David M Berman

Queen's University, Kingston, Ontario, Canada

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Publications (60)518.98 Total impact

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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: 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;
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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: 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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    ABSTRACT: A lack of clinically relevant experimental models of human prostate cancer hampers evaluation of potential therapeutic agents. Currently, androgen deprivation therapy is the gold standard treatment for advanced prostate cancer, but inevitably, a subpopulation of cancer cells survives and repopulates the tumor. Tumor cells that survive androgen withdrawal are critical therapeutic targets for more effective treatments, but current model systems cannot determine when they arise in disease progression and are unable to recapitulate variable patient response to treatment. A model system was developed in which stromal-supported xenografts from multiple patients with early-stage localized disease can be tested for response to castration. The histopathology of these xenografts mimicked the original tumors, and short-term host castration resulted in reduced proliferation and increased apoptosis in tumor cells. After 4 weeks of castration, residual populations of quiescent, stem-like tumor cells remained. Without subsequent treatment, these residual cells displayed regenerative potential, because testosterone readministration resulted in emergence of rapidly proliferating tumors. Therefore, this model may be useful for revealing potential cellular targets in prostate cancer, which exist before the onset of aggressive incurable disease. Specific eradication of these regenerative tumor cells that survive castration could then confer survival benefits for patients.
    Sci Transl Med. 01/2013; 5(187):187ra71.
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    ABSTRACT: Prostate cancer is the second leading cause of cancer death among United States men. However, disease aggressiveness is varied, with low-grade disease often being indolent and high-grade cancer accounting for the greatest density of deaths. Outcomes are also disparate among men with high-grade prostate cancer, with upwards of 65% having disease recurrence even after primary treatment. Identification of men at risk for recurrence and elucidation of the molecular processes that drive their disease is paramount, as these men are the most likely to benefit from multimodal therapy. We previously showed that androgen-induced expression profiles in prostate development are reactivated in aggressive prostate cancers. Herein, we report the down-regulation of one such gene, Sparcl1, a secreted protein, acidic and rich in cysteine (SPARC) family matricellular protein, during invasive phases of prostate development and regeneration. We further demonstrate a parallel process in prostate cancer, with decreased expression of SPARCL1 in high-grade/metastatic prostate cancer. Mechanistically, we demonstrate that SPARCL1 loss increases the migratory and invasive properties of prostate cancer cells through Ras homolog gene family, member C (RHOC), a known mediator of metastatic progression. By using models incorporating clinicopathologic parameters to predict prostate cancer recurrence after treatment, we show that SPARCL1 loss is a significant, independent prognostic marker of disease progression. Thus, SPARCL1 is a potent regulator of cell migration/invasion and its loss is independently associated with prostate cancer recurrence.
    Proceedings of the National Academy of Sciences 09/2012; 109(37):14977-14982. · 9.81 Impact Factor
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    ABSTRACT: Androgens initiate a complex network of signals within the UGS that trigger prostate lineage commitment and bud formation. Given its contributions to organogenesis in other systems, we investigated a role for canonical Wnt signaling in prostate development. We developed a new method to achieve complete deletion of beta-catenin, the transcriptional coactivator required for canonical Wnt signaling, in early prostate development. Beta-catenin deletion abrogated canonical Wnt signaling and yielded prostate rudiments that exhibited dramatically decreased budding and failed to adopt prostatic identity. This requirement for canonical Wnt signaling was limited to a brief critical period during the initial molecular phase of prostate identity specification. Deletion of beta-catenin in the adult prostate did not significantly affect organ homeostasis. Collectively, these data establish that beta-catenin and Wnt signaling play key roles in prostate lineage specification and bud outgrowth.
    Developmental Biology 08/2012; 371(2):246-55. · 3.87 Impact Factor
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    ABSTRACT: Prostate cancer is one of the most common malignancies and the second leading cause of death from cancer in men. The molecular mechanisms driving prostate carcinogenesis are complex; with several lines of evidence suggesting that the reexpression of conserved developmental programs plays a key role. In this study, we used conditional gene targeting and organ grafting, to describe conserved roles for the transcription factor Sox9 in the initiation of both prostate organogenesis and prostate carcinogenesis in murine models. Abrogation of Sox9 expression prior to the initiation of androgen signaling blocks the initiation of prostate development. Similarly, Sox9 deletion in two genetic models of prostate cancer (TRAMP and Hi-Myc) prevented cancer initiation. Expression profiling of Sox9-null prostate epithelial cells revealed that the role of Sox9 in the initiation of prostate development may relate to its regulation of multiple cytokeratins and cell adherence/ polarity. Due to its essential role in cancer initiation, manipulation of Sox9 targets in at-risk men may prove useful in the chemoprevention of prostate cancer.
    Oncotarget 07/2012; 3(6):651-63. · 6.64 Impact Factor
  • The Pediatric Infectious Disease Journal 06/2012; 31(6):661. · 3.57 Impact Factor
  • Clinical Infectious Diseases 06/2012; 54(12):1784, 1814-5. · 9.37 Impact Factor
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    ABSTRACT: The completion of the Human Genome Project and the development of genome-based technologies over the past decade have set the stage for a new era of personalized medicine. By all rights, molecularly trained investigative pathologists should be leading this revolution. Singularly well suited for this work, molecular pathologists have the rare ability to wed genomic tools with unique diagnostic skills and tissue-based pathology techniques for integrated diagnosis of human disease. However, the number of pathologists with expertise in genome-based research has remained relatively low due to outdated training methods and a reluctance among some traditional pathologists to embrace new technologies. Moreover, because budding pathologists may not appreciate the vast selection of jobs available to them, they often end up choosing jobs that focus almost entirely on routine diagnosis rather than new frontiers in molecular pathology. This review calls for changes aimed at rectifying these troubling trends to ensure that pathology continues to guide patient care in a post-genomic era.
    Laboratory Investigation 01/2012; 92(1):4-8. · 3.96 Impact Factor

Publication Stats

5k Citations
518.98 Total Impact Points


  • 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