1832 ◽  
Author(s):  
Ronald J. Cohen ◽  
John E. McNeal ◽  
Marleen Susman ◽  
Loryn N. Sellner ◽  
Barry J. Iacopetta ◽  
...  

Abstract Sarcomatoid renal cell carcinoma (SRCC) is an aggressive tumor variant thought to arise predominantly from dedifferentiation of clear cell carcinoma. A few reports of SRCC associated with non–clear cell tumors led to the presumption that SRCC may arise from any renal cell carcinoma, although direct evidence of this is lacking. Cytogenetic studies on 3 previously documented SRCCs associated with papillary renal cancers showed either 3p deletions or absence of trisomy 7, 17 in the sarcomatoid tumors, suggesting origin from a coexistent clear cell tumor. The present case represents the first conclusive evidence of direct progression of non–clear cell carcinoma to SRCC with both tumor components containing multiple copies of chromosomes 7 and 17. Many genetic anomalies, including p53 mutations, frequently recognized in SRCC were not recognized in this case, highlighting the importance of cytogenetic evaluation of all SRCC. The patient is well and without evidence of tumor progression 1 year after surgery, and the sinister outlook of SRCC in association with clear cell carcinoma may not apply in SRCC of non–clear cell origin.


2018 ◽  
Vol 10 (02) ◽  
pp. 241-244 ◽  
Author(s):  
Manjari Kishore ◽  
Devender Singh Chauhan ◽  
Shruti Dogra

AbstractCutaneous and intraoral metastasis from any malignancy is not common. Cutaneous spread is usually noted in 5%–10% of high-grade malignancies, as in carcinoma breast, lung, colon, ovary, and malignant melanoma. Only 4.6% cases of cutaneous spread are from renal cell carcinoma (RCC). Intraoral spread from RCC is much rarer with an incidence of approximately 1% of all malignant oral tumors, noted sometimes in tongue, palate, buccal mucosa, gingiva, and lips. RCC is a highly aggressive tumor which requires early diagnosis for increasing the chance of cure. In our case, a 54-year-old male presented with swelling over upper lip, scalp, and retromolar area, which on histopathology and immunohistochemistry revealed clear cell carcinoma compatible with metastatic RCC.


Genes ◽  
2020 ◽  
Vol 11 (4) ◽  
pp. 440
Author(s):  
Yitong Zhang ◽  
Jiaxing Wang ◽  
Xiqing Liu

Kidney renal clear cell carcinoma (KIRC) is the most common and fatal subtype of renal cancer. Antagonistic associations between selenium and cancer have been reported in previous studies. Selenium compounds, as anti-cancer agents, have been reported and approved for clinical trials. The main active form of selenium in selenoproteins is selenocysteine (Sec). The process of Sec biosynthesis and incorporation into selenoproteins plays a significant role in biological processes, including anti-carcinogenesis. However, a comprehensive selenoprotein mRNA analysis in KIRC remains absent. In the present study, we examined all 25 selenoproteins and identified key selenoproteins, glutathione peroxidase 3 (GPX3) and type 1 iodothyronine deiodinase (DIO1), with the associated prognostic biomarker leucine-rich repeat containing 19 (LRRC19) in clear cell renal cell carcinoma cases from The Cancer Genome Atlas (TCGA) database. We performed validations for the key gene expression levels by two individual clear cell renal cell carcinoma cohorts, GSE781 and GSE6344, datasets from the Gene Expression Omnibus (GEO) database. Multivariate survival analysis demonstrated that low expression of LRRC19 was an independent risk factor for OS. Gene set enrichment analysis (GSEA) identified tyrosine metabolism, metabolic pathways, peroxisome, and fatty acid degradation as differentially enriched with the high LRRC19 expression in KIRC cases, which are involved in selenium therapy of clear cell renal cell carcinoma. In conclusion, low expression of LRRC19 was identified as an independent risk factor, which will advance our understanding concerning the selenium adjuvant therapy of clear cell renal cell carcinoma.


2019 ◽  
Vol 37 (7_suppl) ◽  
pp. 548-548 ◽  
Author(s):  
Rana R. McKay ◽  
Bradley Alexander McGregor ◽  
Kathryn Gray ◽  
John A. Steinharter ◽  
Meghara K. Walsh ◽  
...  

548 Background: NccRCC and sccRCC have historically been underrepresented in clinical trials. Even with targeted therapy, most patients have inferior survival compared to clear cell renal cell carcinoma. The combination of atezolizumab and bevacizumab has demonstrated safety and efficacy in ccRCC. In this multicenter, phase II, open-label, single arm trial we evaluate the efficacy of atezolizumab and bevacizumab in patients with nccRCC and sccRCC with >20% sarcomatoid differentiation. Methods: Eligible patients had an ECOG performance status of 0-2 and may have received prior therapy. Prior PD-1/PD-L1 therapy was not allowed. Patients underwent a mandatory baseline biopsy and subsequently received atezolizumab 120 mg and bevacizumab 15 mg/kg intravenously every 3 weeks. Patients remained on therapy until radiographic progression, unacceptable adverse events, or withdrawal. The primary end point was overall response rate (ORR) as determined by RECIST version 1.1. Results: 65 patients were enrolled of whom 52 had ≥1 response assessment and were included in this analysis. 36 patients had nccRCC (papillary n=14, chromophobe n=8, unclassified RCC n=3, collecting duct n=3, translocation n=3, other n=5), and 16 patients had sccRCC. 17 patients received prior systemic therapy, 16 of whom had nccRCC. The ORR was 31% in the overall cohort (Table 1). 10 patients (19%) developed grade 3 treatment-related adverse events (AEs), half of which were immune-related. There were no grade 4-5 AEs. Conclusions: In this study, we show that therapy with atezolizumab and bevacizumab was safe and demonstrated anti-tumor activity in nccRCC and sccRCC. Further analyses will report ORR by histologic subtype and PD-L1 expression status. Analysis of tissue and blood-based biomarkers of response are ongoing. Clinical trial information: NCT02724878. [Table: see text]


1991 ◽  
Vol 39 (4) ◽  
pp. 479-484 ◽  
Author(s):  
H Ohtani ◽  
Y Fukushi ◽  
S Orikasa ◽  
H Nagura

Renal cell carcinomas are immunohistochemically positive for oligosaccharides with the Le(x) determinant (Gal beta 1----4[Fuc alpha 1----3]GlcNAc) and its derivatives, as oncofetal antigens, and their expression is closely related to a better prognosis of the patients. This study was designed to clarify the difference in antigen localization at the ultrastructural level between renal cell carcinoma and normal tissues. In normal kidneys, Le(x) detected by monoclonal antibody (MAb) FH 2 and sialylated extended Le(x) (sialyl Le(x)-i) by MAb FH 6 were identified along the plasma membrane of microvilli of proximal tubule epithelial cells, with occasional immunoreactivity along the basolateral plasma membranes. Intracellular localization was very sparse. Renal cell carcinoma showed localization of Le(x) and sialyl Le(x)-i antigens along the cell membrane and in the cytosol as aggregates or filaments. Immunoreactive materials were also observed in the lumen formed among carcinoma cells. The cytosolic immunoreactivity, not observed in the normal kidney, was regarded as "abnormal cytosolic accumulation" of the antigens. This pattern was more pronounced in clear-cell carcinoma. Pretreatment of specimens with chloroform-methanol, which extracts glycolipids, decreased immunoreactivity in carcinoma tissues, particularly that in the cytosol. The extracts contained substances immunoreactive for MAb FH6. Our study has demonstrated that (a) remarkable changes occur in the ultrastructural localization patterns of sialyl Le(x)-i and Le(x) in renal cell carcinoma and (b) considerable amounts of glycolipids are contained in the substances with sialyl Le(x)-i deposited in the cytosol of clear-cell carcinoma.


2014 ◽  
Vol 8 (9-10) ◽  
pp. 744
Author(s):  
Hakan Öztürk ◽  
Serap Karaaslan

Metachronous adrenal metastasis from contralateral renal cell carcinoma (RCC) surgery is an extremely rare condition. Iatrogenic Addison’s disease occurring after metastasectomy (adrenalectomy) is an even rarer clinical entity. We present a case of a 68-year-old male with hematuria and left flank pain 9 years prior. The patient underwent left transperitoneal radical nephrectomy involving the ipsilateral adrenal glands due to a centrally-located, 75-mm in diameter solid mass lesion in the upper pole of the left kidney. The tumour lesion was confined within the renal capsule, and the histopathological examination revealed a Fuhrman nuclear grade II clear cell carcinoma. The patient underwent transperitoneal right adrenalectomy. The histopathological examination revealed metastasis of clear cell carcinoma. The patient was diagnosed with iatrogenic Addison’s disease based on the measurement of serum cortisol levels and the adrenocorticotropic hormone (ACTH) stimulation test, after which glucocorticoid and mineralocorticoid replacement was initiated. The patient did not have local recurrence or new metastasis in the first year of the follow-up. The decision to perform ipsilateral adrenalectomy during radical nephrectomy constitutes a challenge, and the operating surgeon must consider all these rare factors.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ken Ohnita ◽  
Shuntaro Higashi ◽  
Satoshi Hirai ◽  
Ai Kuwahara ◽  
Kana Kakigao ◽  
...  

Abstract Background Esophageal metastasis of renal cell carcinoma (RCC) is extremely rare. We have described herein a case of a 59-year-old man with esophageal metastasis of RCC that was endoscopically resected. Case presentation The case was a 59-year-old man who had undergone left nephrectomy for renal clear cell carcinoma 17 years ago and splenectomy for splenic metastasis 3 years ago. Esophagogastroduodenoscopy (EGD) performed 9 years ago revealed a small reddish elevated lesion with a smooth surface in the middle esophagus; this lesion increased in size 4 years ago. However, no biopsy was performed. The lesion continued to grow in size and was found to have become nodular during the present observation. Biopsy revealed clear cell carcinoma. Endoscopic ultrasound (EUS) revealed that the lesion had not invaded the submucosa, and contrast-enhanced computed tomography did not reveal any other metastasis. The lesion was successfully removed en bloc via endoscopic submucosal dissection (ESD). Pathologically, the tumor was detected in the subepithelium with focal infiltration of the muscularis mucosa. It consisted of monotonous cells with small nuclei and a clear cytoplasm. Immunohistological findings indicated that the tumor was a metastasis of RCC. The lateral and vertical margins were noted to be free. Conclusions We have presented herein a case of esophageal metastasis of RCC that had progressed over 9 years and was then resected en bloc through endoscopic submucosal dissection.


Sign in / Sign up

Export Citation Format

Share Document