David F Jarrard

University of Wisconsin–Madison, Madison, Wisconsin, United States

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Publications (132)635.82 Total impact

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    ABSTRACT: Epidemiologic, preclinical, and early phase I studies of the cruciferous vegetable bioactive metabolite, 3,3'-diindolylmethane (DIM), support its potential prostate cancer chemopreventive ability. We performed a multicenter, double-blind, placebo-controlled trial of DIM in patients diagnosed with prostate cancer and scheduled for radical prostatectomy. A total of 45 patients with organ-confined prostate cancer were randomized to 21-28 days of an absorption-enhanced formulation of DIM (BR-DIM) at doses of 100 or 200 mg per os twice daily or to placebo twice daily. Prostate tissue levels of DIM were the primary endpoint, with selected secondary biomarker endpoints including blood levels of DIM, total prostate-specific antigen, testosterone, and the insulin-like growth factor-1: insulin-like growth factor binding protein-3 ratio and the urinary 2-hydroxyestrone/16-hydroxyestrone ratio, obtained at baseline, at day 15, and before surgery, as well as tissue expression of androgen receptor, prostate-specific antigen, Ki67, caspase 3 with cytochrome p450 mRNA expression and genotyping (polymorphisms). DIM was well tolerated with excellent study compliance and relatively rapid accrual of all 45 patients within 1 year. DIM levels were detected in only seven of 28 prostate tissue specimens. There was a statistically significant difference in the change in the urinary 2-hydroxyestrone/16-hydroxyestrone ratio from baseline until before surgery between the placebo and 400 mg DIM groups, with otherwise statistically nonsignificant changes in plasma biomarker expression. The administration of BR-DIM to prostate cancer patients before prostatectomy yields detectable plasma levels but without consistent or significant tissue accumulation or biomarker modulation. This study demonstrates the feasibility of biologic evaluation of relatively nontoxic preventive agents in the preprostatectomy setting with the potential for rapid accrual.
    European journal of cancer prevention: the official journal of the European Cancer Prevention Organisation (ECP) 08/2015; DOI:10.1097/CEJ.0000000000000189 · 3.03 Impact Factor
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    ABSTRACT: Background: Androgen-deprivation therapy (ADT) has been the backbone of treatment for metastatic prostate cancer since the 1940s. We assessed whether concomitant treatment with ADT plus docetaxel would result in longer overall survival than that with ADT alone. Methods: We assigned men with metastatic, hormone-sensitive prostate cancer to receive either ADT plus docetaxel (at a dose of 75 mg per square meter of body-surface area every 3 weeks for six cycles) or ADT alone. The primary objective was to test the hypothesis that the median overall survival would be 33.3% longer among patients receiving docetaxel added to ADT early during therapy than among patients receiving ADT alone. Results: A total of 790 patients (median age, 63 years) underwent randomization. After a median follow-up of 28.9 months, the median overall survival was 13.6 months longer with ADT plus docetaxel (combination therapy) than with ADT alone (57.6 months vs. 44.0 months; hazard ratio for death in the combination group, 0.61; 95% confidence interval [CI], 0.47 to 0.80; P<0.001). The median time to biochemical, symptomatic, or radiographic progression was 20.2 months in the combination group, as compared with 11.7 months in the ADT-alone group (hazard ratio, 0.61; 95% CI, 0.51 to 0.72; P<0.001). The rate of a prostate-specific antigen level of less than 0.2 ng per milliliter at 12 months was 27.7% in the combination group versus 16.8% in the ADT-alone group (P<0.001). In the combination group, the rate of grade 3 or 4 febrile neutropenia was 6.2%, the rate of grade 3 or 4 infection with neutropenia was 2.3%, and the rate of grade 3 sensory neuropathy and of grade 3 motor neuropathy was 0.5%. Conclusions: Six cycles of docetaxel at the beginning of ADT for metastatic prostate cancer resulted in significantly longer overall survival than that with ADT alone. (Funded by the National Cancer Institute and others; ClinicalTrials.gov number, NCT00309985.).
    New England Journal of Medicine 08/2015; 373(8). DOI:10.1056/NEJMoa1503747 · 55.87 Impact Factor
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    ABSTRACT: No guidelines currently exist that address the need for rebiopsy in patients with a negative diagnosis of prostate cancer on initial biopsy sample analysis. Accurate diagnosis of prostate cancer in these patients is often complicated by continued elevation of serum PSA levels that are suggestive of prostate cancer, resulting in a distinct management challenge. Following negative initial findings of biopsy sample analysis, total serum PSA levels and serum PSA kinetics are ineffective indicators of a need for a repeat biopsy; therefore, patients suspected of having prostate cancer might undergo several unnecessary biopsy procedures. Several alternative strategies exist for identifying men who might be at risk of prostate cancer despite negative findings of biopsy sample analysis. Use of other serum PSA-related measurements enables more sensitive and specific diagnosis and can be combined with knowledge of clinicopathological features to improve outcomes. Other options include the FDA-approved Progensa(®) test and prostate imaging using MRI. Newer tissue-based assays that measure methylation changes in normal prostate tissue are currently being developed. A cost-effective strategy is proposed in order to address this challenging clinical scenario, and potential directions of future studies in this area are also described.
    Nature Reviews Urology 07/2015; 12(8). DOI:10.1038/nrurol.2015.159 · 4.84 Impact Factor
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    ABSTRACT: Purpose: Senescence is a terminal growth arrest that functions as a tumor suppressor in aging and precancerous cells and is a response to selected anticancer compounds. Lysosomal-β-galactosidase (GLB1) hydrolyzes β-galactose from glycoconjugates and is the origin of senescence-associated β-gal activity (SA-β-gal). Using a new GLB1 antibody, senescence biology was investigated in prostate cancer (PCa) tissues. Experimental design: In vitro characterization of GLB1 was determined in primary prostate epithelial cell cultures passaged to replicative senescence and in therapy-induced senescence in PCa lines using chemotherapeutic agents. FFPE tissue microarrays were subjected to immunofluorescent staining for GLB1, Ki67 and HP1γ and automated quantitative imaging initially using AQUA in exploratory samples and Vectra in a validation series. Results: GLB1 expression accumulates in replicative and induced senescence and correlates with senescent morphology and P16 (CDKN2) expression. In tissue arrays, quantitative imaging detects increased GLB1 expression in high-grade prostatic intraepithelial neoplasia (HGPIN), known to contain senescent cells, and cancer compared to benign prostate tissues (p<0.01) and senescent cells contain low Ki67 and elevated HP1γ. Within primary tumors, elevated GLB1 associates with lower T stage (p=0.01), localized versus metastatic disease (p=0.0003) and improved PSA-free survival (p=0.03). Increased GLB1 stratifies better PSA-free survival in intermediate grade PCa (0.01). Tissues that elaborate higher GLB1 display increased uniformity of expression. Conclusion: Increased GLB1 is a valuable marker in formalin-fixed paraffin-embedded (FFPE) tissues for the senescence-like phenotype and associates with improved cancer outcomes. This protein addresses a lack of senescence markers and should be applicable to study the biologic role of senescence in other cancers.
    PLoS ONE 04/2015; 10(4):e0124366. DOI:10.1371/journal.pone.0124366 · 3.23 Impact Factor

  • The Journal of Urology 04/2015; 193(4):e426. DOI:10.1016/j.juro.2015.02.1118 · 4.47 Impact Factor
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    ABSTRACT: Prior reports have suggested that inhibition of the renin-angiotensin system (RAS) may decrease recurrence of non-muscle invasive bladder cancer (NMIBC). The purpose of this study was to evaluate if treatment with ACE-inhibitors (ACE-I) or angiotensin receptor blockers (ARBs) at initial surgery was associated with decreased recurrence or progression in NMIBC patients. An institutional bladder cancer database identified 340 patients with data available for initial TURBT. Progression was defined increase to stage T2. Cox proportional hazards models were used to evaluate associations with recurrence-free (RFS) and progression-free survival (PFS). Median patient age was 69.6. During a median follow-up of 3 years (IQR 1.3-6.1), 200 (59%) patients had recurrence and 14 (4.1%) had stage progression. Of those, 143 patients were taking ACE-I/ARBs at the time of their first TUR. On univariate analysis, factors associated with improved RFS included presence of CIS (p=0.040), bacillus Calmette-Guerin (BCG) therapy (p=0.003), and ACE-I/ARB therapy (p=0.009). Multivariate analysis demonstrated that patients treated with BCG therapy (HR 0.68, 95% CI 0.47-0.87; p=0.002) or ACE-I/ARB therapy (HR 0.61, 95% CI 0.45-0.84; p=0.005), were less likely to experience tumor recurrence. The 5-year RFS rate was 45.6% for patients treated with ACE-I/ARBs and 28.1% for patients not treated with ACE-I/ARBs (p=0.009). Subgroup analysis was performed evaluating patients on BCG therapy alone (n=85) and combined with ACE-I/ARB therapy (n=52) on NMIBC pathology (Ta, T1, CIS). Multivariate analysis revealed that patients treated with BCG alone (HR 2.19, 95% CI 1.01-4.77; p=0.04) were associated with a worse RFS compared to patients treated with BCG and ACE-I/ARB therapy (HR 0.45, 95% CI 0.21-0.98; p=0.04) for stage Ta. Pharmacologic inhibition of RAS is associated with improved outcomes in bladder cancer patients. RAS inhibitor administration in NMIBC should be studied in a prospective randomized trial. Copyright © 2015 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.
    The Journal of Urology 04/2015; 193(4):e296. DOI:10.1016/j.juro.2015.02.1130 · 4.47 Impact Factor

  • The Journal of Urology 04/2015; 193(4):e677. DOI:10.1016/j.juro.2015.02.2054 · 4.47 Impact Factor
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    The Journal of Urology 04/2015; 193(4):e296-e297. DOI:10.1016/j.juro.2015.02.1131 · 4.47 Impact Factor
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    The Journal of Urology 04/2015; 193(4):e445. DOI:10.1016/j.juro.2015.02.1283 · 4.47 Impact Factor
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    ABSTRACT: Percutaneous biopsy obtained from a single location is prone to sampling error in large heterogeneous renal masses, leading to non-diagnostic results or failure to detect poor prognostic features. The purpose of this study was to evaluate the accuracy of percutaneous biopsy for large renal masses using a modified multi-quadrant technique (quadBX) compared to standard biopsy technique (sBX). Clinical and pathologic data for all patients with ≥ cT2 renal masses who underwent percutaneous biopsy from 2009 - 2014 were reviewed. The quadBX technique was defined as multiple core biopsies from at least four separate solid enhancing areas within the tumor. The incidence of non-diagnostic findings, sarcomatoid features, and procedural complications was recorded and concordance between biopsy specimens and nephrectomy pathology was compared. A total of 122 biopsies were performed for 117 tumors in 116 patients (46 using sBX technique and 76 quadBX technique). Median tumor size was 10 cm (IQR 8-12). Biopsy was non-diagnostic in 5/46 (10.9%) sBX and 0/76 (0%) quadBX, p=0.007. RCC was identified in 96/115 (82.0%) tumors and non-RCC tumors were identified in 21 (18.0%). One complication occurred using the sBX technique;, no complications reported using quadBX technique. Sarcomatoid features were present in 23/96 (23.9%) of large RCC tumors studied. Sensitivity for identifying sarcomatoid features was higher using quadBX technique compared to the sBX technique, 13/15 (86.7%) vs. 2/8 (25.0%), p= 0.0062. Multi-quadrant percutaneous biopsy technique increases the ability to identify aggressive pathologic features in large renal tumors and decreases non-diagnostic biopsy rates. Copyright © 2015 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.
    The Journal of urology 03/2015; 194(4). DOI:10.1016/j.juro.2015.03.106 · 4.47 Impact Factor
  • Michael L Blute · Nathan A Damaschke · David F Jarrard ·
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    ABSTRACT: There is a major deficit in our ability to detect and predict the clinical behavior of prostate cancer (PCa). Epigenetic changes are associated with PCa development and progression. This review will focus on recent results in the clinical application of diagnostic and prognostic epigenetic markers. The development of high throughput technology has seen an enormous increase in the discovery of new markers that encompass epigenetic changes including those in DNA methylation and histone modifications. Application of these findings to urine and other biofluids, but also cancer and noncancerous prostate tissue, has resulted in new biomarkers. There has been a recent commercial development of a DNA methylation-based assay for identifying PCa risk from normal biopsy tissue. Other biomarkers are currently in the validation phase and encompass combinations of multiple genes. Epigenetic changes improve the specificity and sensitivity of PCa diagnosis and have the potential to help determine clinical prognosis. Additional studies will not only provide new and better biomarker candidates, but also have the potential to inform new therapeutic strategies given the reversibility of these processes.
    Current Opinion in Urology 01/2015; 25(1):83-8. DOI:10.1097/MOU.0000000000000132 · 2.33 Impact Factor
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    ABSTRACT: Genomic imprinting is an epigenetic mechanism that restricts gene expression to one inherited allele. Improper maintenance of imprinting has been implicated in a number of human diseases and developmental syndromes. Assays are needed that can quantify the contribution of each paternal allele to a gene expression profile. We have developed a rapid, sensitive quantitative assay for the measurement of individual allelic ratios termed Pyrosequencing for Imprinted Expression (PIE). Advantages of PIE over other approaches include shorter experimental time, decreased labor, avoiding the need for restriction endonuclease enzymes at polymorphic sites, and prevent heteroduplex formation which is problematic in quantitative PCR-based methods. We demonstrate the improved sensitivity of PIE including the ability to detect differences in allelic expression down to 1%. The assay is capable of measuring genomic heterozygosity as well as imprinting in a single run. PIE is applied to determine the status of Insulin-like Growth Factor-2 (IGF2) imprinting in human and mouse tissues. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Journal of Cellular Biochemistry 01/2015; 116(7). DOI:10.1002/jcb.25081 · 3.26 Impact Factor
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    ABSTRACT: Abnormal expression and function of chromatin regulators results in the altered chromatin structure seen in cancer. The chromatin regulator CTCF, its cofactor CHD8, and antagonistic paralogue BORIS have wide-ranging effects on gene regulation. Their concurrent expression and regulation was examined in benign, localized, and metastatic prostate cancer (PCa) arrays with extended follow-up using an automated quantitative imaging system, VECTRA. Epithelial staining was quantified and compared against a range of clinicopathologic variables. CHD8 expression was decreased in HGPIN, localized, and metastatic PCa compared to benign (P < .001). CHD8 promoter hypermethylation, assessed by Quantitative Pyrosequencing, occurred in over 45% of primary cancers in this population as well as the TGCA database. Treatment of cell lines with the demethylating agent 5-Aza-2'-deoxycytidine reinduced expression. An interesting dichotomy for CHD8 was observed within primary cancers, with higher nuclear protein expression associated with adverse clinical outcomes including extracapsular extension (P = .007), presence of metastases (P = .025) and worse PSA-recurrence free survival (P = .048). CHD8 outperformed Gleason score and predicted biochemical failure within intermediate grade prostate cancers. The BORIS/CTCF expression ratio increased in localized (P = .03) and metastatic PCa (P = .006) and was associated with higher Gleason score (P = .02), increased tumor volume (P = .02) and positive margins (P = .04). Per cell heterogeneity of expression revealed all protein expression to be more heterogeneous in cancerous tissue (both P < .001), especially high grade (P < .01). In the first detailed analysis in cancer, a marked loss of CHD8 expression and increased BORIS/CTCF ratio indicate frequent disruption of CTCF and its effector genes in PCa. Copyright © 2014 Neoplasia Press, Inc. Published by Elsevier Inc. All rights reserved.
    Neoplasia (New York, N.Y.) 12/2014; 16(12):1018-27. DOI:10.1016/j.neo.2014.10.003 · 4.25 Impact Factor
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    ABSTRACT: Androgen receptor (AR) signaling initiates mouse prostate development by stimulating prostate ductal bud formation and specifying bud patterns. Curiously, however, prostatic bud initiation lags behind the onset of gonadal testosterone synthesis by about three days. This study's objective was to test the hypothesis that DNA methylation controls the timing and scope of prostate ductal development by regulating Ar expression in the urogenital sinus (UGS) from which the prostate derives. We determined that Ar DNA methylation decreases in UGS mesenchyme during prostate bud formation in vivo and that this change correlates with decreased DNA methyltransferase expression in the same cell population during the same time period. To examine the role of DNA methylation in prostate development, fetal UGSs were grown in serum-free medium and 5 alpha dihydrotestosterone (DHT) and the DNA methylation inhibitor 5′-aza-2′-deoxycytidine (5AzadC) were introduced into the medium at specific times. As a measure of prostate development, in situ hybridization was used to visualize and count Nkx3-1 mRNA positive prostatic buds. We determined that inhibiting DNA methylation when prostatic buds are being specified, accelerates the onset of prostatic bud development, increases bud number, and sensitizes the budding response to androgens. Inhibition of DNA methylation also reduces Ar DNA methylation in UGS explants and increases Ar mRNA and protein in UGS mesenchyme and epithelium. Together, these results support a novel mechanism whereby Ar DNA methylation regulates UGS androgen sensitivity to control the rate and number of prostatic buds formed, thereby establishing a developmental checkpoint.
    Developmental Biology 10/2014; 396(2). DOI:10.1016/j.ydbio.2014.10.006 · 3.55 Impact Factor
  • David F Jarrard · Michael L Blute · Mark A Ritter ·
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    ABSTRACT: A 52-year-old patient with a family history of prostate cancer is screened for prostate cancer on the basis of his prostate-specific antigen (PSA) level. The initial value is 10.2 ng/mL, which is confirmed as 11 ng/mL on repeat testing. Clinically, he is found to have no prostate abnormalities on digital rectal examination (T1c). Prostate ultrasound and biopsy reveal two cores that are 90% positive with a Gleason score of 4 + 3 = 7. The options of surveillance, radiation treatment, or surgery are discussed, and the patient elects to undergo radical prostatectomy. Final pathology confirms an adenocarcinoma with a Gleason score of 7 (4 + 3) that extensively involves the left gland. The tumor margins are negative, and there is no seminal vesicle involvement. However, one obturator node is positive (one of 14 pelvic lymph nodes) for adenocarcinoma, making his pathologic staging pT2cN1M0. Initial postoperative PSA obtained 2 months after surgery is found to be undetectable.
    Journal of Clinical Oncology 10/2014; 32(35). DOI:10.1200/JCO.2014.57.8302 · 18.43 Impact Factor
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    ABSTRACT: While perioperative blood transfusion (BT) has been associated with adverse outcomes in multiple malignancies, the importance of BT timing has not been established.
    European Urology 09/2014; 66(6). DOI:10.1016/j.eururo.2014.08.051 · 13.94 Impact Factor
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    ABSTRACT: The mechanisms underlying the potential for aggressive behavior of prostate cancer (PCa) remain elusive. In this study, whole genome and/or transcriptome sequencing was performed on 19 specimens of PCa, matched adjacent benign prostate tissues, matched blood specimens, and organ donor prostates. A set of novel fusion transcripts was discovered in PCa. Eight of these fusion transcripts were validated through multiple approaches. The occurrence of these fusion transcripts was then analyzed in 289 prostate samples from three institutes, with clinical follow-up ranging from 1 to 15 years. The analyses indicated that most patients [69 (91%) of 76] positive for any of these fusion transcripts (TRMT11-GRIK2, SLC45A2-AMACR, MTOR-TP53BP1, LRRC59-FLJ60017, TMEM135-CCDC67, KDM4-AC011523.2, MAN2A1-FER, and CCNH-C5orf30) experienced PCa recurrence, metastases, and/or PCa-specific death after radical prostatectomy. These outcomes occurred in only 37% (58/157) of patients without carrying those fusion transcripts. Three fusion transcripts occurred exclusively in PCa samples from patients who experienced recurrence or PCa–related death. The formation of these fusion transcripts may be the result of genome recombination. A combination of these fusion transcripts in PCa with Gleason's grading or with nomogram significantly improves the prediction rate of PCa recurrence. Our analyses suggest that formation of these fusion transcripts may underlie the aggressive behavior of PCa.
    American Journal Of Pathology 09/2014; 184(10). DOI:10.1016/j.ajpath.2014.06.025 · 4.59 Impact Factor

  • 39th ESMO Congress (ESMO); 09/2014
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    ABSTRACT: Background and Objectives: To evaluate the effect of operative time on the risk of symptomatic venous thromboembolic events (VTEs) in patients undergoing robot-assisted radical prostatectomy (RARP). Methods: We reviewed the records of all patients at our institution who underwent RARP by a single surgeon from January 2007 until April 2011. Clinical and pathologic information and VTE incidence were recorded for each patient and analyzed by use of logistic regression to evaluate for association with VTE risk. All patients had mechanical prophylaxis, and beginning in February 2008, a single dose of unfractionated heparin, 5000 U, was administered before surgery. Results: A total of 549 consecutive patients were identified, with a median follow-up period of 8 months. During the initial 30 days postoperatively, 10 patients (1.8%) had a VTE (deep venous thrombosis in 7 and pulmonary embolism in 3). The median operative time was 177 minutes (range, 121–360 minutes). An increase in operative time of 30 or 60 minutes was associated with 1.6 and 2.8 times increased VTE risks. A 5-point increase in body mass index and need for blood transfusion were also associated with increased risk of VTEs (odds ratios of 2.0 and 11.8, respectively). Heparin prophylaxis was not associated with a significant VTE risk reduction but also was not associated with a significant increase in estimated blood loss (P = .23) or transfusion rate (P = .37). Conclusion: A prolonged operative time increases the risk of symptomatic VTEs after RARP. Future studies are needed to evaluate the best VTE prophylactic approach in patients at risk.
    JSLS: Journal of the Society of Laparoendoscopic Surgeons / Society of Laparoendoscopic Surgeons 06/2014; 18(2):282-287. DOI:10.4293/JSLS.2014.00101 · 0.91 Impact Factor
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    ABSTRACT: The objective of this study was to compare the predictive ability of potential tissue biomarkers to known prognostic factors that predict RCC recurrence using an automated system of immunohistochemical (IHC) analysis. After IRB approval, a tissue (TMA) microarray was constructed using tissue from patients who had partial or radical nephrectomy for RCC. Patients with metastatic disease were excluded. IHC staining of the TMA for Ki-67, C reactive protein (CRP), carbonic anhydrase 9 (CAIX), HIF1α, HIF2α was analyzed using automated image analysis. Univariable and multivariable analysis was performed to evaluate the association of putative biomarkers and known prognostic factors. Of 216 patients who met entrance criteria, 34 (16%) patients developed metastatic recurrence within a median follow-up interval of 60.9 [IQR 13.9-87.1] months. RCC morphotypes analyzed in this study include clear cell (N=156), papillary (N=38), chromophobe (N=16), and collecting duct/unclassified (N=6). Univariable analysis identified that only increased Ki-67 was predictive of RCC recurrence among the proteins evaluated, in addition to other known clinical and pathologic prognostic factors. After multivariable analysis, Ki-67 was identified as an independently predictive risk factor for RCC recurrence HR 3.73 [CI 1.60-8.68]. Other independent predictors of RCC recurrence included tumor diameter HR 1.20 [1.02-1.41] and perinephric fat invasion HR 4.49 [CI 1.11-18.20]. We conclude that Ki-67 positivity is independently predictive of RCC recurrence after surgery in non-metastatic patients. Automated analysis of tissue protein expression can facilitate more objective and expedient investigation of tissue biomarkers for RCC.
    Human pathology 05/2014; 45(5). DOI:10.1016/j.humpath.2014.01.008 · 2.77 Impact Factor

Publication Stats

4k Citations
635.82 Total Impact Points


  • 1998-2015
    • University of Wisconsin–Madison
      • • Department of Urology
      • • Molecular and Environmental Toxicology Center
      • • Department of Surgery
      Madison, Wisconsin, United States
  • 2003-2014
    • University of Wisconsin - Stout
      Menominee, Wisconsin, United States
  • 2012-2013
    • James Madison University
      Harisonburg, Virginia, United States
    • Comprehensive Cancer Centers of Nevada
      Las Vegas, Nevada, United States
  • 2002
    • Stanford University
      Palo Alto, California, United States
  • 1995-1997
    • Johns Hopkins University
      • Department of Medicine
      Baltimore, Maryland, United States
  • 1996
    • Johns Hopkins Medicine
      • Department of Urology
      Baltimore, Maryland, United States