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[Title] Identification of fatty acid binding proteins as markers associated with the initiation and/or progression of renal cell carcinoma.

Renal cell carcinoma (RCC) representing the most common neoplasia of the kidney in Western countries is a histologic diverse disease with an often unpredictable course.

The prognosis of RCC is worsened with the onset of metastasis, and the therapies currently available are of limited success for the treatment of metastatic RCC.

Although gene expression analyses and other methods are promising tools clarifying and standardizing the pathological classification of RCC, novel innovative molecular markers for the diagnosis, prognosis, and for the monitoring of this disease during therapy as well as potential therapeutic targets are urgently needed.

Using proteome-based strategies, a number of RCC-associated markers either over-expressed or down-regulated in tumor lesions in comparison to the normal epithelium have been identified which have been implicated in tumorigenesis, but never linked to the initiation and/or progression of RCC.

These include members of the fatty acid binding protein family, which have the potential to serve as diagnostic or prognostic markers for the screening of RCC patients.

[MeSH-major] Carcinoma, Renal Cell / physiopathology. Carrier Proteins / analysis. Kidney Neoplasms / physiopathology

[MeSH-minor] Biomarkers, Tumor / analysis. Biomarkers, Tumor / isolation & purification. Cell Line, Tumor. DNA Primers. Disease Progression. Electrophoresis, Gel, Two-Dimensional / methods. Fatty Acid-Binding Proteins. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Kidney. Prognosis. Reference Values. Reverse Transcriptase Polymerase Chain Reaction. Urothelium / chemistry. Urothelium / metabolism

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(PMID = 15892167.001).

[ISSN] 1615-9853

[Journal-full-title] Proteomics

[ISO-abbreviation] Proteomics

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / DNA Primers; 0 / Fatty Acid-Binding Proteins

   

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[Title] A man with changes in the urinary bladder: benign metaplasia or adenocarcinoma?

[MeSH-major] Adenocarcinoma / diagnosis. Cystitis / diagnosis. Kidney Neoplasms / diagnosis. Lymphatic Diseases / pathology

[MeSH-minor] Adult. Diagnosis, Differential. Humans. Male. Metaplasia. Nephrolithiasis / complications. Referral and Consultation

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(PMID = 19323300.001).

[ISSN] 0890-9091

[Journal-full-title] Oncology (Williston Park, N.Y.)

[ISO-abbreviation] Oncology (Williston Park, N.Y.)

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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[Title] Invasion of renal sinus fat is not an independent predictor of survival in pT3a renal cell carcinoma.

OBJECTIVE: To clarify the significance of the location of extrarenal tumour extension of renal cell carcinoma (RCC) as in the 2002 Tumour-Nodes-Metastasis classification.

Renal cortical tumours with perirenal fat invasion (PFI) or sinus fat invasion (SFI) are consolidated within the pT3a grouping; tumours with SFI are close to the renal veins, lymphatics and the collecting system.

This might carry a worse prognosis for disease-specific survival (DSS), but reports are limited and contradictory.

PATIENTS AND METHODS: We retrospectively reviewed 1244 patients treated with nephrectomy from 1988 to 2007, to identify patients with pT3a renal tumours.

CONCLUSION: Patients with renal tumours with SFI are more likely to die from RCC than those with PFI.

[MeSH-major] Adipose Tissue / pathology. Carcinoma, Renal Cell / pathology. Kidney Neoplasms / pathology. Kidney Pelvis / pathology

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(PMID = 19154464.001).

[ISSN] 1464-410X

[Journal-full-title] BJU international

[ISO-abbreviation] BJU Int.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

   

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[Title] Efficacy and safety of sorafenib in patients with advanced renal cell carcinoma with and without prior cytokine therapy, a subanalysis of TARGET.

Before the development of targeted therapies, administration of cytokines (e.g., interleukin-2, interferon-alpha) was the primary systemic treatment option for advanced renal cell carcinoma.

Sorafenib, an oral targeted, multikinase inhibitor, significantly prolonged progression-free survival and overall survival in the Treatment Approaches in Renal Cancer Global Evaluation Trial (TARGET), a large (N = 903) phase III, double-blind, randomised, placebo-controlled study of patients with advanced renal cell carcinoma resistant to standard therapy.

Sorafenib demonstrated a consistent, significant clinical benefit against advanced renal cell carcinoma, with a twofold improvement in progression-free survival and disease control rate, with similar toxicities in patients with or without prior cytokine treatment.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Renal Cell / drug therapy. Kidney Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use

[MeSH-minor] Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / adverse effects. Benzenesulfonates / administration & dosage. Benzenesulfonates / adverse effects. Cardiovascular Diseases / chemically induced. Diarrhea / chemically induced. Disease-Free Survival. Double-Blind Method. Female. Hematologic Diseases / chemically induced. Humans. Interferon-alpha / administration & dosage. Interferon-alpha / adverse effects. Interleukin-2 / administration & dosage. Interleukin-2 / adverse effects. Kaplan-Meier Estimate. Male. Middle Aged. Niacinamide / analogs & derivatives. Phenylurea Compounds. Progestins / administration & dosage. Progestins / adverse effects. Pyridines / administration & dosage. Pyridines / adverse effects. Treatment Outcome. Vinca Alkaloids / administration & dosage. Vinca Alkaloids / adverse effects

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[Cites] J Clin Oncol. 2007 Aug 1;25(22):3296-301 [17664477.001]

[Cites] Cancer Res. 2004 Oct 1;64(19):7099-109 [15466206.001]

[Cites] Nature. 1999 May 20;399(6733):271-5 [10353251.001]

[Cites] Lancet. 1998 Nov 21;352(9141):1691-6 [9853456.001]

[Cites] J Clin Oncol. 1999 Jul;17 (7):2039-43 [10561255.001]

[Cites] N Engl J Med. 1996 Sep 19;335(12):865-75 [8778606.001]

[Cites] Ann Oncol. 2006 Aug;17(8):1185-96 [16418310.001]

[Cites] Clin Cancer Res. 2004 Sep 15;10 (18 Pt 2):6388S-92S [15448036.001]

[Cites] Semin Oncol. 2006 Oct;33(5):527-33 [17045081.001]

[Cites] N Engl J Med. 2007 Jan 11;356(2):125-34 [17215530.001]

[Cites] Nat Genet. 1994 May;7(1):85-90 [7915601.001]

[Cites] J Clin Oncol. 1999 Aug;17(8):2530-40 [10561319.001]

[Cites] Mol Cancer Ther. 2008 Oct;7(10 ):3129-40 [18852116.001]

[Cites] Curr Treat Options Oncol. 2001 Oct;2(5):437-45 [12057107.001]

[Cites] Nat Clin Pract Urol. 2006 Sep;3(9):478-84 [16964189.001]

[Cites] J Clin Oncol. 2009 Jul 10;27(20):3312-8 [19451442.001]

[Cites] N Engl J Med. 1998 Apr 30;338(18):1265-71 [9562580.001]

[Cites] J Clin Oncol. 1995 Mar;13(3):688-96 [7884429.001]

[Cites] N Engl J Med. 1998 Apr 30;338(18):1272-8 [9562581.001]

[Cites] J Clin Oncol. 2007 Aug 1;25(22):3288-95 [17664476.001]

[Cites] Cancer Res. 2003 Oct 1;63(19):6130-4 [14559790.001]

[Cites] Semin Oncol. 2000 Apr;27(2):124-37 [10768592.001]

[Cites] Nat Clin Pract Urol. 2007 Apr;4(4):205-17 [17415353.001]

[Cites] Blood. 2006 Aug 15;108(4):1374-6 [16645167.001]

[Cites] Ann Oncol. 2002 Sep;13(9):1460-8 [12196373.001]

[Cites] J Clin Oncol. 1996 Aug;14(8):2410-1 [8708739.001]

[Cites] J Clin Oncol. 2000 May;18(9):1928-35 [10784634.001]

[Cites] J Clin Oncol. 2003 Nov 1;21(21):3987-94 [14581421.001]

[Cites] Cochrane Database Syst Rev. 2005 Jan 25;(1):CD001425 [15674877.001]

(PMID = 19757215.001).

[ISSN] 1559-131X

[Journal-full-title] Medical oncology (Northwood, London, England)

[ISO-abbreviation] Med. Oncol.

[Language] eng

[Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial

[Publication-country] United States

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Benzenesulfonates; 0 / Interferon-alpha; 0 / Interleukin-2; 0 / Phenylurea Compounds; 0 / Progestins; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 0 / Vinca Alkaloids; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib

   

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[Title] [Systemic therapy of metastatic renal cell carcinoma].

Cytokine-based immunotherapy was the only viable option in metastatic, nonresectable renal cell carcinoma (RCC) for many years.

In this context, interleukin-2 (IL-2) and interferon-alpha (IFN-alpha) turned out to be the most effective single agents in RCC.

Such small molecules like tyrosine kinase inhibitors, monoclonal antibodies, or the mTOR inhibitor CCI-779 may dramatically change the established concepts of systemic RCC treatment.

This paper gives an overview of established, current, and evolving concepts of systemic therapy in RCC.

[MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Renal Cell / drug therapy. Carcinoma, Renal Cell / secondary. Drug Delivery Systems / methods. Immunotherapy / methods. Kidney Neoplasms / drug therapy

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[Cites] Cancer Chemother Pharmacol. 2006 Apr;57(4):533-9 [16052341.001]

[Cites] N Engl J Med. 2001 Dec 6;345(23 ):1655-9 [11759643.001]

[Cites] Invest New Drugs. 2006 Jan;24(1):85-8 [16380835.001]

[Cites] N Engl J Med. 1996 Sep 19;335(12):865-75 [8778606.001]

[Cites] Br J Urol. 1995 May;75(5):586-9 [7613793.001]

[Cites] Urologe A. 2002 May;41(3):282-7 [12132280.001]

[Cites] Semin Oncol. 2000 Apr;27(2):177-86 [10768596.001]

[Cites] J Clin Oncol. 2005 Nov 1;23(31):7889-96 [16204015.001]

[Cites] Lancet. 2001 Sep 22;358(9286):966-70 [11583750.001]

[Cites] Semin Oncol. 1991 Oct;18(5 Suppl 7):108-12 [1948123.001]

[Cites] Eur Urol. 2006 Jan;49(1):76-81 [16310929.001]

[Cites] Cancer. 2004 Oct 1;101(7):1545-51 [15378501.001]

[Cites] J Clin Oncol. 2002 Jan 1;20(1):289-96 [11773181.001]

[Cites] Curr Treat Options Oncol. 2003 Oct;4(5):385-90 [12941198.001]

[Cites] Br J Cancer. 2004 Mar 8;90(5):985-90 [14997194.001]

[Cites] J Clin Oncol. 2005 Jan 1;23 (1):133-41 [15625368.001]

[Cites] J Urol. 2004 Jun;171(6 Pt 1):2176-80 [15126780.001]

[Cites] N Engl J Med. 2003 Jul 31;349(5):427-34 [12890841.001]

[Cites] Urologe A. 2006 Mar;45(3):328, 330-5 [16465522.001]

[Cites] J Clin Oncol. 1999 Sep;17 (9):2859-67 [10561363.001]

[Cites] Presse Med. 1987 Nov 21;16(39):1953-6 [2962158.001]

[Cites] J Clin Oncol. 2004 Mar 1;22(5):909-18 [14990647.001]

[Cites] J Clin Oncol. 2006 Jan 1;24(1):16-24 [16330672.001]

[Cites] Br J Cancer. 2005 Mar 14;92 (5):843-6 [15756254.001]

[Cites] Cochrane Database Syst Rev. 2005 Jan 25;(1):CD001425 [15674877.001]

(PMID = 16622645.001).

[ISSN] 0340-2592

[Journal-full-title] Der Urologe. Ausg. A

[ISO-abbreviation] Urologe A

[Language] ger

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Germany

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents

[Number-of-references] 35

   

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[Title] Stauffer's syndrome with jaundice, a paraneoplastic manifestation of renal cell carcinoma: a case report.

OBJECTIVE: To report an infrequent case of Stauffer's Syndrome with jaundice as a paraneoplastic syndrome of a metastatic renal cancer.

METHODS: We describe the set up of cholestatic jaundice without neoplastic liver infiltration in a patient with a metastatic renal cell carcinoma, which turned back with surgery and systemic treatment.

RESULTS: Proper treatment of baseline disease enables turn back paraneoplastic signs and symptoms of Stauffer's Syndrome.

CONCLUSIONS: Reversible cholestatic jaundice without evidence of hepatic disease is an infrequent form of the Stauffer's syndrome.

This paraneoplastic syndrome is associated particularly with renal carcinoma but was described in lymphoproliferative diseases, prostate cancer and broncogenic tumors.

[MeSH-major] Carcinoma, Renal Cell / complications. Jaundice, Obstructive / etiology. Kidney Neoplasms / complications. Paraneoplastic Syndromes / etiology

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(PMID = 20378939.001).

[ISSN] 1576-8260

[Journal-full-title] Archivos españoles de urología

[ISO-abbreviation] Arch. Esp. Urol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Spain

   

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[Title] Robot-assisted extraperitoneal radical prostatectomy in a patient with a pelvic kidney.

The ectopic position of a pelvic kidney can present a unique challenge to the success of robot-assisted radical prostatectomy while preserving function in the kidney.

We describe our experience of performing extraperitoneal robot-assisted radical prostatectomy in a patient with a pelvic kidney.

[MeSH-major] Adenocarcinoma / surgery. Kidney / abnormalities. Prostatectomy / methods. Prostatic Neoplasms / surgery. Robotics

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(PMID = 17095077.001).

[ISSN] 1527-9995

[Journal-full-title] Urology

[ISO-abbreviation] Urology

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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[Title] Recent advances in the therapy of renal cancer.

Metastatic clear cell renal cell cancer has traditionally been treated with cytokines (interferon or interleukin-2).

Vascular endothelial growth factor, the related receptor and the mTOR signal transduction pathway have particularly been exploited.

The future of the therapy of renal cancer appears promising owing to the efficacy of these novel agents.

[MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Renal Cell / drug therapy. Kidney Neoplasms / drug therapy

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(PMID = 17250461.001).

[ISSN] 1744-7682

[Journal-full-title] Expert opinion on biological therapy

[ISO-abbreviation] Expert Opin Biol Ther

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents

[Number-of-references] 68

   

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[Title] Neuroendocrine breast carcinoma metastatic to renal cell carcinoma and ipsilateral adrenal gland.

We report on a 60-year-old woman with neuroendocrine carcinoma of the left breast metastasizing to renal cell carcinoma (RCC) of the left kidney and to adrenal gland.

A yellow, well-circumscribed tumor, 11 cm in largest diameter and limited to the kidney, was found.

Histopathology revealed RCC with foci of neuroendocrine differentiation.

Solid sheets of hyperchromatic epithelioid cells with high mitotic activity were found between typical clear cells of RCC.

These cells were CAM5,2 and E-cadherin focally positive, synaptophysin and NSE weakly positive, CK19 moderately positive, and AE1-AE3 and EMA strongly positive.

The left adrenal gland contained multiple, separate foci of a tumor composed of neuroendocrine components.

Because of the biphasic tumor in the kidney, extensive clinical examination and further analyses were recommended.

Tumor in the left breast was revealed.

The tumor was histologically and immunohistochemically similar to the neuroendocrine component within RCC.

To our knowledge, this is the first case of neuroendocrine breast carcinoma with metastasis to renal cell carcinoma and ipsilateral adrenal gland.

[MeSH-major] Breast Neoplasms / pathology. Carcinoma, Neuroendocrine / secondary. Carcinoma, Renal Cell / pathology. Kidney Neoplasms / pathology. Neoplasms, Multiple Primary / pathology

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(PMID = 18538946.001).

[ISSN] 0344-0338

[Journal-full-title] Pathology, research and practice

[ISO-abbreviation] Pathol. Res. Pract.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

   

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[Title] Identification of membrane type-1 matrix metalloproteinase as a target of hypoxia-inducible factor-2 alpha in von Hippel-Lindau renal cell carcinoma.

Metastatic renal cell carcinoma (RCC) resulting from the hereditary loss of the von Hippel-Lindau (VHL) tumor suppressor gene is the leading cause of death in VHL patients due to the deleterious effects of the metastatic tumor(s).

The process of tumor invasion and metastasis involves the destruction of the extracellular matrix, which is accomplished primarily by the matrix metalloproteinase (MMP) family of enzymes.

Here, we describe a connection between the loss of VHL tumor suppressor function and the upregulation of membrane type-1 MMP (MT1-MMP) gene expression and protein.

Specifically, MT1-MMP is upregulated in VHL-/- RCC cells through an increase in gene transcription, which is mediated by the cooperative effects of the transcription factors, HIF-2 and Sp1.

To our knowledge, this is the first report to show direct regulation of MT1-MMP by HIF-2 and to provide a direct link between the loss of VHL tumor suppressor function and an increase in MMP gene and protein expression.

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[Cites] Trends Mol Med. 2004 Sep;10(9):466-72 [15350900.001]

[Cites] J Urol. 1999 Sep;162(3 Pt 1):905-9 [10458406.001]

[Cites] J Biol Chem. 1995 Mar 10;270(10):5331-8 [7890645.001]

[Cites] Nat Med. 1995 Aug;1(8):822-6 [7585187.001]

[Cites] J Biol Chem. 1996 Jul 26;271(30):17771-8 [8663540.001]

[Cites] Genes Dev. 1997 Jan 1;11(1):72-82 [9000051.001]

[Cites] Medicine (Baltimore). 1997 Nov;76(6):381-91 [9413424.001]

[Cites] Mech Dev. 1998 Apr;73(1):117-23 [9545558.001]

[Cites] J Intern Med. 1998 Jun;243(6):527-33 [9681854.001]

[Cites] Biochem J. 1998 Sep 1;334 ( Pt 2):345-53 [9716492.001]

[Cites] Blood. 1998 Oct 1;92(7):2260-8 [9746763.001]

[Cites] Nature. 1999 May 20;399(6733):271-5 [10353251.001]

[Cites] Nucleic Acids Res. 1999 Sep 1;27(17):3402-9 [10446226.001]

[Cites] Gene. 2000 Jan 25;242(1-2):75-86 [10721699.001]

[Cites] J Cell Biol. 2000 Jun 12;149(6):1309-23 [10851027.001]

[Cites] Curr Opin Cell Biol. 2001 Oct;13(5):534-40 [11544020.001]

[Cites] Br J Cancer. 2001 Sep 14;85(6):881-90 [11556841.001]

[Cites] Surv Ophthalmol. 2001 Sep-Oct;46(2):117-42 [11578646.001]

[Cites] Neth J Med. 2001 Nov;59(5):225-34 [11705642.001]

[Cites] Nat Rev Cancer. 2002 Jan;2(1):38-47 [11902584.001]

[Cites] Nat Rev Cancer. 2002 Mar;2(3):161-74 [11990853.001]

[Cites] Carcinogenesis. 2002 May;23(5):769-76 [12016149.001]

[Cites] Cancer Cell. 2002 Apr;1(3):237-46 [12086860.001]

[Cites] Cancer Cell. 2002 Apr;1(3):247-55 [12086861.001]

[Cites] EMBO J. 2002 Aug 1;21(15):3949-59 [12145196.001]

[Cites] Nat Rev Cancer. 2002 Sep;2(9):673-82 [12209156.001]

[Cites] J Biol Chem. 2002 Oct 11;277(41):38737-45 [12138160.001]

[Cites] J Biol Chem. 2002 Nov 15;277(46):43799-808 [12228247.001]

[Cites] Cancer Lett. 2003 May 8;194(1):1-11 [12706853.001]

[Cites] Circ Res. 2003 May 2;92(8):827-39 [12730128.001]

[Cites] Stem Cells. 2003;21(3):337-47 [12743328.001]

[Cites] Cell. 2003 Jul 11;114(1):33-45 [12859896.001]

[Cites] Nature. 2003 Sep 18;425(6955):307-11 [13679920.001]

[Cites] Oncogene. 2003 Sep 29;22(42):6524-36 [14528277.001]

[Cites] J Urol. 2003 Dec;170(6 Pt 1):2163-72 [14634372.001]

[Cites] Oncogene. 2003 Nov 27;22(54):8716-22 [14647466.001]

[Cites] J Mol Biol. 2004 Feb 6;336(1):9-24 [14741200.001]

[Cites] J Invest Dermatol. 2004 Jan;122(1):167-76 [14962105.001]

[Cites] Mol Cancer Res. 2004 Feb;2(2):89-95 [14985465.001]

[Cites] PLoS Biol. 2003 Dec;1(3):E83 [14691554.001]

[Cites] Cancer Res. 2004 Apr 1;64(7):2534-43 [15059909.001]

[Cites] J Biol Chem. 2004 Apr 9;279(15):15025-31 [14742449.001]

[Cites] Mol Vis. 2004 May 17;10:341-50 [15162095.001]

[Cites] Clin Cancer Res. 2004 Jun 15;10(12 Pt 1):4038-47 [15217936.001]

[Cites] Mol Cell Biol. 1999 Sep;19(9):5902-12 [10454537.001]

[Cites] Nature. 1994 Jul 7;370(6484):61-5 [8015608.001]

(PMID = 15592504.001).

[ISSN] 0950-9232

[Journal-full-title] Oncogene

[ISO-abbreviation] Oncogene

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA-77267; United States / NCI NIH HHS / CA / R01 CA077267; United States / NIAMS NIH HHS / AR / AR-26599; United States / NIAMS NIH HHS / AR / R01 AR026599; United States / NIAMS NIH HHS / AR / R37 AR026599; United States / NIAID NIH HHS / AI / T32 AI007363

[Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.

[Publication-country] England

[Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Trans-Activators; 0 / Tumor Suppressor Proteins; 0 / endothelial PAS domain-containing protein 1; EC 3.4.24.- / Matrix Metalloproteinases, Membrane-Associated; EC 3.4.24.- / Metalloendopeptidases; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein

[Other-IDs] NLM/ NIHMS15822; NLM/ PMC1847637

   

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[Title] Preoperative prognostic nomogram (probability table) for renal cell carcinoma based on TNM classification.

PURPOSE: Recently several prognostic nomograms have been developed to predict the prognosis of malignant diseases, including renal cell carcinoma.

However, to our knowledge a preoperative prognostic nomogram that predicts survival in patients with renal cell carcinoma is not available.

We developed a preoperative nomogram based on the TNM classification that predicts cause specific survival in patients with renal cell carcinoma.

MATERIALS AND METHODS: A total of 545 patients with renal cell carcinoma, including metastatic disease, who underwent radical nephrectomy or nephron sparing surgery at our institution were included in the study.

Cases were staged according to the 2002 UICC TNM system, 6th edition.

CONCLUSIONS: The preoperative information shown by this nomogram may be important for obtaining informed consent from patients with renal cell carcinoma who have indications for surgery.

[MeSH-major] Carcinoma, Renal Cell / mortality. Carcinoma, Renal Cell / pathology. Kidney Neoplasms / mortality. Kidney Neoplasms / pathology. Neoplasm Invasiveness / pathology. Nomograms

[MeSH-minor] Aged. Aged, 80 and over. Cohort Studies. Confidence Intervals. Disease-Free Survival. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Nephrectomy / methods. Nephrectomy / mortality. Predictive Value of Tests. Preoperative Care / methods. Probability. Prognosis. Proportional Hazards Models. Retrospective Studies. Risk Assessment. Sensitivity and Specificity. Survival Rate. Treatment Outcome

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(PMID = 19100568.001).

[ISSN] 1527-3792

[Journal-full-title] The Journal of urology

[ISO-abbreviation] J. Urol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Dysregulation of kallikrein-related peptidases in renal cell carcinoma: potential targets of miRNAs.

Renal cell carcinoma (RCC) accounts for 3% of all adult malignancies and currently no diagnostic marker exists.

Kallikrein-related peptidases (KLKs) have been implicated in numerous cancers including ovarian, prostate, and breast carcinoma.

KLKs 5, 6, 10, and 11 have decreased expression in RCC when compared to normal kidney tissue.

Our bioinformatic analysis indicated that the KLK 1, 6, and 7 genes have decreased expression in RCC.

We experimentally verified these results and found that decreased expression of KLKs 1 and 3 were significantly associated with the clear cell RCC subtype (p<0.001).

An analysis of miRNAs differentially expressed in RCC showed that 61 of the 117 miRNAs that were reported to be dysregulated in RCC were predicted to target KLKs.

Transfection of miR-224 into HEK-293 cells resulted in decreased KLK1 protein levels.

A luciferase assay demonstrated that hsa-let-7f can target KLK10 in the RCC cell line ACHN.

Our results, showing differential expression of KLKs in RCC, suggest that KLKs could be novel diagnostic markers for RCC and that their dysregulation could be under miRNA control.

[MeSH-major] Carcinoma, Renal Cell / metabolism. Kallikreins / metabolism. Kidney Neoplasms / metabolism. MicroRNAs / metabolism

[MeSH-minor] Biomarkers, Tumor / metabolism. Chromosome Aberrations. Computational Biology. Evolution, Molecular. Gene Expression Regulation, Neoplastic. Humans. Phylogeny. Reproducibility of Results

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(PMID = 20180642.001).

[ISSN] 1437-4315

[Journal-full-title] Biological chemistry

[ISO-abbreviation] Biol. Chem.

[Language] eng

[Grant] Canada / Canadian Institutes of Health Research / / 86490

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MicroRNAs; EC 3.4.21.- / Kallikreins

   

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[Title] Histologic predictors of renal cell carcinoma response to interleukin-2-based therapy.

The authors examined pathology from patients with renal cancer (RCC) treated with IL-2 to determine response rates for clear cell and variant RCC and to identify histologic features that predict response.

Of 163 primary RCCs, the response rate was 21% (30/146) for patients with clear cell versus 6% (1/17) for patients with variant or indeterminate type RCC (P = 0.20).

For clear cell carcinomas, response to IL-2 was associated with the presence of alveolar features and the absence of papillary and granular features.

Patients with more than 50% alveolar features and no granular or papillary features had a 39% response rate (14/36).

Patients with alveolar and granular features representing less than 50% of the specimen and no papillary features had a 19% response rate (15/77).

Response rates in the three prognostic groups and for patients with non-clear cell cancers were 25% (5/20), 9% (2/22), 0% (0/16), and 0% (0/10), respectively.

Median survivals for all patients with clear cell tumors by risk group were 2.87, 1.36, and 0.87 years, respectively (P < 0.001).

These data suggest that patients with non-clear cell RCC or with clear cell RCC with papillary, no alveolar, and/or more than 50% granular features respond poorly to IL-2 and should be considered for alternative treatments.

Investigation of other tumor-related predictors of IL-2 responsiveness is warranted.

[MeSH-major] Carcinoma, Renal Cell / pathology. Carcinoma, Renal Cell / therapy. Immunotherapy / methods. Interleukin-2 / therapeutic use. Kidney Neoplasms / pathology. Kidney Neoplasms / therapy

[MeSH-minor] Adenocarcinoma, Clear Cell / therapy. Aged. Cell Line, Tumor. Cytoplasm / metabolism. Female. Humans. Immunohistochemistry. Kidney / pathology. Male. Middle Aged. Neoplasm Metastasis. Prognosis. Risk. Time Factors. Treatment Outcome

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(PMID = 16113605.001).

[ISSN] 1524-9557

[Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)

[ISO-abbreviation] J. Immunother.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Interleukin-2

   

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[Title] Adult Xp11 translocation renal cell carcinoma diagnosed by cytogenetics and immunohistochemistry.

PURPOSE: To determine the incidence of Xp11 translocation renal cell carcinoma (RCC) in adult patients using cytogenetics and immunohistochemstry.

EXPERIMENTAL DESIGN: Cytogenetic studies were prospectively done using tumor samples from 443 consecutive adult Japanese patients (ages 15-89 years) who underwent nephrectomy for RCC.

Clinicopathologic characteristics of Xp11 translocation RCC were examined.

RESULTS: Mitotic cells suitable for cytogenetic analysis were obtained in 244 tumor samples (55%); among these, we identified 4 cases (1.6%) of Xp11 translocation RCC.

The median age of the 7 patients was 41 years (range, 15-59 years), and 15% of RCC patients (4 of 26) who were younger than ages 45 years had this type of RCC.

Of the four Xp11 translocation RCC patients whose karyotypes were determined, two had an ASPL-TFE3 gene fusion.

Of these 2, 1 had pulmonary metastasis at presentation, and the other developed liver metastasis 12 months after nephrectomy and died of the disease.

Both had nodal involvement but remained disease free for 3 and 5 years, respectively, after surgical resection of lymph node metastases.

CONCLUSIONS: This is the first report to determine the incidence of Xp11 translocation RCC in adult patients.

We found that this disease is relatively common in young adults.

[MeSH-major] Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / analysis. Carcinoma, Renal Cell / genetics. Chromosomes, Human, X. Kidney Neoplasms / genetics. Translocation, Genetic

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(PMID = 19228722.001).

[ISSN] 1078-0432

[Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research

[ISO-abbreviation] Clin. Cancer Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / Receptors, Growth Factor; 0 / TFE3 protein, human; EC 2.7.10.1 / MET protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-met

   

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[Title] [Clinicopathologic study of renal cell carcinoma with rhabdoid features].

OBJECTIVE: To study the clinicopathologic features and biologic behavior of renal cell carcinoma (RCC) with rhabdoid features.

METHODS: Ten cases of RCC with rhabdoid features collected during the period from 1995 to 2005 were enrolled into the study.

Histologically, the rhabdoid foci were characterized by loosely cohesive trabeculae, acini, lobules and clusters of rhabdoid cells in otherwise clear cell RCC (9 cases) or papillary RCC (1 case).

The rhabdoid cells were round to polygonal in shape and contained globular eosinophilic inclusion bodies in the cytoplasm, eccentric nuclei, vesicular chromatin pattern and prominent nucleoli.

Coagulative tumor necrosis was commonly seen.

Immunohistochemical study showed that the rhabdoid cells were diffusely positive for CD10 (10/10), cytokeratin AE1/AE3 (10/10), epithelial membrane antigen (10/10) and vimentin (10/10).

The mean Ki-67 labeling index of the rhabdoid component was higher than that of the non-rhabdoid component (P < 0.05).

While 6 patients are still alive without recurrence, 2 patients died of the disease 6 and 29 months respectively after the operation.

CONCLUSIONS: RCC with rhabdoid elements are mainly observed in clear cell RCC and need to be distinguished from oncocytic renal tumors and malignant rhabdoid tumor of kidney.

[MeSH-major] Carcinoma, Renal Cell / pathology. Kidney Neoplasms / pathology. Rhabdoid Tumor / pathology

[MeSH-minor] Adult. Aged. Carcinoma, Transitional Cell / metabolism. Carcinoma, Transitional Cell / pathology. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Immunohistochemistry. Keratins / metabolism. Lymphatic Metastasis. Male. Middle Aged. Mucin-1 / metabolism. Nephrectomy. Neprilysin / metabolism. Vimentin / metabolism

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(PMID = 17535682.001).

[ISSN] 0529-5807

[Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology

[ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Mucin-1; 0 / Vimentin; 68238-35-7 / Keratins; EC 3.4.24.11 / Neprilysin

   

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[Title] Tuberous sclerosis and the kidney: from mesenchyme to epithelium, and beyond.

The renal manifestations of tuberous sclerosis complex (TSC) are remarkably diverse, including polycystic kidney disease, oncocytomas, renal cell carcinomas, and both benign and malignant angiomyolipomas.

What is particularly unusual about TSC, setting it apart from virtually all other inherited forms of renal disease, is the abnormalities of both mesenchymal cells (angiomyolipomas) and epithelial cells (cysts, oncocytomas, and carcinomas).

Recently, the TSC1/TSC2 protein complex was shown to inhibit the kinase mTOR (mammalian target of rapamycin).

This places TSC1/TSC2 at center stage in signaling pathways that regulate cell growth.

Here, we will address the genetic, cellular and biochemical mechanisms that may contribute to the unusually broad spectrum of renal disease in cells with TSC1 or TSC2 mutations, and consider how the TSC signaling pathways may be linked to other renal diseases such as polycystic kidney disease and renal cell carcinoma.

[MeSH-major] Angiomyolipoma / etiology. Carcinoma / etiology. Kidney Neoplasms / etiology. Tuberous Sclerosis / complications

[MeSH-minor] Humans. Mutation. Repressor Proteins / genetics. Repressor Proteins / metabolism. Signal Transduction. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism

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[Cites] Nat Cell Biol. 2000 May;2(5):281-7 [10806479.001]

[Cites] Am J Hum Genet. 2001 Jan;68(1):64-80 [11112665.001]

[Cites] Cancer Cell. 2003 Aug;4(2):147-58 [12957289.001]

[Cites] Cell. 1993 Dec 31;75(7):1305-15 [8269512.001]

[Cites] Am J Pathol. 2003 Feb;162(2):457-68 [12547704.001]

[Cites] Am J Hum Genet. 1999 May;64(5):1305-15 [10205261.001]

[Cites] Oncogene. 2002 Sep 12;21(41):6356-65 [12214276.001]

[Cites] Am J Physiol Lung Cell Mol Physiol. 2004 Apr;286(4):L694-700 [12922981.001]

[Cites] Am J Hum Genet. 2001 Sep;69(3):493-503 [11468687.001]

[Cites] Oncogene. 2004 Apr 19;23(18):3151-71 [15094765.001]

[Cites] Oncogene. 2002 Dec 5;21(55):8470-6 [12466966.001]

[Cites] Hum Mol Genet. 1998 Jun;7(6):1053-7 [9580671.001]

[Cites] J Urol. 1998 Jul;160(1):141-5 [9628635.001]

[Cites] Pediatr Radiol. 2002 Sep;32(9):677-80 [12195309.001]

[Cites] Lancet. 2003 Apr 19;361(9366):1348-9 [12711473.001]

[Cites] Am J Surg Pathol. 1998 Feb;22(2):180-7 [9500218.001]

[Cites] Cell. 2003 Nov 26;115(5):577-90 [14651849.001]

[Cites] Am J Pathol. 2003 Feb;162(2):491-500 [12547707.001]

[Cites] Cancer. 1998 Nov 15;83(10):2208-16 [9827727.001]

[Cites] Cancer Res. 1998 Nov 1;58(21):4766-70 [9809973.001]

[Cites] Am J Surg Pathol. 1998 Jun;22(6):663-72 [9630173.001]

[Cites] Mod Pathol. 2002 Mar;15(3):205-10 [11904337.001]

[Cites] J Urol. 2003 Dec;170(6 Pt 1):2163-72 [14634372.001]

[Cites] J Biol Chem. 2004 Jul 16;279(29):29930-7 [15150271.001]

[Cites] Cancer Res. 2003 May 15;63(10):2675-80 [12750296.001]

[Cites] Mayo Clin Proc. 1991 Aug;66(8):792-6 [1861550.001]

[Cites] J Biol Chem. 2003 Dec 19;278(51):51372-9 [14551205.001]

[Cites] Am J Pathol. 1996 Oct;149(4):1201-8 [8863669.001]

[Cites] Mol Cell. 2001 Apr;7(4):823-32 [11336705.001]

[Cites] J Clin Invest. 1997 Jan 15;99(2):194-9 [9005987.001]

[Cites] Am J Hum Genet. 1996 Aug;59(2):400-6 [8755927.001]

[Cites] Urology. 1991 Apr;37(4):340-3 [2014599.001]

[Cites] Eur J Radiol. 1998 May;27(2):131-8 [9639138.001]

[Cites] Nat Genet. 1994 Dec;8(4):328-32 [7894481.001]

[Cites] Nat Genet. 1994 Feb;6(2):193-6 [8162074.001]

[Cites] Hum Mol Genet. 1994 Oct;3(10):1829-32 [7849708.001]

[Cites] Kidney Int. 2004 Sep;66(3):924-34 [15327383.001]

[Cites] J Pediatr Surg. 1996 May;31(5):729-30 [8861495.001]

[Cites] Am J Surg Pathol. 2000 Jun;24(6):889-94 [10843294.001]

[Cites] Hum Mol Genet. 1994 Oct;3(10):1833-4 [7849709.001]

[Cites] Science. 1997 Aug 8;277(5327):805-8 [9242607.001]

(PMID = 15856327.001).

[ISSN] 0931-041X

[Journal-full-title] Pediatric nephrology (Berlin, Germany)

[ISO-abbreviation] Pediatr. Nephrol.

[Language] eng

[Grant] United States / NIDDK NIH HHS / DK / DK 51052

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review

[Publication-country] Germany

[Chemical-registry-number] 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins; 0 / tuberous sclerosis complex 1 protein; 4JG2LF96VF / tuberous sclerosis complex 2 protein

[Number-of-references] 43

   

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[Title] Efficacy and safety of TachoSil as haemostatic treatment versus standard suturing in kidney tumour resection: a randomised prospective study.

OBJECTIVE: Elective nephron-sparing surgery (NSS) for renal cell carcinoma (RCC) has gained general acceptance as an alternative to radical nephrectomy.

To achieve haemostasis without risk of local ischaemia and necrosis of kidney parenchyma after standard haemostatic suturing, we investigated TachoSil's efficacy and safety as atraumatic haemostatic treatment after kidney tumour resection.

METHODS: A total of 185 patients scheduled for NSS for small, superficial kidney tumours were included in an open, randomised, prospective, multicentre, parallel-group trial.

CONCLUSION: TachoSil was superior to standard suturing in obtaining intraoperative control of haemorrhage and was as well tolerated as standard haemostatic treatment during NSS.

[MeSH-major] Carcinoma, Renal Cell / surgery. Fibrinogen / therapeutic use. Hemostatics / therapeutic use. Kidney Neoplasms / surgery. Surgical Sponges. Thrombin / therapeutic use

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[CommentIn] Eur Urol. 2007 Oct;52(4):1162-3 [17467888.001]

(PMID = 17467884.001).

[ISSN] 0302-2838

[Journal-full-title] European urology

[ISO-abbreviation] Eur. Urol.

[Language] eng

[Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Drug Combinations; 0 / Hemoglobins; 0 / Hemostatics; 0 / TachoSil; 9001-32-5 / Fibrinogen; EC 3.4.21.5 / Thrombin

   

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[Title] Prognostic significance of perinephric fat infiltration and tumor size in renal cell carcinoma.

PURPOSES: It is controversial that perinephric fat infiltration has an impact on survival in patients with renal cell carcinoma.

Therefore, we evaluated the influence of perinephric fat infiltration and tumor size on patient survival.

MATERIALS AND METHODS: We retrospectively reviewed the medical records of 783 and 77 patients with pT1-2 (cN0M0) and pT3a (cN0M0) renal cell carcinoma, respectively.

Sporadic unilocular noncystic renal cell carcinoma was included.

Univariate and multivariate analyses of prognostic factors, including perinephric fat infiltration, on cancer specific and disease-free survival were performed.

RESULTS: Patients with pT1-2 and pT3a tumors had a 5-year cancer specific survival rate of 96.1% and 84.9%, and a 5-year disease-free survival rate of 93.4% and 74.7%, respectively (each p <0.01).

Age, tumor size and Fuhrman nuclear grade were independent prognostic factors for cancer specific and disease-free survival, whereas perinephric fat infiltration was significant only for disease-free survival.

However, perinephric fat infiltration had a significant effect on cancer specific survival in patients with pT3a tumors more than 7 cm (p = 0.001).

In contrast, patients with pT3a tumors 7 cm or less had cancer specific and disease-free survival similar to that of patients with pT2 tumors.

Recurrence of pT3a tumors greater than 7 cm was observed in 44% of patients but in only 14.6% of those with pT3a tumors 7 cm or less (p = 0.029).

In contrast to the recurrence of tumors 7 cm or less, recurrence of pT3a tumors more than 7 cm usually developed at multiple sites with a large tumor burden and it progressed rapidly.

Consequently 85% of patients with recurrence of pT3a tumors larger than 7 cm died of renal cell carcinoma compared with 33% of those with recurrence of pT3a tumors 7 cm or less (p = 0.001).

CONCLUSIONS: In pT3a renal cell carcinoma tumor size was the strongest prognostic factor of disease-free and cancer specific survival.

Perinephric fat infiltration was an independent prognostic factor for disease-free survival but not for cancer specific survival due to the less aggressive behavior of small (7 cm or less) pT3a tumors after recurrence.

Tumor size and perinephric fat infiltration should be included in T3a renal cell carcinoma staging.

[MeSH-major] Adipose Tissue / pathology. Carcinoma, Renal Cell / mortality. Carcinoma, Renal Cell / pathology. Kidney Neoplasms / mortality. Kidney Neoplasms / pathology. Tumor Burden

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(PMID = 18550101.001).

[ISSN] 1527-3792

[Journal-full-title] The Journal of urology

[ISO-abbreviation] J. Urol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] The role of lymph node dissection in renal cell carcinoma: the pendulum swings back.

The incidence of regional lymph node metastases in patients with renal cell carcinoma ranges from 13% to over 30%, and portends a poor prognosis in both locally advanced and metastatic settings.

Patients with small, organ confined tumors are at low risk for regional lymph node metastases and lymph node dissection can be omitted in these patients.

Patients with locally advanced primary tumors but no clinical evidence of lymphadenopathy can be selectively targeted for aggressive lymph node dissection as an adjunct to radical nephrectomy, based on their individual risk of harboring micrometastatic lymph node disease.

Although early identification of micrometastatic nodal disease in this group of patients has not conclusively been shown to improve survival, accurate pathologic nodal staging allows for early implementation of adjuvant systemic therapies in these high-risk patients.

[MeSH-major] Carcinoma, Renal Cell / pathology. Kidney Neoplasms / pathology. Lymph Node Excision

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(PMID = 18836335.001).

[ISSN] 1528-9117

[Journal-full-title] Cancer journal (Sudbury, Mass.)

[ISO-abbreviation] Cancer J

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Long-lasting remission of pulmonary metastases of renal cell cancer under IFN-beta therapy in a patient with multiple sclerosis.

BACKGROUND: Immunomodulary therapy based on interferon (IFN)-a has been shown to be effective in a subset of patients with advanced renal cell carcinoma (RCC).

IFN-Beta has occasionally been reported to induce remissions in RCC, but is well established in the treatment of multiple sclerosis (MS).

There is an ongoing debate whether hyperactivation of the immune system may convey protection against the development of cancer in MS patients.

PATIENTS AND METHODS: A 54-year-old female MS patient underwent tumor nephrectomy for RCC in 1994.

CONCLUSION: To our knowledge, this is the longest remission under IFN-Beta treatment ever reported in an RCC patient.

We conclude that IFN-Beta should be particularly considered as a therapeutic option in the rare occasion of metastatic RCC in patients with MS.

[MeSH-major] Carcinoma, Renal Cell / prevention & control. Carcinoma, Renal Cell / secondary. Interferon-beta / therapeutic use. Kidney Neoplasms / drug therapy. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Multiple Sclerosis / drug therapy

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(PMID = 16974116.001).

[ISSN] 0378-584X

[Journal-full-title] Onkologie

[ISO-abbreviation] Onkologie

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Switzerland

[Chemical-registry-number] 77238-31-4 / Interferon-beta

   

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Rutaceline was evaluated for its antiproliferative capacity on the human colorectal adenocarcinoma (Caco-2) and the African green monkey kidney (Vero) cell lines.

The 50% inhibition of cell growth (IC50) obtained after 24 h incubation was similar for both cells lines (110-115 microg/ml, i.e.

269-281 microM), but at 48 h the IC50 value for the Caco-2 cells was lower than for the Vero cells (20 microg/lml, i.e.

220 microM) indicating a higher cell growth inhibitory effect on the colon adenocarcinoma cells.

At the respective IC50 concentrations, Rutaceline did not significantly induce apoptosis but induced cell cycle arrest in the GO/G1 phase, as well as a decrease of cells in S phase.

Rutaceline also induced DNA fragmentation in both cell lines, as revealed by agarose gel electrophoresis, and a dose-dependent clastogenic effect in both cell lines as revealed by the Comet assay.

[MeSH-minor] Adenocarcinoma. Animals. Cell Line. Cell Line, Tumor. Cercopithecus aethiops. Colorectal Neoplasms. Humans. Kidney / drug effects. Kinetics. Madagascar. Vero Cells

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(PMID = 17436597.001).

[ISSN] 0258-851X

[Journal-full-title] In vivo (Athens, Greece)

[ISO-abbreviation] In Vivo

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Greece

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzophenanthridines

   

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[Title] Food groups and renal cell carcinoma: a case-control study from Italy.

Although nutrition and diet have been related to renal cell carcinoma (RCC), the role of specific foods or nutrients on this cancer is still controversial.

We evaluated the relation between a wide range of foods and the risk of RCC in an Italian case-control study including 767 patients (494 men and 273 women) younger than 79 years with incident, histologically confirmed RCC, and 1,534 controls (988 men and 546 women) admitted to the same hospitals as cases for a wide spectrum of acute, non-neoplastic conditions, not related to long term diet modifications.

A validated and reproducible food frequency questionnaire, including 78 foods and beverages, plus a separate section on alcohol drinking, was used to assess patients' dietary habits 2 years before diagnosis or hospital admission.

Poultry (OR = 0.74), processed meat (OR = 0.64) and vegetables (OR = 0.65) were inversely associated with RCC risk.

No relation was found for coffee and tea, soups, eggs, red meat, fish, cheese, pulses, potatoes, fruits, desserts and sugars.

The results of this study provide further indications on dietary correlates of RCC, and in particular indicate that a diet rich in refined cereals and poor in vegetables may have an unfavorable role on RCC.

[MeSH-major] Carcinoma, Renal Cell / pathology. Carcinoma, Renal Cell / physiopathology. Energy Intake / physiology. Food. Kidney Neoplasms / pathology

[MeSH-minor] Aged. Alcohol Drinking. Body Mass Index. Case-Control Studies. Diet. Educational Status. Female. Humans. Italy. Male. Middle Aged. Multivariate Analysis. Odds Ratio. Risk Factors. Smoking

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[CommentIn] Int J Cancer. 2007 Nov 1;121(9):2116-7 [17640056.001]

(PMID = 17058282.001).

[ISSN] 0020-7136

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Resection of recurrent inferior vena cava tumor after radical nephrectomy for renal cell carcinoma.

Management of recurrent tumor in the inferior vena cava (IVC) after radical nephrectomy is surgically challenging.

We report 3 cases of recurrent renal cell carcinoma within the IVC managed by three different surgical techniques.

One patient was treated with tumor thrombus removal and primary cavotomy closure.

Although technically difficult, repeat resection of IVC tumor recurrence after nephrectomy for renal cell carcinoma is an acceptable method of treatment.

[MeSH-major] Carcinoma, Renal Cell / surgery. Kidney Neoplasms / surgery. Neoplasm Recurrence, Local / surgery. Vascular Neoplasms / surgery. Vena Cava, Inferior

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(PMID = 16698379.001).

[ISSN] 1527-9995

[Journal-full-title] Urology

[ISO-abbreviation] Urology

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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[Title] Plasma activity of prolyl endopeptidase in relation to psychopathology during immunotherapy with IFN-alpha in patients with renal cell carcinoma.

In 24 patients (16 men, 8 women, median age 60.5 years, range 47-72 years) with metastatic renal cell carcinoma (RCC), psychiatric assessment and blood sampling were performed before and at 4 and 8 weeks and at 6 months after initiation of treatment with IFN-alpha.

[MeSH-major] Carcinoma, Renal Cell / drug therapy. Carcinoma, Renal Cell / psychology. Immunotherapy. Interferon-alpha / therapeutic use. Kidney Neoplasms / drug therapy. Kidney Neoplasms / psychology. Serine Endopeptidases / blood

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(PMID = 18547158.001).

[ISSN] 1079-9907

[Journal-full-title] Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research

[ISO-abbreviation] J. Interferon Cytokine Res.

[Language] eng

[Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Interferon-alpha; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.26 / prolyl oligopeptidase

   

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[Title] [Experiences of open transperitoneal radical nephrectomy for large renal masses].

OBJECTIVE: To evaluate the effect of technical improvements of transperitoneal radical nephrectomy on the patients with large renal cell carcinoma.

METHODS: From May 2002 until May 2009, 45 patients with large (> 12 cm) renal cell carcinoma underwent transperitoneal radical nephrectomy.

The modified operative methods included exposing the operative field via a liver retractor and initially ligating renal artery to block the blood supply of kidney and tumor.

The method of tumor-free tissue dissociation was applied.

RESULTS: The tumor diameter was from 12.2 cm to 28.3 cm with a mean of 14.5 cm.

The pathological diagnoses were all of renal cell carcinoma.

The pathological stage included T(2)N(0 approximately 1)M(0 approximately 1)(n = 13), T(3)N(0 approximately 1)M(0 approximately 1)(n = 23), T(4)N(0 approximately 1)M(0 approximately 1)(n = 9).

After a follow-up period of 3 - 63 months, 3 cases of tumor recurrence were found in primary renal clutch.

CONCLUSION: Improved radical nephrectomy is feasible for large renal cell carcinoma.

[MeSH-major] Abdominal Cavity / surgery. Kidney Neoplasms / surgery. Nephrectomy / methods

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(PMID = 20646430.001).

[ISSN] 0376-2491

[Journal-full-title] Zhonghua yi xue za zhi

[ISO-abbreviation] Zhonghua Yi Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Evaluation Studies; Journal Article

[Publication-country] China

   

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[Title] Tuberin haploinsufficiency is associated with the loss of OGG1 in rat kidney tumors.

BACKGROUND: Tuberous sclerosis complex (TSC) is caused by defects in one of two tumor suppressor genes, TSC-1 or TSC-2.

TSC-2 gene encodes tuberin, a protein involved in the pathogenesis of kidney tumors.

Loss of heterozygosity (LOH) at the TSC2 locus has been detected in TSC-associated renal cell carcinoma (RCC) and in RCC in the Eker rat.

Tuberin downregulates the DNA repair enzyme 8-oxoguanine DNA-glycosylase (OGG1) with important functional consequences, compromising the ability of cells to repair damaged DNA resulting in the accumulation of the mutagenic oxidized DNA, 8-oxo-dG.

Loss of function mutations of OGG1 also occurs in human kidney clear cell carcinoma and may contribute to tumorgenesis.

We investigated the distribution of protein expression and the activity of OGG1 and 8-oxo-dG and correlated it with the expression of tuberin in kidneys of wild type and Eker rats and tumor from Eker rat.

RESULTS: Tuberin expression, OGG1 protein expression and activity were higher in kidney cortex than in medulla or papilla in both wild type and Eker rats.

In kidney tumors from Eker rats, the loss of the second TSC2 allele is associated with loss of OGG1 expression.

Immunostaining of kidney tissue shows localization of tuberin and OGG1 mainly in the cortex.

CONCLUSION: These results demonstrate that OGG1 localizes with tuberin preferentially in kidney cortex.

In addition, the predominant expression of OGG1 in the cortex and its decreased expression and activity in the Eker rat may account for the predominant cortical localization of renal cell carcinoma.

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[Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3523-8 [11904416.001]

[Cites] Am J Physiol Renal Physiol. 2008 Jan;294(1):F281-90 [17989114.001]

[Cites] Carcinogenesis. 2003 Mar;24(3):573-82 [12663520.001]

[Cites] Antioxid Redox Signal. 2004 Jun;6(3):561-70 [15130282.001]

[Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]

[Cites] J Urol. 1984 Dec;132(6):1170-4 [6502814.001]

[Cites] J Urol. 1987 Sep;138(3):477-81 [3625844.001]

[Cites] Cancer Res. 1991 Jun 15;51(12):3075-9 [2039987.001]

[Cites] J Biol Chem. 1992 Jan 5;267(1):166-72 [1730583.001]

[Cites] Science. 1992 Mar 27;255(5052):1693-5 [1553556.001]

[Cites] J Biol Chem. 1993 Nov 5;268(31):23524-30 [8226881.001]

[Cites] Biochimie. 2000 Jan;82(1):59-64 [10717388.001]

[Cites] Cancer Res. 2000 Sep 1;60(17):4740-4 [10987279.001]

[Cites] Regul Toxicol Pharmacol. 2000 Dec;32(3):264-75 [11162720.001]

[Cites] Cancer Lett. 2001 May 10;166(1):65-9 [11295288.001]

[Cites] Cancer Res. 2001 Jul 15;61(14):5378-81 [11454679.001]

[Cites] Environ Mol Mutagen. 2001;38(2-3):180-90 [11746753.001]

[Cites] J Biol Chem. 1994 May 27;269(21):15318-24 [7515054.001]

[Cites] J Toxicol Environ Health B Crit Rev. 1998 Jul-Sep;1(3):181-97 [9644327.001]

[Cites] Oncogene. 1998 Jun 11;16(23):3083-6 [9662341.001]

[Cites] Jpn J Cancer Res. 1998 Aug;89(8):825-8 [9765618.001]

[Cites] Cancer. 1998 Nov 15;83(10):2208-16 [9827727.001]

[Cites] J Histochem Cytochem. 1999 Apr;47(4):533-44 [10082755.001]

[Cites] DNA Repair (Amst). 2006 Nov 8;5(11):1337-45 [16861056.001]

[Cites] DNA Repair (Amst). 2007 Apr 1;6(4):544-59 [17112792.001]

[Cites] Toxicol Pathol. 2002 Nov-Dec;30(6):675-80 [12512868.001]

(PMID = 18218111.001).

[ISSN] 1476-4598

[Journal-full-title] Molecular cancer

[ISO-abbreviation] Mol. Cancer

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / P50 DK061597; United States / NIDDK NIH HHS / DK / R37 DK33665

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Tumor Suppressor Proteins; 4JG2LF96VF / tuberous sclerosis complex 2 protein; 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / OGG1 protein, rat; G9481N71RO / Deoxyguanosine

[Other-IDs] NLM/ PMC2265742

   

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[Title] Ubiquitin COOH-terminal hydrolase 1: a biomarker of renal cell carcinoma associated with enhanced tumor cell proliferation and migration.

PURPOSE: Renal cell carcinoma (RCC) accounts for 2% to 3% of all malignancies.

It represents one of the most radiation- and chemotherapy-resistant tumors and surgical resections are only effective in organ-defined disease.

However, RCC is an immunogenic tumor with response rates to immunotherapies between 10% and 20% of the treated patients.

Due to the currently inefficient therapies and the low 5-year survival rates of RCC patients, novel diagnostic, prognostic, and therapeutic markers are urgently needed for this disease.

EXPERIMENTAL DESIGN: Proteome-based approaches were used to identify (a) differentially expressed proteins in RCC compared with normal kidney epithelium and (b) proteins that are able to induce an antibody response in RCC patients.

RESULTS: The ubiquitin COOH-terminal hydrolase L1 (UCHL1) was found to be differentially expressed in both RCC lesions and RCC cell lines and immunoreactive using patients' sera.

UCHL1 expression was often down-regulated in primary RCC when compared with normal kidney epithelium but dependent on the RCC subtype, the von Hippel-Lindau phenotype, and the tumor grading.

Moreover, the frequency and the level of UCHL1 expression were higher in metastases when compared with primary RCC lesions.

Gain-of-function transfectants exhibited a significant higher proliferation and migration rate than UCHL1-negative RCC cells.

CONCLUSIONS: UCHL1 expression seems to be associated with the metastatic phenotype of RCC and therefore might serve as potential biomarker for the diagnosis and prognosis of RCC patients.

[MeSH-major] Biomarkers, Tumor. Carcinoma, Renal Cell / drug therapy. Gene Expression Regulation, Neoplastic. Kidney Neoplasms / drug therapy. Ubiquitin Thiolesterase / biosynthesis

[MeSH-minor] Antineoplastic Agents / pharmacology. Cell Line, Tumor. Cell Movement. Cell Proliferation. Humans. Kidney / metabolism. Neoplasm Metastasis. Phenotype. Protein Structure, Tertiary. Proteomics / methods

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(PMID = 17200335.001).

[ISSN] 1078-0432

[Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research

[ISO-abbreviation] Clin. Cancer Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; EC 3.1.2.15 / UCHL1 protein, human; EC 3.1.2.15 / Ubiquitin Thiolesterase

   

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[Title] [Pathological prognostic indicators in renal cell carcinoma].

[Transliterated title] Indicadores pronósticos anatomopatológicos del cáncer de riñón.

OBJECTIVE: To analyze histological factors not routinely assessed as potential prognostic factors in renal cell carcinoma, such as tumor necrosis, microscopic vascular invasion, and sinus fat invasion.

MATERIALS AND METHODS: A retrospective, analytical study was conducted of surgical specimens from 139 patients with localized renal cell carcinoma who underwent nephrectomy from 1993 to 2005.

Tumor necrosis, microscopic vascular invasion, and sinus fat invasion were analyzed and compared to the classical factors: TNM classification, Fuhrman grade, and tumor size.

For statistical analysis, variables analyzed were categorized as pT1, 2 vs pT3, 4; Fuhrman grade 1, 2 vs 3, 4; tumor size < 7 cm vs >or= 7cm; tumor necrosis vs no tumor necrosis; microvascular invasion of sinus fat vs no invasion.

Cancer-specific survival probability and disease-free survival were calculated.

Dependent variables were used to analyze cancer-specific survival rates.

Disease-free survival was estimated using a Cox regression model and Kaplan-Meier curves.

RESULTS: In the univariate analysis, all variables analyzed had a significant influence on death for renal cell carcinoma.

The variables significantly influencing disease-free survival, estimated by the Cox method, were the pT stage (p = 0.038) and Fuhrman grade (p = 0.048).

CONCLUSIONS: In patients with clinically localized renal cell carcinoma undergoing nephrectomy, pT stage and Fuhrman grade are the most important prognostic factors for survival and disease-free survival.

Tumor necrosis, microscopic vascular invasion, and sinus fat invasion are prognostic factors for death from renal carcinoma which are associated to TNM classification, Fuhrman grade, and tumor size.

[MeSH-major] Carcinoma, Renal Cell / pathology. Kidney Neoplasms / pathology

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(PMID = 20223135.001).

[ISSN] 1699-7980

[Journal-full-title] Actas urologicas españolas

[ISO-abbreviation] Actas Urol Esp

[Language] spa

[Publication-type] English Abstract; Journal Article

[Publication-country] Spain

   

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[Title] Renal oncocytoma with bilateral synchronous renal cell carcinoma in a patient undergoing long-term hemodialysis.

We report a case of bilateral synchronous renal cell carcinoma and renal oncocytoma in a 56-year-old male who had been treated with hemodialysis for 32 years.

Because anemia gradually worsened, computed tomography and magnetic resonance imaging were carried out and revealed bilateral renal tumors within acquired cystic disease of the kidney.

Bilateral nephrectomy was carried out, and the patient was diagnosed with multiple renal cell carcinomas and a single renal oncocytoma.

To our knowledge, this is the first reported case of renal oncocytoma with synchronous renal cell carcinoma in a patient undergoing long-term hemodialysis.

[MeSH-major] Adenoma, Oxyphilic / etiology. Carcinoma, Renal Cell / etiology. Kidney Neoplasms / etiology. Neoplasms, Multiple Primary / etiology. Renal Dialysis / adverse effects

[MeSH-minor] Humans. Kidney Failure, Chronic / complications. Kidney Failure, Chronic / therapy. Male. Middle Aged

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(PMID = 18184181.001).

[ISSN] 1442-2042

[Journal-full-title] International journal of urology : official journal of the Japanese Urological Association

[ISO-abbreviation] Int. J. Urol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Australia

   

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[Title] Overexpression of the myc target gene Mina53 in advanced renal cell carcinoma.

The myc target gene Mina53 was reported to be overexpressed in esophageal cancer with a poor prognosis.

The purpose of the present study was to examined Mina53 expression and its relationship to clinicopathological parameters in human renal cell carcinoma (RCC).

Mina53 and Ki-67 expression was examined on immunohistochemistry for 64 surgically resected RCC and non-cancerous tissue.

In addition, the relationship between Mina53 expression and clinicopathological prognostic factors of RCC such as age, stage, microvenous invasion (MVI), histological subtype, Ki-67 labeling index (LI), and prognosis, was examined.

Mina53 was expressed in the nuclei of tumor cells and tubular nuclei of normal renal tissue.

The expression level of Mina53 was significantly higher in patients with poor prognostic factors (stage IV, MVI-positive, and sarcomatoid RCC, and high Ki-67 LI).

The prognosis of high Mina53-expressing tumors was significantly poorer than that of non-Mina53-high tumors (P < 0.0001).

In conclusion, Mina53 is overexpressed in RCC tissue from patients with poor prognostic factors, suggesting that Mina53 overexpression is one of the factors for poor prognosis in RCC.

[MeSH-major] Carcinoma, Renal Cell / genetics. Gene Expression Regulation, Neoplastic. Kidney Neoplasms / genetics. Nuclear Proteins / genetics

[MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Cell Line, Tumor. Cell Nucleus / metabolism. Female. Humans. Immunoenzyme Techniques. Japan / epidemiology. Ki-67 Antigen / metabolism. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Nephrectomy. Prognosis. Survival Rate

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(PMID = 17803656.001).

[ISSN] 1320-5463

[Journal-full-title] Pathology international

[ISO-abbreviation] Pathol. Int.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Australia

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / MINA protein, human; 0 / Nuclear Proteins

   

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[Title] A case of complete clinical response with sorafenib in a patient with thyroid gland metastases from renal cell carcinoma 17 years from diagnosis.

[MeSH-major] Antineoplastic Agents / therapeutic use. Benzenesulfonates / therapeutic use. Carcinoma, Renal Cell / drug therapy. Carcinoma, Renal Cell / secondary. Kidney Neoplasms / pathology. Pyridines / therapeutic use. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / secondary

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(PMID = 19688987.001).

[ISSN] 0300-8916

[Journal-full-title] Tumori

[ISO-abbreviation] Tumori

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] United States

[Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib

   

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[Title] [Outcome of surgical management of renal cell carcinoma with renal vein or inferior vena cava tumor thrombus].

OBJECTIVE: To investigate the prognosis of surgical treatment for renal cell carcinoma with renal vein or inferior vena cava tumor thrombus.

METHODS: Between August 1994 and July 2004, 33 patients with renal cell carcinoma with renal vein or inferior vena cava tumor thrombus underwent radical nephrectomy and thrombectomy.

Level of tumor thrombus was renal vein in 15 patients, infrahepatic (level I) in 9, intrahepatic (level II) in 5, suprahepatic (level III) in 1, and right atrial extension (level IV) in 3.

The mean survival time of patients with renal vein involvement [(49.9 +/- 9.8) months] versus level I [(16.7 +/- 1.9) months] was significantly different (P < 0.05).

CONCLUSIONS: Radical nephrectomy plus thrombectomy is a valuable method for the treatment of renal cell carcinoma with renal vein or inferior vena cava involvement.

Patients with renal vein tumor thrombus appear to have better survival compared to patients with inferior vena cava tumor thrombus.

[MeSH-major] Carcinoma, Renal Cell / surgery. Embolectomy / methods. Kidney Neoplasms / surgery. Neoplastic Cells, Circulating. Nephrectomy / methods. Renal Veins / surgery. Vena Cava, Inferior / surgery

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(PMID = 16784678.001).

[ISSN] 0529-5815

[Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]

[ISO-abbreviation] Zhonghua Wai Ke Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

   

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[Title] Isolated gastric metastasis from renal cell carcinoma 10 years after radical nephrectomy.

[MeSH-major] Carcinoma, Renal Cell / secondary. Kidney Neoplasms / pathology. Stomach Neoplasms / secondary

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(PMID = 17201902.001).

[ISSN] 0815-9319

[Journal-full-title] Journal of gastroenterology and hepatology

[ISO-abbreviation] J. Gastroenterol. Hepatol.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] Australia

   

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[Title] Critical role of fine needle aspiration cytology and immunocytochemistry in preoperative diagnosis of pediatric renal tumors.

OBJECTIVE: To evaluate accuracy and role of immunocytochemistry (ICC) in cytologic diagnosis of pediatric renal tumors.

STUDY DESIGN: Fine needle aspirates from 75 cases of pediatric renal tumors were studied.

Smears were screened without the knowledge of final histologic diagnosis.

Subsequently, clinical details, final histology and diagnosis rendered by the original cytologist were noted to judge accuracy of diagnosis by a sensitized cytologist.

Five neuroblastomas that entered close differentials for Wilms tumor were also evaluated.

RESULTS: Of 58 Wilms tumors, 5 were misdiagnosed; 3 renal rhabdoid tumors and 1 clear cell sarcoma were missed on cytology.

Non-Hodgkin's lymphomas presenting as renal masses were accurately diagnosed on cytology, but primitive neuroectodermal tumors (n = 3) and renal cell carcinomas (n = 2) were not accurately diagnosed.

Accuracy rate improved from 65% to 92% on review by a cytologist aware of cytologic features of pediatric renal tumors.

CONCLUSION: A good accuracy rate of diagnosis of pediatric renal tumors can be achieved by priming pathologists to typical features of tumors.

Immunocytochemistry plays a supportive role in cases with atypical morphology or unusual presentations.

[MeSH-major] Kidney / pathology. Kidney Neoplasms / diagnosis. Kidney Neoplasms / pathology. Preoperative Care

[MeSH-minor] Adolescent. Azure Stains. Biopsy, Fine-Needle. Carcinoma, Renal Cell / diagnosis. Carcinoma, Renal Cell / pathology. Cell Nucleus / pathology. Child. Child, Preschool. Humans. Immunohistochemistry. Infant. Neuroectodermal Tumors, Primitive, Peripheral / diagnosis. Neuroectodermal Tumors, Primitive, Peripheral / pathology. Rhabdoid Tumor / diagnosis. Rhabdoid Tumor / pathology. Wilms Tumor / diagnosis. Wilms Tumor / pathology

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(PMID = 17910341.001).

[ISSN] 0001-5547

[Journal-full-title] Acta cytologica

[ISO-abbreviation] Acta Cytol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Azure Stains

   

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[Title] Von Hippel-Lindau gene product modulates TIS11B expression in renal cell carcinoma: impact on vascular endothelial growth factor expression in hypoxia.

TIS11B has been shown to regulate vascular endothelial growth factor (VEGF) mRNA stability in adrenocorticotropic hormone-stimulated primary adrenocortical cells.

TIS11B has also been documented as a negative regulator of VEGF during development, but nothing has yet been reported in the context of human cancers.

The Von Hippel-Lindau (VHL) tumor suppressor protein regulates VEGF gene expression at both the transcriptional and post-transcriptional levels in normoxia.

Here, we report a unique regulatory function of VHL in VEGF expression in hypoxia that is mediated through modulation of TIS11B protein levels in renal cancer cells.

In normoxia, we detected increased expression of the microRNA hsa-miR-29b in the VHL-overexpressing renal cancer cell line 786-O.

In contrast, in hypoxia, increased TIS11B expression paralleled an increased TIS11B mRNA stability in VHL-overexpressing 786-O cells.

This VHL-mediated TIS11B up-regulation in hypoxia may be important for TIS11B-regulated gene expression: we observed a down-regulation of VEGF mRNA in hypoxia in VHL-overexpressing cells compared with parental 786-O cells, and this effect was reversible by silencing TIS11B expression.

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[Cites] Semin Cancer Biol. 2004 Apr;14(2):123-30 [15018896.001]

[Cites] Arch Biochem Biophys. 2007 Jun 15;462(2):278-85 [17517366.001]

[Cites] Science. 1983 Feb 25;219(4587):983-5 [6823562.001]

[Cites] Science. 1987 Jan 23;235(4787):442-7 [2432664.001]

[Cites] Nature. 1989 May 4;339(6219):58-61 [2469964.001]

[Cites] Science. 1989 Dec 8;246(4935):1306-9 [2479986.001]

[Cites] Mol Cell Biol. 1991 Mar;11(3):1754-8 [1996120.001]

[Cites] FEBS Lett. 1992 Jul 13;306(1):1-4 [1628738.001]

[Cites] Nature. 1992 Oct 29;359(6398):843-5 [1279431.001]

[Cites] Nature. 1993 Apr 29;362(6423):841-4 [7683111.001]

[Cites] Science. 1993 May 28;260(5112):1317-20 [8493574.001]

[Cites] Am J Pathol. 1993 Nov;143(5):1255-62 [8238242.001]

[Cites] Nature. 1994 Feb 10;367(6463):576-9 [8107827.001]

[Cites] Cancer Res. 1994 Aug 1;54(15):4233-7 [7518352.001]

[Cites] Proc Natl Acad Sci U S A. 1995 Jan 31;92(3):768-72 [7531342.001]

[Cites] Cancer Res. 1995 Mar 15;55(6):1358-64 [7533661.001]

[Cites] FEBS Lett. 1995 Jul 10;368(1):160-4 [7615073.001]

[Cites] Nat Med. 1995 Aug;1(8):822-6 [7585187.001]

[Cites] Trends Biochem Sci. 1995 Nov;20(11):465-70 [8578590.001]

[Cites] Cancer Res. 1996 May 15;56(10):2299-301 [8625303.001]

[Cites] Sci Am. 1996 Sep;275(3):150-4 [8701285.001]

[Cites] Cell. 1996 Aug 23;86(4):517-20 [8752206.001]

[Cites] Proc Natl Acad Sci U S A. 1996 Oct 1;93(20):10589-94 [8855222.001]

[Cites] Proc Natl Acad Sci U S A. 1996 Oct 1;93(20):10595-9 [8855223.001]

[Cites] Kidney Int. 1997 Feb;51(2):575-8 [9027742.001]

[Cites] Mol Cell Biol. 1997 Sep;17(9):5629-39 [9271438.001]

[Cites] Eur J Cell Biol. 2008 Jan;87(1):31-8 [17889962.001]

[Cites] Proc Natl Acad Sci U S A. 2008 Sep 2;105(35):12885-90 [18728182.001]

[Cites] Medicine (Baltimore). 1997 Nov;76(6):381-91 [9413424.001]

[Cites] J Biol Chem. 1998 Mar 13;273(11):6417-23 [9497373.001]

[Cites] Nature. 1998 Jul 30;394(6692):485-90 [9697772.001]

[Cites] Trends Genet. 1998 Oct;14(10):423-6 [9820032.001]

[Cites] Nature. 1999 May 20;399(6733):271-5 [10353251.001]

[Cites] Oncogene. 2004 Nov 11;23(53):8673-80 [15467755.001]

[Cites] Oncogene. 2005 Nov 24;24(53):7850-8 [16170373.001]

[Cites] Nucleic Acids Res. 2006 Jan 1;34(Database issue):D140-4 [16381832.001]

[Cites] Genes Dev. 2006 Mar 1;20(5):515-24 [16510870.001]

[Cites] Mol Endocrinol. 2006 Apr;20(4):916-30 [16306087.001]

[Cites] J Natl Cancer Inst. 2001 Feb 21;93(4):266-76 [11181773.001]

[Cites] Science. 2001 Apr 20;292(5516):464-8 [11292862.001]

[Cites] Science. 2001 Apr 20;292(5516):468-72 [11292861.001]

[Cites] Dev Dyn. 2006 Nov;235(11):3144-55 [17013884.001]

[Cites] Mol Cell Biol. 2004 Jul;24(14):6445-55 [15226444.001]

(PMID = 19801654.001).

[ISSN] 1083-351X

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA078383; United States / NCI NIH HHS / CA / R29 CA078383; United States / NCI NIH HHS / CA / CA78383

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Butyrate Response Factor 1; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; 0 / ZFP36L1 protein, human; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein; S88TT14065 / Oxygen

[Other-IDs] NLM/ PMC2781675

   

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[Title] Characterization and gene expression analysis of novel matched primary and metastatic renal cell carcinoma cell lines.

Despite recent advances in molecular biology that have clarified the mechanisms involved in the metastasis of several types of cancer, the molecular mechanism underlying the metastasis of renal cell carcinoma (RCC) remains unclear.

Two RCC cell lines were successfully established from the surgical specimens of a matched primary tumor and adrenal metastasis from the same RCC patient, and were designated as TMK-1P and TMK-1M, respectively.

DNA microarray analysis showed a large differential expression of genes related to cell adhesion and the extracellular matrix molecules of which hexabrachion (tenascin-C), epidermal growth factor receptor, cadherin-6, and beta1-catenin were down-regulated, and the 67 kDa laminin receptor 1 and transforming growth factor-beta-induced 68 kDa protein (betaig-h3) were up-regulated in TMK-1M.

Real-time RT-PCR analysis confirmed this differential gene expression between the two cell lines.

The RCC cell lines may be useful in studying tumor invasion and screening markers for metastasis.

[MeSH-major] Adrenal Gland Neoplasms / genetics. Biomarkers, Tumor / genetics. Carcinoma, Renal Cell / genetics. Gene Expression Regulation, Neoplastic. Kidney Neoplasms / genetics. Kidney Neoplasms / pathology

[MeSH-minor] Cell Line, Tumor. Gene Expression Profiling. Humans. Karyotyping. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 18695898.001).

[ISSN] 1021-335X

[Journal-full-title] Oncology reports

[ISO-abbreviation] Oncol. Rep.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Greece

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / RNA, Neoplasm

   

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[Title] Renal cell carcinoma presenting with paraneoplastic hypercalcemic coma: a case report and review of the literature.

We report a case of a 62-year-old woman with renal cell carcinoma (RCC) presenting with a hypercalcemia-induced coma.

Initial imaging was negative, but PET scan identified a mass in the upper pole of the left kidney.

Our patient underwent partial nephrectomy, and the mass was identified as RCC on final pathology.

This case report describes a patient with RCC with the unusual presentation of hypercalcemic coma.

We review the differential diagnosis of malignant hypercalcemia and the evaluation of hypercalcemia occurring with RCC.

[MeSH-major] Carcinoma, Renal Cell / complications. Coma / etiology. Hypercalcemia / etiology. Kidney Neoplasms / complications

[MeSH-minor] Diagnosis, Differential. Female. Humans. Interleukin-6 / blood. Middle Aged. Parathyroid Hormone / blood. Receptor, Parathyroid Hormone, Type 1 / blood

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[Cites] JAMA. 1999 May 5;281(17):1628-31 [10235157.001]

[Cites] Radiol Med. 2006 Dec;111(8):1146-55 [17171520.001]

[Cites] Radiology. 2005 Jan;234(1):227-34 [15564390.001]

[Cites] N Engl J Med. 2005 Jan 27;352(4):373-9 [15673803.001]

[Cites] Eur J Nucl Med Mol Imaging. 2005 May;32(5):589-92 [15726356.001]

[Cites] Clin Cancer Res. 2005 Jun 1;11(11):4198-203 [15930357.001]

[Cites] Tumour Biol. 2005 Jul-Aug;26(4):201-6 [16006777.001]

[Cites] N Engl J Med. 2005 Dec 8;353(23):2477-90 [16339096.001]

[Cites] Am J Med Sci. 2006 Mar;331(3):119-23 [16538071.001]

[Cites] Clin Calcium. 2006 Apr;16(4):665-69 [16582519.001]

[Cites] Kidney Int Suppl. 2006 Jul;(102):S29-33 [16810307.001]

[Cites] Endocr Pract. 2006 Sep-Oct;12(5):535-41 [17002928.001]

[Cites] Semin Oncol. 2006 Oct;33(5):527-33 [17045081.001]

[Cites] N Engl J Med. 2000 Jan 20;342(3):177-85 [10639544.001]

[Cites] Int J Urol. 2000 Jun;7(6):239-42 [10843457.001]

[Cites] Clin Chim Acta. 2000 Dec;302(1-2):59-68 [11074064.001]

[Cites] Prog Urol. 2001 Apr;11(2):368-75 [11400511.001]

[Cites] Urol Int. 2002;68(3):202-3 [11919470.001]

[Cites] Mil Med. 2002 Dec;167(12):986-9 [12502172.001]

[Cites] J Clin Endocrinol Metab. 2003 Apr;88(4):1603-9 [12679445.001]

[Cites] Endocr Relat Cancer. 2003 Sep;10(3):403-7 [14503917.001]

[Cites] Curr Opin Urol. 2003 Nov;13(6):433-8 [14560134.001]

[Cites] Endocrinology. 1970 Jun;86(6):1436-40 [4315103.001]

[Cites] N Engl J Med. 1974 Jun 11;291(2):83-5 [4835887.001]

[Cites] J Clin Endocrinol Metab. 1975 Jul;41(1):164-7 [1150858.001]

[Cites] J Urol. 1977 Nov;118(5):720-3 [916087.001]

[Cites] Eur J Clin Invest. 1978 Dec;8(6):425-6 [217693.001]

[Cites] Cancer. 1980 May 15;45(10):2652-4 [6155196.001]

[Cites] J Clin Endocrinol Metab. 1982 Aug;55(2):219-27 [7085851.001]

[Cites] Am J Med. 1982 Nov;73(5):751-5 [6291389.001]

[Cites] J Surg Oncol. 1983 Apr;22(4):265-8 [6601207.001]

[Cites] Clin Endocrinol (Oxf). 1986 Jan;24(1):57-62 [3085989.001]

[Cites] Science. 1987 Aug 21;237(4817):893-6 [3616618.001]

[Cites] Urology. 1989 Mar;33(3):167-70 [2521966.001]

[Cites] Endocrinology. 1997 May;138(5):1879-85 [9112382.001]

[Cites] Bone. 1998 Mar;22(3):285-8 [9514222.001]

[Cites] Mayo Clin Proc. 1990 Nov;65(11):1399-407 [1700240.001]

[Cites] J Urol. 1991 Feb;145(2):248-50 [1988711.001]

[Cites] Crit Rev Diagn Imaging. 1990;31(1):81-115 [2288659.001]

[Cites] J Biol Chem. 1992 Sep 5;267(25):18236-43 [1517251.001]

[Cites] Cancer. 1993 Feb 15;71(4):1309-12 [8382106.001]

[Cites] Arch Intern Med. 1993 Sep 13;153(17):2043-5 [8357289.001]

[Cites] Urology. 1993 Sep;42(3):250-7; discussion 257-8 [8379024.001]

[Cites] N Engl J Med. 1996 Sep 19;335(12):865-75 [8778606.001]

[Cites] Semin Urol Oncol. 1996 Nov;14(4):216-22 [8946620.001]

[Cites] Cancer. 1999 Sep 15;86(6):1028-34 [10491530.001]

(PMID = 17443359.001).

[ISSN] 1525-1497

[Journal-full-title] Journal of general internal medicine

[ISO-abbreviation] J Gen Intern Med

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Interleukin-6; 0 / PTH1R protein, human; 0 / Parathyroid Hormone; 0 / Receptor, Parathyroid Hormone, Type 1

[Number-of-references] 48

[Other-IDs] NLM/ PMC2219737

   

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[Title] Tyrosine kinase inhibitors in advanced renal cell carcinoma: the evolving treatment paradigm.

[MeSH-major] Carcinoma, Renal Cell / drug therapy. Kidney Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors

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[CommentOn] Clin Genitourin Cancer. 2009 Jan;7(1):20-3 [19213663.001]

[CommentOn] Clin Genitourin Cancer. 2009 Jan;7(1):11-9 [19213662.001]

(PMID = 19213661.001).

[ISSN] 1558-7673

[Journal-full-title] Clinical genitourinary cancer

[ISO-abbreviation] Clin Genitourin Cancer

[Language] eng

[Publication-type] Comment; Editorial

[Publication-country] United States

[Chemical-registry-number] 0 / Benzenesulfonates; 0 / Indoles; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 0 / Pyrroles; 0 / sunitinib; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / Protein-Tyrosine Kinases

   

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[Title] Comparison of laparoscopic and open partial nephrectomies in t1a renal cell carcinoma: a korean multicenter experience.

PURPOSE: We analyzed a series of patients who had undergone laparoscopic partial nephrectomies (LPNs) and open partial nephrectomies (OPNs) to compare outcomes of the two procedures in patients with pathologic T1a renal cell carcinomas (RCCs).

MATERIALS AND METHODS: From January 1998 to May 2009, 417 LPNs and 345 OPNs were performed on patients with small renal tumors in 15 institutions in Korea.

Of the patients, 273 and 279 patients, respectively, were confirmed to have pT1a RCC.

Although the tumor location was more exophytic (51% vs. 44%, p=0.047) and smaller (2.1 cm vs. 2.3 cm, p=0.026) in the LPN cohort, the OPN cohort demonstrated shorter ischemia times (23.4 min vs. 33.3 min, p<0.001).

The LPN may be an acceptable surgical option in patients with small RCC in Korea.

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[Cites] Curr Opin Urol. 2003 May;13(3):209-14 [12692443.001]

[Cites] Urology. 2003 Jan;61(1):73-7 [12559270.001]

[Cites] Ann Intern Med. 2003 Jul 15;139(2):137-47 [12859163.001]

[Cites] J Urol. 2004 Jun;171(6 Pt 1):2181-5, quiz 2435 [15126781.001]

[Cites] Urology. 2004 Jul;64(1):38-42 [15245930.001]

[Cites] J Urol. 2004 Dec;172(6 Pt 1):2292-5 [15538251.001]

[Cites] J Endourol. 2005 Apr;19(3):406-9 [15865537.001]

[Cites] BJU Int. 2005 Oct;96(6):811-4 [16153207.001]

[Cites] BJU Int. 2007 Feb;99(2):286-9 [17155985.001]

[Cites] J Urol. 2007 Jan;177(1):70-4; discussion 74 [17162003.001]

[Cites] J Urol. 2007 Jun;177(6):2067-73; discussion 2073 [17509287.001]

[Cites] J Urol. 2007 Jul;178(1):41-6 [17574056.001]

[Cites] Eur Urol. 2008 Mar;53(3):590-6 [17997214.001]

[Cites] J Urol. 2008 Mar;179(3):847-51; discussion 852 [18221958.001]

[Cites] Eur Urol. 2008 Apr;53(4):732-42; discussion 742-3 [18222599.001]

[Cites] Curr Opin Urol. 2008 Mar;18(2):145-9 [18303534.001]

[Cites] J Endourol. 2008 May;22(5):953-7 [18363510.001]

[Cites] Eur Urol. 2009 May;55(5):1171-8 [19232819.001]

[Cites] J Am Soc Nephrol. 2009 Nov;20(11):2305-13 [19833901.001]

[Cites] J Urol. 1996 Jun;155(6):1868-73 [8618276.001]

[Cites] J Urol. 1999 Jan;161(1):33-4; discussion 34-5 [10037361.001]

[Cites] J Clin Oncol. 1999 Sep;17(9):2868-75 [10561364.001]

[Cites] J Urol. 2000 Feb;163(2):442-5 [10647650.001]

[Cites] J Urol. 2001 Jul;166(1):6-18 [11435813.001]

[Cites] J Urol. 2002 Feb;167(2 Pt 1):469-7; discussion 475-6 [11792899.001]

[Cites] Urology. 2003 May;61(5):906-9 [12736001.001]

(PMID = 20664779.001).

[ISSN] 2005-6745

[Journal-full-title] Korean journal of urology

[ISO-abbreviation] Korean J Urol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Korea (South)

[Other-IDs] NLM/ PMC2907495

[Keywords] NOTNLM ; Glomerular filtration rate / Kidney neoplasms / Nephrectomy / Outcomes assessment

   

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[Title] Clear cell hidradenoma: a mimic of metastatic clear cell tumors.

Clear cell hidradenoma is a benign skin appendage tumor that may mimic conventional-type renal cell carcinoma.

Histologically, clear cell hidradenoma contains small ductular lumens, focal apocrine and squamoid change, and a less prominent vascular pattern than renal cell carcinoma.

Furthermore, immunohistochemical studies can aid in distinguishing the 2 tumors.

Detailed clinical history, physical findings, and ancillary studies are essential for correct diagnosis and categorization of these tumors.

We report the rare case of a patient with renal cell carcinoma who underwent excision of an axillary clear cell hidradenoma, which was clinically suggestive of cutaneous metastatic disease.

[MeSH-major] Adenoma, Sweat Gland / diagnosis. Carcinoma, Renal Cell / diagnosis. Kidney Neoplasms / diagnosis. Neoplasms, Multiple Primary / diagnosis. Sweat Gland Neoplasms / diagnosis

[MeSH-minor] Axilla. Biomarkers, Tumor / analysis. Diagnosis, Differential. Humans. Immunohistochemistry. Lymph Nodes / pathology. Lymph Nodes / surgery. Male. Middle Aged. Mitotic Index. Neoplasm Metastasis / diagnosis. Treatment Outcome

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(PMID = 15859654.001).

[ISSN] 1543-2165

[Journal-full-title] Archives of pathology & laboratory medicine

[ISO-abbreviation] Arch. Pathol. Lab. Med.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor

   

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[Title] The prognostic value of the width of the surgical margin in the enucleoresection of small renal cell carcinoma: an intermediate-term follow-up.

OBJECTIVES: To assess the prognostic value of the width of a healthy surgical margin in the enucleoresection of small renal cell carcinoma, in which 68% of cases had a margin width of 3.0 mm or less.

METHODS: We retrospectively reviewed 98 consecutive enucleoresections regarding the width of healthy margin and tumor recurrence in 96 patients followed up for more than 3 years after surgery.

RESULTS: The mean tumor size was 2.8 cm (range, 1.0-6.1).

Only 1 patient developed tumor recurrence during follow-up, excluding a patient with von Hippel Lindau disease.

CONCLUSIONS: The width of the surgical margin was not associated with the oncological prognosis in our enucleoresection series of small renal cell carcinoma, in which the width of the margin was 3.0 mm or less in more than two-thirds of the cases.

[MeSH-major] Carcinoma, Renal Cell / pathology. Carcinoma, Renal Cell / surgery. Kidney Neoplasms / pathology. Kidney Neoplasms / surgery

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[Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.

(PMID = 20346491.001).

[ISSN] 1527-9995

[Journal-full-title] Urology

[ISO-abbreviation] Urology

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Bilateral renal-cell carcinoma associated with an acquired VHL mutation and long-term trichloroethylene exposure.

BACKGROUND/AIMS: The genetic basis for clear-cell renal carcinomas has been established in familial and many sporadic forms.

METHODS: PCR amplification and sequencing of VHL exons 1 - 3 were performed on peripheral blood and tumor tissue.

RESULTS: The tumor alone had a previously undescribed mutation in exon 1 of the VHL gene: deletion of a cytidine residue at position 291 relative to the first ATG start codon of the wild-type sequence.

There is loss of suppressor function when substrates such as hypoxia-inducible factor have impaired degradation: they accumulate and ultimately cause uncontrolled cell turnover.

This association of a proposed occupational cause and occurrence of renal-cell carcinoma emphasizes the availability and use of VHL sequencing for both studying the pathophysiology of malignant transformation and potentially playing a clinical role in genetic counseling or risk assessment.

[MeSH-major] Carcinoma, Renal Cell / genetics. Kidney Neoplasms / genetics. Mutation. Occupational Exposure / adverse effects. Solvents / adverse effects. Trichloroethylene / adverse effects

[MeSH-minor] Humans. Kidney / pathology. Male. Middle Aged. Nephrectomy. Tomography, X-Ray Computed. Von Hippel-Lindau Tumor Suppressor Protein / genetics

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(PMID = 19473641.001).

[ISSN] 0301-0430

[Journal-full-title] Clinical nephrology

[ISO-abbreviation] Clin. Nephrol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Solvents; 290YE8AR51 / Trichloroethylene; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein

   

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[Title] Significance of B7-H1 overexpression in kidney cancer.

B7-H1 is a cell surface glycoprotein belonging to the B7 family of costimulatory molecules.

Constitutive protein expression is restricted to a fraction of macrophage-lineage cells, although B7-H1 can be induced on activated T lymphocytes.

In addition, some human tumor cells can acquire the ability to aberrantly express B7-H1.

In vitro studies demonstrate that B7-H1, expressed by tumor cells or activated lymphocytes, impairs T-cell function and survival and enhances apoptosis of activated tumor-specific T cells.

Consistent with this, in vivo monoclonal antibody blockade of B7-H1 has been shown to potentiate antitumor responses in several murine cancer models.

Thus, tumor-associated B7-H1 has recently garnered much attention as a potential inhibitor of host antitumor immunity.

We describe herein the published investigations looking at the role of B7-H1 in renal cell carcinoma (RCC).

Clinical observations demonstrate that B7-H1 is aberrantly expressed in primary and metastatic RCC.

All patients had clear-cell RCC, and pathologic evaluation was performed by a single urologic pathologist.

Their results demonstrated that B7-H1, expressed by tumor cells or lymphocytes, is associated with aggressive pathologic features, including TNM stage, nuclear grade, tumor size, and coagulative necrosis.

With a median clinical follow-up of 11 years, patients with tumor B7-H1 were at significant risk of disease progression, cancer-specific death, and overall mortality even after multivariate analyses.

Five-year cancer-specific survival rates were 42% and 83% for patients with and without tumor B7-H1, respectively.

The basis for these associations could relate to the recognized ability of B7-H1 to inhibit antitumor T-cell-mediated immunity.

Based on the current literature, B7-H1 is an independent predictor of prognosis in RCC and represents a promising target for immune manipulation in this refractory tumor.

[MeSH-major] Antigens, CD / metabolism. Carcinoma, Renal Cell / diagnosis. Kidney Neoplasms / diagnosis

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(PMID = 17239274.001).

[ISSN] 1558-7673

[Journal-full-title] Clinical genitourinary cancer

[ISO-abbreviation] Clin Genitourin Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD274; 0 / CD274 protein, human

[Number-of-references] 39

   

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We demonstrate that ZONAB/DbpA and symplekin form a complex in kidney and intestinal epithelial cells that can be immunoprecipitated and that exists in the nucleus.

RNAi experiments indicate that symplekin depletion reduces the nuclear accumulation and the transcriptional activity of ZONAB/DbpA in colon adenocarcinoma cells, resulting in inhibition of proliferation and reduced expression of the ZONAB/DbpA-target gene cyclin D1.

[MeSH-minor] Animals. Caco-2 Cells. Cell Line. Cell Line, Tumor. Dogs. Epithelial Cells / metabolism. Fluorescent Antibody Technique. Humans. Immunoprecipitation. Protein Binding. RNA Interference. Receptor, ErbB-2 / genetics. Receptor, ErbB-2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tight Junctions / genetics. Tight Junctions / metabolism. Zonula Occludens-1 Protein

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(PMID = 17158914.001).

[ISSN] 0021-9533

[Journal-full-title] Journal of cell science

[ISO-abbreviation] J. Cell. Sci.

[Language] eng

[Grant] United Kingdom / Wellcome Trust / / 063661; United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/C514458/1; United Kingdom / Wellcome Trust / / 066100; United Kingdom / Medical Research Council / / G0100200; United Kingdom / Medical Research Council / / G0400678

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Membrane Proteins; 0 / Nuclear Proteins; 0 / Phosphoproteins; 0 / SYMPK protein, human; 0 / TJP1 protein, human; 0 / Transcription Factors; 0 / ZONAB protein, Canis familiaris; 0 / Zonula Occludens-1 Protein; EC 2.7.10.1 / Receptor, ErbB-2

   

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[Title] Proposal for revision of the TNM classification system for renal cell carcinoma.

BACKGROUND: The current study defined an optimal tumor size breakpoint to stratify localized renal cell carcinoma (RCC) into groups with significantly different cancer-related outcomes and proposed a revision of the TNM classification system.

METHODS: The authors analyzed the data from 1138 patients who had undergone partial or radical nephrectomy for localized RCC at 7 European urologic centers.

The scatterplot of tumor size versus expected risk of death per patient suggested that an interval of 5-6 cm was appropriate.

A total of 720 (63.3%) and 418 (36.7%) patients had tumors measuring < or = 5.5-cm and tumors measuring > 5.5-cm, respectively.

Significant cancer-specific survival differences between the two groups of patients were reported in the series by all the centers participating in the study.

On univariate analysis, the other variables found to be associated with cancer-specific survival were the patient's age, symptomatic tumor presentation, and the Fuhrman nuclear grade.

On multivariate analysis, the pathologic stage of the primary tumor defined according to the 5.5-cm breakpoint was found to be an independent predictor of cancer-specific survival, as well as age, mode of presentation, and nuclear grade.

1) patients with < or = 5.5-cm incidentally detected RCC;.

2) patients with < or = 5.5-cm symptomatic RCC; and 3) patients with > 5.5-cm RCC.

This cancer-related outcome stratification was valid regardless of the patient's age.

CONCLUSIONS: The 5.5-cm breakpoint was found to be the optimal tumor size breakpoint with which to stratify patients with organ-confined RCC.

The study supported the upgrade of the TNM classification system according to this breakpoint.

[MeSH-major] Carcinoma, Renal Cell / classification. Carcinoma, Renal Cell / pathology. Kidney Neoplasms / classification. Kidney Neoplasms / pathology

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[Copyright] Copyright 2005 American Cancer Society

(PMID = 16208703.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Publication-type] Journal Article; Multicenter Study

[Publication-country] United States

   

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[Title] Renal cell carcinoma: case report and literature review.

Renal cell carcinoma arising from epithelial cells of the renal tubule is a highly aggressive and malignant tumor in all ages.

Tumor is presented with characteristic findings of flank pain, gross hematuria, and palpable mass.

Although one half of the patients have metastasis at the time of diagnosis, most cases are currently being incidentally detected using improved imaging techniques.

Tumor stage and complete surgical resection have been reported as the most meaningful prognostic factors for the outcome.

The incidence of metastatic disease is same as in adults.

Cure is the most likely consequence in localized and completely resected tumors.

Here, we present an 8-year-old boy with renal cell carcinoma demonstrating only hematuria without any pathological physical examination findings.

The mass was described by abdominal ultrasonography and computed tomography in the left kidney.

[MeSH-major] Carcinoma, Renal Cell / surgery. Kidney Neoplasms / surgery

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(PMID = 15937800.001).

[ISSN] 1531-5037

[Journal-full-title] Journal of pediatric surgery

[ISO-abbreviation] J. Pediatr. Surg.

[Language] eng

[Publication-type] Case Reports; Journal Article; Review

[Publication-country] United States

[Number-of-references] 30

   

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[Title] D2-40, a novel monoclonal antibody against the M2A antigen as a marker to distinguish hemangioblastomas from renal cell carcinomas.

Hemangioblastomas (HB) are characterized by the presence of vacuolated tumor cells resembling the tumor cells seen in clear cell renal cell carcinomas (CRCC).

The issue is further complicated by the possibility of both HB and metastatic CRCC in brains of patients with Von Hippel Lindau (VHL) disease.

The vacuolated tumor cells in all HB were stained positively with D2-40.

Nineteen of 23 (83%) HB showed strong, membranous staining in the vacuolated tumor cells, and 4 of 23 (17%) showed weaker staining.

No expression was seen in CRCC, either primary in the kidney (0/20), or metastatic CRCC in the brain (0/8).

Three of the patients with HB also had VHL disease, and no difference was seen in D2-40 staining of HB in patients with or without VHL disease.

Two of these three VHL disease patients had both primary CRCC and HB resected at our institution.

In these two patients, strong D2-40 expression was seen in the HB, but no expression was seen in the CRCC, underlying the utility of this marker in distinguishing HB from CRCC in patients with VHL disease in addition to sporadic cases.

[MeSH-major] Antibodies, Monoclonal. Antigens, Neoplasm / immunology. Biomarkers, Tumor / metabolism. Carcinoma, Renal Cell / metabolism. Hemangioblastoma / metabolism

[MeSH-minor] Adult. Aged. Female. Humans. Immunohistochemistry / methods. Inhibins / metabolism. Male. Middle Aged. Staining and Labeling / methods. von Hippel-Lindau Disease / diagnosis. von Hippel-Lindau Disease / metabolism

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(PMID = 15864611.001).

[ISSN] 0001-6322

[Journal-full-title] Acta neuropathologica

[ISO-abbreviation] Acta Neuropathol.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / oncofetal antigens; 57285-09-3 / Inhibins

   

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[Title] [Molecular imaging for PET-CT reporter gene in breast adenocarcinoma (HSV1-tk) of subcutaneous xenografts in living nude mice].

OBJECTIVE: To study the in vitro accumulation of (18)F-FHBG, its in vivo distribution and (18)F-FHBG PET-CT imaging for reporter gene (HSV1-tk) in nude mice with a xenograft of breast adenocarcinoma.

METHODS: The in vitro uptake of (18)F-FHBG in tumor cells of T47D and T47D-tk and the distribution of (18)F-FHBG in normal Kunming mice and nude mice with breast adenocarcinoma xenograft were detected by well-type gamma counter.

Reporter gene PET-CT imaging with (18)F-FHBG was performed in nude mice with a xenograft of breast adenocarcinoma.

RESULTS: The in vitro uptake of (18)F-FHBG in T47D-tk cells (143.67 dpm/10(4) +/- 5.82 dpm/10(4) cells) was significantly higher than that in T47D cells (2.23 dpm/10(4) +/- 0.23 dpm/10(4) cells) at 60 and 120 min post-injection (P < 0.001) and reaches a plateau at 60 min.

In normal Kunming mice, (18)F-FHBG was mainly distributed in liver, intestine, kidney and bladder while there was no obvious radioactive accumulation in brain. (18)F-FHBG accumulated at a significantly higher level in T47D-tk tumors than in T47D tumors and its accumulation yielded the best image effect at 2 h by PET-CT imaging in nude mice.

CONCLUSION: The in vitro uptake of (18)F-FHBG in T47D-tk cells is significantly higher than that in T47D cells. (18)F-FHBG is mainly excreted by digestive tract and urinary tract in mice.

This study will offer a monitoring method and scientific base for (18)F-FHBG reporter gene imaging and HSV1-tk gene therapy in tumors.

[MeSH-major] Adenocarcinoma / radionuclide imaging. Breast Neoplasms / radionuclide imaging. Genes, Reporter. Positron-Emission Tomography

[MeSH-minor] Animals. Cell Line, Tumor. Female. Fluorine Radioisotopes. Genetic Therapy. Guanine / analogs & derivatives. Humans. Mice. Mice, Inbred BALB C. Mice, Inbred Strains. Mice, Nude. Neoplasm Transplantation

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(PMID = 20223118.001).

[ISSN] 0376-2491

[Journal-full-title] Zhonghua yi xue za zhi

[ISO-abbreviation] Zhonghua Yi Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / 9-(4-fluoro-3-hydroxymethylbutyl)guanine; 0 / Fluorine Radioisotopes; 5Z93L87A1R / Guanine

   

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[Title] How do symptoms have an impact on the prognosis of renal cell carcinoma?

AIM: Symptomatic renal cell carcinoma (RCC) is well known to have a characteristic behavior.

We therefore evaluated the impact of systemic symptoms on the prognosis of RCC.

METHODS: Patard's criteria were used to classify symptoms before operation into three groups defined as: S1 (incidental tumor), S2 (localized symptoms) and S3 (systemic symptoms).

Selected clinicopathological factors including gender, maximum tumor diameter, clinical stage, hemoglobin, C-reactive protein (CRP) and immunosuppressive acidic protein, nuclear grade and venous invasion were measured preoperatively in 252 patients.

To determine impacts of them on the prognosis of RCC, we compared quantitative results using Cox multivariate analysis.

RESULTS: The cancer-specific five-year survival rates were 93.1%, 71.0%, and 20.2% for S1 (144 patients), S2 (80 patients) and S3 (28 patients), respectively (P < 0.0001).

[MeSH-major] Carcinoma, Renal Cell / diagnosis. Kidney Neoplasms / diagnosis

[MeSH-minor] Aged. Biomarkers, Tumor / blood. C-Reactive Protein / metabolism. Female. Hemoglobins / metabolism. Humans. Kidney / pathology. Male. Middle Aged. Neoplasm Proteins / blood. Prognosis. Retrospective Studies

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(PMID = 18380815.001).

[ISSN] 1442-2042

[Journal-full-title] International journal of urology : official journal of the Japanese Urological Association

[ISO-abbreviation] Int. J. Urol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Australia

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Hemoglobins; 0 / Neoplasm Proteins; 0 / immunosuppressive acidic protein; 9007-41-4 / C-Reactive Protein

   

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Helicobacter pylori (H. pylori) cagA-positive strains are associated with gastritis, peptic ulcerations, and gastric adenocarcinoma.

Upon delivery into gastric epithelial cells, the cagA-encoded CagA protein specifically binds and aberrantly activates SHP-2 oncoprotein in a manner that is dependent on CagA tyrosine phosphorylation.

CagA-deregulated SHP-2 then elicits aberrant Erk activation while causing an elongated cell shape known as the hummingbird phenotype.

In polarized epithelial cells, CagA also binds to PAR1b/MARK2 and inhibits the PAR1b kinase activity, thereby disrupting tight junctions and epithelial cell polarity independent of CagA tyrosine phosphorylation.

We show here that the CagA-multimerization (CM) sequence that mediates interaction of CagA with PAR1b is not only essential for the CagA-triggered junctional defects but also plays an important role in induction of the hummingbird phenotype by potentiating CagA-SHP-2 complex formation.

[MeSH-minor] Adenoviridae / genetics. Amino Acid Sequence. Animals. COS Cells. Cell Line. Cell Polarity. Cercopithecus aethiops. Dogs. Epithelial Cells / cytology. Epithelial Cells / metabolism. Epithelial Cells / physiology. Genetic Vectors. Humans. Kidney / cytology. Molecular Sequence Data. Mutation. Phosphorylation. Protein Tyrosine Phosphatase, Non-Receptor Type 11 / metabolism. Stomach / cytology. Tight Junctions / metabolism. Transduction, Genetic. Transfection. Virulence / genetics

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(PMID = 19016760.001).

[ISSN] 1349-7006

[Journal-full-title] Cancer science

[ISO-abbreviation] Cancer Sci.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Bacterial Proteins; 0 / Calgranulin A; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11

   

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[Title] Nephron-sparing surgery is equally effective to radical nephrectomy for T1BN0M0 renal cell carcinoma: a population-based assessment.

OBJECTIVES: To test the effect of nephron-sparing surgery (NSS) vs radical nephrectomy (RN) on cancer-specific mortality (CSM) in patients with T1bN0M0 renal cell carcinoma (RCC) in a population-based cohort.

To date, only few series from tertiary care centers supported the use of NSS for T1bN0M0 (range 4-7 cm) RCC.

METHODS: The Surveillance, Epidemiology, and End Results database allowed us to identify 275 NSS (5.3%) and 4866 RN (94.7%) patients treated for T1bN0M0 RCC between 1988 and 2004.

Analyses matched for age, year of surgery, tumor size, and Fuhrman grade addressed the effect of nephrectomy type (NSS vs RN) on CSM.

RESULTS: Five years after surgery, the surviving proportions of NSS and RN patients matched for age, tumor size, and year of surgery were respectively 91.4 and 95.3% and 90.1 and 93.8% in the cohort, where additional matching for Fuhrman grade was performed.

Neither of the matched analyses resulted in statistically significant CSM difference (P = .1 and .4) between NSS and RN.

CONCLUSIONS: Our study represents the largest and the only population-based analysis of cancer control efficacy of NSS vs RN in T1bN0M0 RCC.

It indicates that NSS does provide equivalent cancer control relative to RN.

In consequence, based on cancer control equivalence, NSS should be given equal consideration to RN in patients with T1bN0M0 lesions.

[MeSH-major] Carcinoma, Renal Cell / pathology. Carcinoma, Renal Cell / surgery. Kidney Neoplasms / pathology. Kidney Neoplasms / surgery. Nephrectomy / methods

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[Copyright] Crown Copyright 2010. Published by Elsevier Inc. All rights reserved.

[CommentIn] Urology. 2010 Feb;75(2):275-6; author reply 276 [20152477.001]

(PMID = 19962740.001).

[ISSN] 1527-9995

[Journal-full-title] Urology

[ISO-abbreviation] Urology

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States