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• W2004103067 abstract "We report a rare case of regression of metastatic renal cell cancer after stopping treatment with the tyrosine kinase inhibitor sunitinib. The 63-year-old female patient was diagnosed with primary metastatic clear cell renal cell cancer in December 2007. She was found to have a right renal tumour with invasion of the right renal vein and the vena cava, bilateral adrenal metastases, multiple lung metastases and a solitary lytic bone metastasis in the left 10th rib laterally. The patient was treated with sunitinib 50 mg 4 weeks on/2 weeks off starting in January 2008. A computed tomography (CT) scan after 4 weeks of treatment showed decrease in size of all involved tumour sites. Response to treatment was maintained and last seen on a CT scan in August 2008. In November 2008, obvious disease progression was demonstrated on CT with progression of the primary tumour, both adrenal metastases and the lung metastases and new mediastinal lymph-node metastases (Figures 1 and 2).Figure 2Kidney tumour.View Large Image Figure ViewerDownload (PPT) Treatment was therefore stopped and the patient was considered for participation in the expanded access trial with RAD001, a novel orally available mammalian target of rapamycin inhibitor. At this time, she was symptomatic from the bone metastasis in her rib and fatigue. A screening CT scan was carried out for trial purposes at the end of December 2008, which at this point revealed disease regression in all tumour locations—the right kidney (6.3–4.2 cm), both adrenals (3.7–1.5 cm and 2.8–1.7 cm), lymph nodes and the lung—compared with the scan from November 2008. We decided not to treat the patient systemically and postponed enrolment on the trial and adopted an active surveillance approach. A repeat CT evaluation in mid-February 2009 (Figures 3 and 4) confirmed disease regression in the lung and the right kidney.Figure 4Disease regression in the right kidney.View Large Image Figure ViewerDownload (PPT) Fatigue has resolved since stopping sunitinib. Due to persisting pain in the 10th rib, we have decided to give palliative analgetic radiotherapy to this site and continue the active surveillance strategy otherwise. Spontaneous regression in renal cell cancer is a well-recognised phenomenon and has been reported before [1.Bumpus H.C. The apparent disappearance of pulmonary metastasis in a case of hypernephroma following nephrectomy.J Urol. 1928; 20: 185-191Crossref Google Scholar]. In many case reports of the so-called spontaneous regression, the primary tumour is surgically removed [2.Lekanidi K. Vlachou P.A. Morgan B. et al.Spontaneous regression of metastatic renal cell carcinoma: case report.J Med Case Reports. 2007; 1: 89Crossref PubMed Scopus (22) Google Scholar], irradiated [3.MacManus M.P. Harte R.J. Stranex S. Spontaneous regression of metastatic renal cell carcinoma following palliative irradiation of the primary tumor.Ir J Med Sci. 1994; 163: 461-463Crossref PubMed Scopus (34) Google Scholar] or ablated [4.Sánchez-Ortiz R.F. Tannir N. Ahrar K. et al.Spontaneous regression of pulmonary metastases from renal cell carcinoma after radio frequency ablation of the primary tumor: an in situ tumor vaccine?.J Urol. 2003; 170: 178-179Crossref PubMed Scopus (88) Google Scholar], but elimination of the primary tumour does not seem to be necessary since regressions are also reported in the absence of nephrectomy or other primary tumour manipulations [5.Lokich J. Spontaneous regression of metastatic renal cancer. Case report and literature review.Am J Clin Oncol. 1997; 20: 416-418Crossref PubMed Scopus (109) Google Scholar]. The mechanism underlying spontaneous regression in renal cell cancer patients remains unclear, although immunologic effects as a basis of this phenomenon have been postulated. Regression of metastatic clear cell renal cell carcinoma without active treatment and after progression on treatment with a tyrosine kinase inhibitor has not been reported before. In contrary, discontinuation of vascular endothelial growth factor (VEGF) inhibition has been feared to accelerate angiogenesis and tumour growth due to simultaneous induction of VEGF and other proangiogenic pathways. And there is preclinical evidence to support this theory [6.Mancuso M.R. Davis R. Norberg S.M. et al.Rapid vascular regrowth in tumors after reversal of VEGF inhibition.J Clin Invest. 2006; 116: 2610-2621Crossref PubMed Scopus (691) Google Scholar]. The key and ongoing role of VEGF in angiogenesis provided the rationale for continuous anti-VEGF therapy until, and possibly beyond, disease progression [7.Tobelem G. VEGF: a key therapeutic target for the treatment of cancer—insights into its role and pharmacological inhibition.Targeted Oncology. 2007; 2: 153-164Crossref Scopus (12) Google Scholar]. However, it may be hypothesised that in our case either stopping the tyrosine kinase inhibitor had a positive effect or spontaneous regression occurred. In analogy to prostate cancer, where androgen receptor mutant forms can proliferate and avoid apoptosis by using antiandrogens as substitute for androgens [8.Zhao X.Y. Malloy P.J. Krishnan A.V. et al.Glucocorticoids can promote androgen-independent growth of prostate cancer cells through a mutated androgen receptor.Nat Med. 2000; 6: 703-706Crossref PubMed Scopus (438) Google Scholar] and withdrawal of these antiandrogens can promote disease regression, VEGF and platelet-derived growth factor receptor mutations or subtle modifications may occur in renal cell cancer and initiate a switch from antagonicity to agonicity. There is also a complex crosstalk between VEGF receptors and it is perceivable that interfering with these regulatory mechanisms can have anti- as well as proangiogenic effects. In our case, the CT scan was only carried out for trial requirements and we would have attributed the regression to treatment with RAD001 without this repeat imaging. Such regressions may very well occur more frequently but remain undetected due to instant initiation of a second-line therapy without new staging since so many treatment options in renal cell cancer are available now." @default.
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• W2004103067 date "2009-06-01" @default.
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• W2004103067 title "‘Sunitinib withdrawal phenomenon’ or spontaneous regression in renal cell cancer" @default.
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• W2004103067 doi "https://doi.org/10.1093/annonc/mdp239" @default.
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