David M Berman

Queen's University, Kingston, Ontario, Canada

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Publications (72)536.67 Total impact

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    ABSTRACT: To describe the relationships between procedure volume and late survival after cystectomy for muscle-invasive bladder cancer (MIBC) and explore variables explaining any effect. Electronic records of treatment and surgical pathology reports were linked to a population-based registry to identify patients who underwent cystectomy during 1994-2008 in Ontario, Canada. Explanatory variables included adjuvant chemotherapy, lymph node dissection (LND), and margin status. A Cox proportional hazards regression model was used to explore associations between volume and cancer-specific survival (CSS) as well as overall survival. The cohort included 2802 MIBC patients treated with cystectomy. High-volume hospitals were more likely to have used adjuvant chemotherapy (25% vs 18%; P <.001), more likely to have performed an LND (83% vs 53%; P <.001), and associated with a lower 90-day mortality (6% vs 10%; P = .032). Low-volume hospitals had a lower 5-year CSS rate of 32% (28%-36%) compared with those of high-volume centers at 38% (33%-42%). Individual surgeon volume was similarly associated with both early- and long-term outcomes. In multivariate analysis, both surgeon and hospital volumes were associated with CSS and overall survival. The surgeon volume effect on long-term outcomes was modestly modified by indicators of the quality of the LND, with little effect of the other explanatory variables. Higher provider volume is associated with higher CSS in patients with MIBC in the general population. The volume effect was modestly mediated by the quality of LND. Copyright © 2014 Elsevier Inc. All rights reserved.
    Urology 10/2014; · 2.42 Impact Factor
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    ABSTRACT: Inflammation is associated with several diseases of the prostate including benign enlargement and cancer, but a causal relationship has not been established. Our objective was to characterize the prostate inflammatory microenvironment after infection with a human prostate derived bacterial strain and to determine the effect of inflammation on prostate cancer progression. To this end, we mimicked typical human prostate infection with retrograde urethral instillation of CP1, a human prostatic isolate of Escherichia coli. CP1 bacteria were tropic for the accessory sex glands and induced acute inflammation in the prostate and seminal vesicles with chronic inflammation lasting at least one year. Compared to controls, infection induced both acute and chronic inflammation with epithelial hyperplasia, stromal hyperplasia, and inflammatory cell infiltrates. In areas of inflammation, epithelial proliferation and hyperplasia often persist despite decreased expression of androgen receptor (AR). Inflammatory cells in the prostates of CP1 infected mice were characterized at 8 weeks post-infection by flow cytometry, which showed an increase in macrophages and lymphocytes, particularly Th17 cells. Inflammation was additionally assessed in the context of carcinogenesis. Multiplex cytokine profiles of inflamed prostates showed distinct inflammatory cytokines were expressed during prostate inflammation and cancer, with a subset of cytokines synergistically increased during concurrent inflammation and cancer. Furthermore, CP1 infection in the Hi-Myc mouse model of prostate cancer accelerated the development of invasive prostate adenocarcinoma with 70% more mice developing cancer by 4.5 months of age. This study provides direct evidence that prostate inflammation accelerates prostate cancer progression, and gives insight into the microenvironment changes induced by inflammation that may accelerate tumour initiation or progression.
    The Journal of Pathology 10/2014; · 7.59 Impact Factor
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    ABSTRACT: Objectives To investigate reporting patterns and outcomes associated with lymphovascular invasion in a general population setting.Methods We identified all cystectomy patients with muscle-invasive urothelial cancer in Ontario, Canada, 1994–2008. Surgical pathology reports were analyzed for pathological variables including lymphovascular invasion. Lymphovascular invasion reporting patterns were described over time. A Cox proportional hazards model was used to evaluate the association of lymphovascular invasion with survival.ResultsOf the 2802 cases identified, lymphovascular invasion status was reported in 75%. Lymphovascular invasion reporting significantly improved over the study period and was correlated with poor prognostic pathological features (T stage and N stage). Comprehensive cancer center status was not consistently associated with lymphovascular invasion reporting. Patients with lymphovascular invasion had substantially lower survival than patients who were lymphovascular invasion-negative or whose lymphovascular invasion status was unstated (P < 0.001). Lymphovascular invasion was independently associated with survival in patients regardless of lymph node metastasis. After adjusting for age, stage, comorbidity, margin status and adjuvant chemotherapy, lymphovascular invasion remained strongly associated with reduced survival (hazard ratio 1.98, 95% confidence interval 1.71–2.29).Conclusions Although routine reporting of lymphovascular invasion has improved over the years, pathologists appear to be biased towards evaluating lymphovascular invasion in patients with high-stage disease. Despite this bias, lymphovascular invasion remains an important prognostic factor among patients treated by cystectomy. Pathologists in general practice should report lymphovascular invasion status more consistently and urologists should hold their pathology colleagues to a higher standard.
    International Journal of Urology 10/2014; · 1.73 Impact Factor
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    ABSTRACT: Objective To evaluate whether pathologic factors are associated with differential effect of ACT.Patients and Methods In this population-based retrospective cohort study we linked electronic records of treatment and surgical pathology to the Ontario Cancer Registry. The study population included all patients with MIBC undergoing cystectomy in Ontario 1994-2008. Factors associated with overall (OS) and cancer-specific survival (CSS) were evaluated using Cox proportional hazards. We tested for interaction between the following variables and ACT effect-size: N stage, margin status, T stage, and lymphovascular invasion (LVI).ResultsThe study population included 2802 patients; 19% were treated with ACT. Interaction terms with ACT for OS/CSS are: N stage (p<0.001/p<0.001); margin status (p=0.054/p=0.048); T stage (p=0.509/p=0.286); and LVI (p=0.361/p=0.405). Magnitude of effect for ACT was greater for patients with node-positive disease (OS HR 0.56, [95%CI 0.47-0.67], CSS HR 0.60 [0.49-0.72]) than for patients with node-negative disease (OS HR 0.80 [0.61-1.03], CSS HR 0.79 [0.59-1.07]). ACT was also associated with greater effect among patients with involved margins (OS HR 0.45 [95%CI 0.33-0.62], CSS HR 0.40 [0.28-0.57]) compared to patients with negative margins (OS HR 0.75 [0.65-0.87], CSS HR 0.79 [0.67-0.93]).Conclusions In this population-based cohort study we observe evidence of interaction between ACT effect and nodal stage and surgical margin status. Our results suggest that patients at highest risk of disease recurrence may derive greatest benefit from ACT.
    BJU International 08/2014; · 3.05 Impact Factor
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    ABSTRACT: Background:Key challenges of biopsy-based determination of prostate cancer aggressiveness include tumour heterogeneity, biopsy-sampling error, and variations in biopsy interpretation. The resulting uncertainty in risk assessment leads to significant overtreatment, with associated costs and morbidity. We developed a performance-based strategy to identify protein biomarkers predictive of prostate cancer aggressiveness and lethality regardless of biopsy-sampling variation.Methods:Prostatectomy samples from a large patient cohort with long follow-up were blindly assessed by expert pathologists who identified the tissue regions with the highest and lowest Gleason grade from each patient. To simulate biopsy-sampling error, a core from a high- and a low-Gleason area from each patient sample was used to generate a 'high' and a 'low' tumour microarray, respectively.Results:Using a quantitative proteomics approach, we identified from 160 candidates 12 biomarkers that predicted prostate cancer aggressiveness (surgical Gleason and TNM stage) and lethal outcome robustly in both high- and low-Gleason areas. Conversely, a previously reported lethal outcome-predictive marker signature for prostatectomy tissue was unable to perform under circumstances of maximal sampling error.Conclusions:Our results have important implications for cancer biomarker discovery in general and development of a sampling error-resistant clinical biopsy test for prediction of prostate cancer aggressiveness.British Journal of Cancer advance online publication, 17 July 2014; doi:10.1038/bjc.2014.396 www.bjcancer.com.
    British journal of cancer. 07/2014;
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    ABSTRACT: When distinguishing between indolent and potentially harmful prostate cancers, the Gleason score is the most important variable, but may be inaccurate in biopsies due to tumor under-sampling. This study investigated whether a molecular feature, PTEN protein loss, could help identify which Gleason score 6 tumors on biopsy are likely to be upgraded at radical prostatectomy. Seventy one patients with Gleason score 6 tumors on biopsy upgraded to Gleason score 7 or higher at prostatectomy (cases) were compared with 103 patients with Gleason score 6 on both biopsy and prostatectomy (controls). A validated immunohistochemical assay for PTEN was performed, followed by fluorescence in situ hybridization (FISH) to detect PTEN gene deletion in a subset. PTEN protein loss and clinical-pathologic variables were assessed by logistic regression. Upgraded patients were older than controls (61.8 vs 59.3 years), had higher pre-operative PSA levels (6.5 vs 5.3 ng/ml) and a higher fraction of involved cores (0.42 vs 0.36). PTEN loss by immunohistochemistry was found in 18% (13/71) of upgraded cases compared with 7% (7/103) of controls (P=0.02). Comparison between PTEN immunohistochemistry and PTEN FISH showed the assays were highly concordant, with 97% (65/67) of evaluated biopsies with intact PTEN protein lacking PTEN gene deletion, and 81% (13/16) of the biopsies with PTEN protein loss showing homozygous PTEN gene deletion. Tumors with PTEN protein loss were more likely to be upgraded at radical prostatectomy than those without loss, even after adjusting for age, preoperative PSA, clinical stage and race (odds ratio=3.04 (1.08-8.55; P=0.035)). PTEN loss in Gleason score 6 biopsies identifies a subset of prostate tumors at increased risk of upgrading at radical prostatectomy. These data provide evidence that a genetic event can improve Gleason score accuracy and highlight a path toward the clinical use of molecular markers to augment pathologic grading.Modern Pathology advance online publication, 4 July 2014; doi:10.1038/modpathol.2014.85.
    Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc. 07/2014;
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    ABSTRACT: Definitive therapy of bladder cancer involves cystectomy or radiotherapy; controversy exists regarding optimal management. Here we describe the management and outcomes of patients treated in routine practice.
    Clinical oncology (Royal College of Radiologists (Great Britain)). 06/2014;
  • David M Berman, Jonathan I Epstein
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    ABSTRACT: Several investigators have challenged the idea that low-grade cancers are a cause for concern, suggesting that the term cancer should not be applied to these tumors. This article reviews the defining features of cancer, and the diagnostic and prognostic classification systems currently used for prostate cancer. Logical, morphologic, and molecular evidence is presented to show that low-grade prostate cancers are correctly classified as cancer. The authors suggest, however, that 6 out of 10 on an aggressiveness scale is inappropriate for indolent cancer, and that a proposed reinterpretation of Gleason grading categories is a more logical way to address overtreatment.
    Urologic Clinics of North America 05/2014; 41(2):339-346. · 1.39 Impact Factor
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    ABSTRACT: While fibroblast growth factor receptor 3 (FGFR3) is frequently mutated or overexpressed in nonmuscle-invasive urothelial carcinoma (UC), the prevalence of FGFR3 protein expression and mutation remains unknown in muscle-invasive disease. FGFR3 protein and mRNA expression, mutational status, and copy number variation were retrospectively analyzed in 231 patients with formalin-fixed paraffin-embedded primary UCs, 33 metastases, and 14 paired primary and metastatic tumors using the following methods: immunohistochemistry, NanoString nCounterTM, OncoMap or Affymetrix OncoScanTM array, and Gain and Loss of Analysis of DNA and Genomic Identification of Significant Targets in Cancer software. FGFR3 immunohistochemistry staining was present in 29% of primary UCs and 49% of metastases and did not impact overall survival (P = 0.89, primary tumors; P = 0.78, metastases). FGFR3 mutations were observed in 2% of primary tumors and 9% of metastases. Mutant tumors expressed higher levels of FGFR3 mRNA than wild-type tumors (P < 0.001). FGFR3 copy number gain and loss were rare events in primary and metastatic tumors (0.8% each; 3.0% and 12.3%, respectively). FGFR3 immunohistochemistry staining is present in one third of primary muscle-invasive UCs and half of metastases, while FGFR3 mutations and copy number changes are relatively uncommon.
    Cancer Medicine 05/2014;
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    ABSTRACT: INTRODUCTIONBy regulating cell fate, proliferation, and survival, Notch pathway signaling provides critical input into differentiation, organization, and function of multiple tissues. Notch signaling is also becoming an increasingly recognized feature in malignancy, including prostate cancer, where it may play oncogenic or tumor suppressive roles.METHODS Based on an electronic literature search from 2000 to 2013 we identified, summarized, and integrated published research on Notch signaling dynamics in prostate homeostasis and prostate cancer.RESULTSIn benign prostate, Notch controls the differentiation state and architecture of the gland. In prostate cancer, similar features correlate with lethal potential and may be influenced by Notch. Increased Notch1 can confer a survival advantage on prostate cancer cells, and levels of Notch family members, such as Jagged2, Notch3, and Hes6 increase with higher cancer grade. However, Notch signaling can also antagonize growth and survival of both benign and malignant prostate cells, possibly through antagonistic effects of the Notch target HEY1 on androgen receptor function.DISCUSSIONNotch signaling can dramatically influence prostate development and disease. Determining the cellular contexts where Notch promotes or suppresses prostate growth could open opportunities for diagnostic and therapeutic interventions. Prostate © 2014 Wiley Periodicals, Inc.
    The Prostate 04/2014; · 3.84 Impact Factor
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    ABSTRACT: BACKGROUND Practice guidelines recommend neoadjuvant chemotherapy (NACT) for bladder cancer. However, the evidence in support of adjuvant chemotherapy (ACT) is less robust. Here we describe whether the evidence of efficacy for NACT/ACT was sufficient to change clinical practice and whether the efficacy demonstrated in clinical trials was translated into effectiveness in the general population.METHODS Electronic records of treatment were linked to the population-based Ontario Cancer Registry to identify all patients with bladder cancer treated with cystectomy in Ontario 1994-2008. Utilization of NACT/ACT was compared across 1994-1998, 1999-2003, and 2004-2008. Logistic regression was used to analyze factors associated with NACT/ACT. Cox model and propensity score analyses were used to explore the association between ACT and survival.RESULTSTwo thousand forty-four patients underwent cystectomy for muscle-invasive bladder cancer (MIBC). Use of NACT remained stable (mean, 4%), whereas utilization of ACT increased over time (16%, 18%, 22%; P = .001). Advanced stage (T3/T4; OR, 1.83; 95% CI, 1.38-2.46) and node-positive disease (OR, 8.10; 95% CI, 6.20-10.7) were associated with greater utilization of ACT. Five-year overall survival (OS) and cancer-specific survival (CSS) for all patients was 29% (95% CI, 28%-31%) and 33% (95% CI, 31%-35%), respectively. Utilization of ACT was associated with improved OS (HR, 0.71; 95% CI, 0.62-0.81) and CSS (HR, 0.73; 95% CI, 0.64-0.84). Results were consistent in propensity score analyses.CONCLUSIONSNACT remains substantially underutilized in routine clinical practice. Our results suggest that perioperative chemotherapy is associated with a substantial survival benefit in the general population. Patients who are planning to undergo cystectomy for bladder cancer should be reviewed by a multidisciplinary team. Cancer 2013. © 2013 American Cancer Society.
    Cancer 04/2014; · 5.20 Impact Factor
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    ABSTRACT: Metastatic urothelial carcinoma (UC) of the bladder is associated with multiple somatic copy number alterations (SCNAs). We evaluated SCNAs to identify predictors of poor survival in patients with metastatic UC treated with platinum-based chemotherapy. We obtained overall survival (OS) and array DNA copy number data from metastatic UC patients in two cohorts. Associations between recurrent SCNAs and OS were determined by a Cox proportional hazard model adjusting for performance status and visceral disease. mRNA expression was evaluated for potential candidate genes by Nanostring nCounter to identify transcripts from the region that are associated with copy number gain. In addition, expression data from an independent cohort was used to identify candidate genes. Multiple areas of recurrent significant gains and losses were identified. Gain of 1q23.3 was independently associated with a shortened OS in the both cohorts (adjusted HR 2.96; 95% CI, 1.35 to 6.48; P = 0.01 and adjusted HR 5.03; 95% CI 1.43-17.73; P < 0.001). The F11R, PFDN2, PPOX, USP21 and DEDD genes, all located on 1q23.3, were closely associated with poor outcome. 1q23.3 copy number gain displayed association with poor survival in two cohorts of metastatic UC. The identification of the target of this copy number gain is ongoing, and exploration of this finding in other disease states may be useful for the early identification of poor risk UC patients. Prospective validation of the survival association is necessary to demonstrate clinical relevance.
    Clinical Cancer Research 01/2014; · 7.84 Impact Factor
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    ABSTRACT: Infection after implantation of spinal rods is a significant complication of this procedure. Optimal treatment of surgical implants often involves device removal. This approach is problematic when treating spinal implant related infections, because device removal may cause significant morbidity. Medical management of these infections is therefore necessary, but treatment regimens are not standardized. We conducted a retrospective review of pediatric patients with spinal implant-related infections at a regional spinal center for a 6 year period. We describe clinical course, duration of treatment and outcomes. We reviewed records of patients with spinal implant-related infections from 2005-2010. Data collection included demographics, underlying diagnosis, surgical hardware, timing to infection after implantation, signs and symptoms of infection, duration of antimicrobials, adverse drug events, and long-term outcomes. We enrolled 23 patients with spinal implant infections, ages 8-20 years. Wound drainage was the most common presenting symptom (82.6%). Median time from surgery to first infection was 16 days (range 8-1052 days). Median length of antimicrobial therapy was 131 days (range 42-597 days). Seventy eight percent were cured with antibiotics alone with implanted devices retained. Four patients failed medical therapy, and required device removal. A wide range of antibiotic duration was used (42 days to > 597 days). Seven patients (30.4%) experienced at least one adverse drug event. Infection related to spinal instrumentation procedures can be managed medically with long term antibiotic therapy. Careful monitoring for not only efficacy but also for adverse drug events is advised. Further research is needed to determine the optimal duration of antibiotics for spinal implant-related infections.
    The Pediatric Infectious Disease Journal 01/2014; · 3.57 Impact Factor
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    ABSTRACT: Anaplastic lymphoma kinase (ALK) genomic alterations have emerged as a potent predictor of benefit from treatment with ALK inhibitors in several cancers. Currently, there is no information about ALK gene alterations in urothelial carcinoma (UC) and its correlation with clinical or pathologic features and outcome.
    PLoS ONE 01/2014; 9(8):e103325. · 3.53 Impact Factor
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    ABSTRACT: Aims Definitive therapy of bladder cancer involves cystectomy or radiotherapy; controversy exists regarding optimal management. Here we describe the management and outcomes of patients treated in routine practice. Materials and methods Treatment records were linked to the Ontario Cancer Registry to identify all cases of bladder cancer in Ontario treated with cystectomy or radiotherapy in 1994–2008. Practice patterns are described in three study periods: 1994–1998, 1999–2003, 2004–2008. Logistic regression, Cox model and propensity score analyses were used to evaluate factors associated with treatment choice and survival. Results In total, 3879 cases (74%) underwent cystectomy and 1380 (26%) were treated with primary radiotherapy. Cystectomy use increased over time (66, 75, 78%), whereas radiotherapy decreased (34, 25, 22%), P < 0.001. There was substantial regional variation in the proportion of cases undergoing radiotherapy (range 16–51%). Five year cancer-specific survival (CSS) and overall survival were 40 and 36% for surgical cases and 35 and 26% for radiotherapy cases (P < 0.001). In multivariate Cox model and propensity score analyses, there was no significant difference in CSS between surgery and radiotherapy (hazard ratio 0.99, 95% confidence interval 0.91–1.08); radiotherapy was associated with slightly inferior overall survival (hazard ratio 1.08, 95% confidence interval 1.00–1.16). Conclusion Utilisation of cystectomy for bladder cancer in routine practice has increased over time with no evidence of a significant difference in CSS between radiotherapy and cystectomy.
    Clinical Oncology. 01/2014;
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    ABSTRACT: We have witnessed significant progress in gene-based approaches to cancer prognostication, promising early intervention for high-risk patients and avoidance of overtreatment for low-risk patients. However, there has been less advancement in protein-based approaches, even though perturbed protein levels and post-translational modifications are more directly linked with phenotype. Most current, gene expression-based platforms require tissue lysis resulting in loss of structural and molecular information, and hence are blind to tumor heterogeneity and morphological features.
    Proteome Science 01/2014; 12:40. · 2.42 Impact Factor
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    ABSTRACT: Micro ribonucleic acid (miR) expression is altered in urologic malignancies, including bladder cancer (BC). Individual miRs have been shown to modulate multiple signaling pathways that contribute to BC. We reviewed the primary literature on the role of miRs in BC; we provide a general introduction to the processing, regulation, and function of miRs as tumor suppressors and oncogenes and critically evaluate the literature on the implications of altered miR expression in BC. We searched the English language literature for original and review articles in PubMed from 1993 to March 2013, using the terms "microRNA" and "bladder cancer," "transitional cell carcinoma," or "urothelial carcinoma." This search yielded 133 unique articles with more than 85% of them published within the last 3 years. To date, the majority of miR studies in BC use profiling to describe dynamic changes in miR expression across stage and grade. Generalized down-regulation of miRs, including those that target the fibroblast growth factor 3 pathway, such as miR-145, miR-101, miR-100, and miR-99a, has been observed in low-grade, non-muscle invasive BC. In contrast, generalized increased expression of miRs is observed in high-grade, muscle-invasive BC compared with adjacent normal bladder urothelium, including miRs predicted to target p53, such as miR-21 and miR-373. Furthermore, p53 suppresses transcriptional factors that promote mesenchymal differentiation, ZEB-1 and ZEB-2, through regulation of the miR200 family. Aberrations in miR expression identified between non-muscle invasive BC and muscle-invasive BC provide insight into the molecular alterations known to distinguish the two parallel pathways of bladder carcinogenesis. The heterogeneity of tumor specimens and research methods limits the reproducibility of changes in miR expression profiles between studies and underscores the importance of in vivo validation in a field that utilizes in silico miR target-prediction models.
    Urologic Oncology 08/2013; · 3.65 Impact Factor
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    ABSTRACT: Circulating tumor cells (CTCs) have received intense scientific scrutiny because they travel in the bloodstream and are therefore well situated to mediate hematogenous metastasis. However, the potential of CTCs to actually form new tumors has not been tested. Popular methods of isolating CTCs are biased towards larger, more differentiated, non-viable cells, creating a barrier to testing their tumor forming potential. Without relying on cell size or the expression of differentiation markers, our objective was to isolate viable prostate CTCs from mice and humans and assay their ability to initiate new tumors. Therefore, blood was collected from transgenic adenocarcinoma of the mouse prostate (TRAMP) mice and from human patients with metastatic castration-resistant prostate cancer (PCa). Gradient density centrifugation or red cell lysis was used to remove erythrocytes, and then leukocytes were depleted by magnetic separation using CD45 immunoaffinity beads. CTCs fractions from TRAMP mice and PCa patients were verified by immunocytochemical staining for cytokeratin 8 and EpCAM, and inoculated into immunodeficient mice. TRAMP tumor growth was monitored by palpation. Human tumor growth formation was monitored up to 8 months by ultrasensitive PSA assays performed on mouse serum. We found viable tumor cells present in the bloodstream that were successfully isolated from mice without relying on cell surface markers. Two out of nine immunodeficient mice inoculated with TRAMP CTCs developed massive liver metastases. CTCs were identified in blood from PCa patients but did not form tumors. In conclusion, viable CTCs can be isolated without relying on epithelial surface markers or size fractionation. TRAMP CTCs were tumorigenic, so CTCs isolated in this way contain viable tumor-initiating cells. Only two of nine hosts grew TRAMP tumors and none of the human CTCs formed tumors, which suggests that most CTCs have relatively low tumor-forming potential. Future studies should identify and target the highly tumorigenic cells.
    Oncotarget 03/2013; · 6.64 Impact Factor
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    2nd Canadian Cancer Research Conference; 01/2013
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    64th CAP-ACP Annual Meeting; 01/2013

Publication Stats

5k Citations
536.67 Total Impact Points

Institutions

  • 2014
    • Queen's University
      • Department of Pathology and Molecular Medicine
      Kingston, Ontario, Canada
  • 2002–2014
    • Johns Hopkins University
      • • Department of Pathology
      • • Department of Medicine
      • • Department of Molecular Biology and Genetics
      Baltimore, Maryland, United States
    • University of Washington Seattle
      Seattle, Washington, United States
  • 2013
    • Dana-Farber Cancer Institute
      Boston, Massachusetts, United States
  • 2009–2012
    • Johns Hopkins Medicine
      • • Department of Pathology
      • • Department of Pediatrics
      Baltimore, MD, United States
    • University of Alabama at Birmingham
      • Division of Infectious Diseases
      Birmingham, AL, United States
  • 2007
    • Centre for Cancer Biology
      Tarndarnya, South Australia, Australia
  • 2006
    • University of Texas MD Anderson Cancer Center
      • Department of Epidemiology
      Houston, TX, United States
  • 2004–2006
    • National Cancer Institute (USA)
      • • Center for Cancer Research
      • • Laboratory of Pathology
      Bethesda, MD, United States
    • National Institutes of Health
      • Laboratory of Pathology
      Bethesda, MD, United States
  • 2003–2004
    • Howard Hughes Medical Institute
      Ashburn, Virginia, United States