Systemic therapy for sarcomatoid renal cell carcinoma

2011 ◽  
Vol 11 (6) ◽  
pp. 913-920 ◽  
Author(s):  
Lance C Pagliaro ◽  
Nizar Tannir ◽  
Kanishka Sircar ◽  
Eric Jonasch
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Systemic Therapy ◽  
Renal Cell ◽  
Sarcomatoid Renal Cell Carcinoma

scholarly journals Long-term progression-free survival of patients with metastatic melanoma or renal cell carcinoma following high-dose interleukin-2

2021 ◽  
Vol 69 (4) ◽  
pp. 888-892
Author(s):  
Joseph I Clark ◽  
Brendan Curti ◽  
Elizabeth J Davis ◽  
Howard Kaufman ◽  
Asim Amin ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Metastatic Melanoma ◽  
Systemic Therapy ◽  
Renal Cell ◽  
Interleukin 2 ◽  
Progression Free Survival ◽  
High Dose ◽  
Free Survival

High-dose interleukin-2 (HD IL-2) was approved in the 1990s after demonstrating durable complete responses (CRs) in some patients with metastatic melanoma (mM) and metastatic renal cell carcinoma (mRCC). Patients who achieve this level of disease control have also demonstrated improved survival compared with patients who progress, but limited data are available describing the long-term course. The aim of this study was to better characterize long-term survival following successful HD IL-2 treatment in patients with no subsequent systemic therapy. Eleven HD IL-2 treatment centers identified patients with survival ≥5 years after HD IL-2, with no subsequent systemic therapy. Survival was evaluated from the date of IL-2 treatment to June 2017. Treatment courses consisted of 2 1-week cycles of HD IL-2. Patients were treated with HD IL-2 alone, or HD IL-2 followed by local therapy to achieve maximal response. 100 patients are reported: 54 patients with mM and 46 patients with mRCC. Progression-free survival (PFS) after HD IL-2 ranges from 5+ years to 30+ years, with a median follow-up of 10+ years. 27 mRCC and 32 mM are alive ≥10 years after IL-2. Thus, a small subset of patients with mM and mRCC achieve long-term PFS (≥5 years) after treatment with HD IL-2 as their only systemic therapy. The ability of HD IL-2 therapy to induce prolonged PFS should be a major consideration in studies of new immunotherapy combinations for mM and mRCC.

Sarcomatoid renal cell carcinoma with foci of chromophobe carcinoma

2002 ◽  
Vol 8 (2) ◽  
pp. 142-144 ◽  
Author(s):  
Gábor Cserni ◽  
Rita Beáta Kovács ◽  
Miklós Tarján ◽  
Zoltán Sápi ◽  
Zsolt Domján ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Sarcomatoid Renal Cell Carcinoma

Response to systemic therapy in fumarate hydratase–deficient renal cell carcinoma

2021 ◽  
Vol 151 ◽  
pp. 106-114
Author(s):  
Lucia Carril-Ajuria ◽  
Emeline Colomba ◽  
Luigi Cerbone ◽  
Carmen Romero-Ferreiro ◽  
Laurence Crouzet ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Systemic Therapy ◽  
Renal Cell ◽  
Fumarate Hydratase

Sarcomatoid Renal Cell Carcinoma of Papillary Origin

2000 ◽  
Vol 124 (12) ◽  
pp. 1830-1832 ◽  
Author(s):  
Ronald J. Cohen ◽  
John E. McNeal ◽  
Marleen Susman ◽  
Loryn N. Sellner ◽  
Barry J. Iacopetta ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Clear Cell ◽  
Clear Cell Carcinoma ◽  
Conclusive Evidence ◽  
Clear Cell Tumor ◽  
Multiple Copies ◽  
Sarcomatoid Renal Cell Carcinoma ◽  
Trisomy 7

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.

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