Multifocal Renal Cortical Tumors: Frequency, Associated Clinicopathological Features and Impact on Survival

Richstone, Lee; Scherr, Douglas S.; Reuter, Vincent; Snyder, Mark E.; Rabbani, Farhang; Kattan, Michael W.; Russo, Paul

doi:10.1097/01.ju.0000106955.19813.f6

Cited by 97 publications

(80 citation statements)

References 20 publications

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“…Multifocal disease is present in 5 -21% of patients presenting with RCC in current series (18)(19)(20). The presence of multifocal disease on presentation does not impact survival in patients undergoing nephrectomy (19,20). Our data did suggest that clinically localized multifocal and solitary tumors have similar growth rates.…”

Section: Discussionsupporting

confidence: 59%

“…This is the first report to our knowledge that compares the growth rates of multifocal and solitary renal lesions under surveillance. Multifocal disease is present in 5 -21% of patients presenting with RCC in current series (18)(19)(20). The presence of multifocal disease on presentation does not impact survival in patients undergoing nephrectomy (19,20).…”

Section: Discussionmentioning

confidence: 99%

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Predicting growth of solid renal masses under active surveillance

Crispen

Wong

Greenberg

et al. 2008

Urologic Oncology: Seminars and Original Investigations

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Objectives-The natural history and growth rates of untreated solid enhancing renal tumors is being defined through active surveillance series. Serial radiographic evaluation of patients who are not surgical candidates or refuse surgical treatment provides an opportunity to characterize the growth of untreated enhancing renal tumors. Here we evaluate factors which may help predict for radiographic growth during observation.Methods and Materials-We reviewed our renal cancer database for enhancing renal masses that were radiographically observed for a period of at least 12 months. Variables examined included patient age, gender, lesion size on presentation, radiographic tumor characteristics, duration of active surveillance, linear growth rate, surgical pathology, development of new renal tumors, and stage progression.Results-109 patients with 124 sporadic enhancing renal tumors were identified undergoing a period of active surveillance of at least 12 months. Median patient age was 73 years (mean 69.8, range 35-87). 72% (78/109) of patients were males. Median duration of active surveillance was 26 months (mean 33.4, range 12-156). Multifocal disease was present in 9% (10/109) patients on presentation, accounting for 20% (25/124) of all tumors. Tumor size on presentation was a median of 2.0 cm (mean 2.61, range 0.4 -12.0). Overall median tumor growth rate was 0.21cm/yr (mean 0.28, range −1.4 -2.47). Observed linear growth rates were independent of patient age, gender, tumor size on presentation, multifocality, and radiographic characteristics (solid versus cystic), p > 0.05. Of the patients initiating a period of active surveillance 36% (39/109) eventually underwent definitive therapy. Malignant pathology was present in 90% (35/39) of patients undergoing treatment. In patients continuing active surveillance (64% (70/109)), 2.9% (2/70) developed de novo renal lesions and 1.4% (1/70) developed metastatic disease.Conclusions-Currently, no clinical predictors of tumor growth or disease progression have been identified; although, the risk of developing progressive disease over the short term appears low. Clinical and molecular markers of disease progression are needed prior to offering active surveillance to otherwise acceptable surgical candidates.

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Predicting growth of solid renal masses under active surveillance

Crispen

Wong

Greenberg

et al. 2008

Urologic Oncology: Seminars and Original Investigations

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“…Patients with multifocal CCRCCs have a higher risk of developing contralateral CCRCC, synchronously or metachronously, than patients with unilateral solitary CCRCCs (16,17). The presence of multifocality does not correlate with a significantly increased risk of cancer progression and metastasis, a finding that argues against the likelihood of intrarenal metastasis as an explanation for this finding in such cases (7,17,18).…”

contrasting

confidence: 44%

Evidence for Polyclonal Origin of Multifocal Clear Cell Renal Cell Carcinoma

Liu

MacLennan

Zhang³

et al. 2008

Clinical Cancer Research

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Purpose: Renal cell carcinomas are often multifocal. We investigated the genomic signatures of multifocal clear cell renal cell carcinoma to determine whether multiple tumors in the same kidney bear a clonal relationship to one another. Experimental Design: A total of 62 tumors from 26 patients who underwent radical nephrectomy were examined. All patients had multiple separate clear cell renal carcinomas. Loss of heterozygosity analyses were done using five microsatellite polymorphic markers that represent putative tumor suppressor genes on chromosome 3p14 (D3S1300), 7q31 (D7S522), 8p22 (D8S261), 9p21 (D9S171), and 17p13 (TP53). X chromosome inactivation analyses were also done on the renal tumors from the 10 female patients. Chromosome 3p deletion status was determined by dual color interphase fluorescence in situ hybridization analysis in all tumors. Results: Nineteen of the 26 (73%) patients with multifocal clear cell renal cell carcinoma showed allelic loss in at least 1of 5 microsatellite loci in separate tumors analyzed. A disconcordant pattern of allelic loss between coexisting kidney tumors was observed in 7 cases. Six cases showed discordant 3p deletion patterns by dual color interphase fluorescence in situ hybridization analysis. Of the eight informative female cases studied by X chromosome inactivation, one showed a discordant nonrandom pattern of X chromosome inactivation. Overall, evidence of independent origin of the multifocal renal tumors was observed in 12 of 26 cases (46%). Conclusions: Our data suggest that in a significant number of cases of multifocal clear cell renal cell carcinoma, the spatially separate tumors are of different clonal origin and arise independently.

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“…The literature contends that as many as 5% of renal CCs may be multifocal. 11,12 However, the concept of retrograde venous extension in renal CC may not have been considered in these studies. As cortical veins lack a smooth muscle media, it is difficult on histologic grounds to investigate this possibility except for microscopic foci.…”

Section: Renal Sinus Involvement In Clear Cell Renal CCmentioning

confidence: 99%

Renal veins and venous extension in clear cell renal cell carcinoma

Bonsib

2007

Modern Pathology

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The 2002 TNM formulation defines a pT3b tumor as one that 'extends into the renal vein or its segmental (muscle containing) branches.' This definition elicits uncertainty when veins with little muscle are involved or the relationship to the main renal vein is unknown. The diameter and medial thickness of 10 normal renal venous systems were studied and compared to sinus veins involved in 54 pT3b clear cell renal cell carcinomas (CC). All tumors were grossly examined and sampled for histology by the author. An immunoperoxidase cocktail containing CD 31 and actin, Masson trichrome and elastic stains were employed to aid identification of intravenous tumor. The venous dissections showed variable numbers of primary and secondary divisions with substantial overlap in diameter and medial thickness. The medial thickness decreased with each proximal division and ranged from being nonexistent to being thick. Study of the 54 pT3b CC revealed that the initial phase of extrarenal extension involved large caliber veins draining the primary tumor. With extensive venous involvement, tumor invaded through the vein wall into sinus fat or demonstrated retrograde venous extension into adjacent cortex. Correlation between gross and histology revealed that most nodules of tumor within the sinus fat contained evidence of pre-existing veins. The following observations were made: (1) the diameter of a sinus vein or the quantity of muscle is a poor indicator of vein segment or relationship to the main renal vein; therefore, the wording used to define pT3b should be clarified; (2) extrarenal spread in CC begins with intravenous extension whereas sinus fat invasion is usually secondary; (3) retrograde venous extension occurs in cases with massive renal vein involvement; and (4) nodules within the sinus fat usually represent venous involvement. Modern Pathology (2007) 20, 44-53.

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Multifocal Renal Cortical Tumors: Frequency, Associated Clinicopathological Features and Impact on Survival

Abstract: We report a 5.3% frequency of multifocal renal cortical tumors and a 3.5% frequency of clinically unsuspected multifocal tumors. Multifocality had no apparent effect on recurrence or survival in patients who underwent radical nephrectomy.

Cited by 97 publications

References 20 publications

Predicting growth of solid renal masses under active surveillance

Predicting growth of solid renal masses under active surveillance

Evidence for Polyclonal Origin of Multifocal Clear Cell Renal Cell Carcinoma

Renal veins and venous extension in clear cell renal cell carcinoma

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