Christopher J Sweeney

Harvard Medical School, Boston, Massachusetts, United States

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Publications (109)620.98 Total impact

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    ABSTRACT: Second-line treatment options for patients with advanced urothelial carcinoma (UC) are limited. Fibroblast growth factor receptor 3 (FGFR3) is dysregulated in UC by activating mutations or protein overexpression in non-mutant tumours. In this study, the efficacy, pharmacodynamics and safety of dovitinib-a broad-targeted inhibitor of tyrosine kinases, including FGFR3-were evaluated in patients with previously treated advanced UC with and without FGFR3 mutations. Forty-four adults with advanced UC who had progressed after one to three platinum-based and/or combination chemotherapy regimens were classified as having mutant (FGFR3(MUT); n=12), wild-type (FGFR3(WT); n=31), or unknown (n=1) FGFR3 status. Patients received 500mg dovitinib once daily on a 5-days-on/2-days-off schedule. The primary end-point of this two-stage study was the investigator-assessed overall response rate (ORR). Most of the patients were men (75%) and over half of the patients were aged ⩾65years (61%). All patients had received ⩾1 prior antineoplastic therapy for UC. The study was terminated at the end of stage 1, when it was determined by investigator review that the ORR of both the FGFR3(MUT) (0%; 95% confidence interval [CI], 0.0-26.5) and FGFR3(WT) (3.2%; 95% CI, 0.1-16.7) groups did not meet the criteria to continue to stage 2. The most common grade 3/4 adverse events, suspected to be study-drug related, included thrombocytopenia (9%), fatigue (9%), and asthenia (9%). Although generally well tolerated, dovitinib has very limited single-agent activity in patients with previously treated advanced UC, regardless of FGFR3 mutation status. clinicaltrials.gov NCT00790426. Copyright © 2014 Elsevier Ltd. All rights reserved.
    European journal of cancer (Oxford, England: 1990) 12/2014; 50(18):3145-52. · 4.12 Impact Factor
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    ABSTRACT: Definitive treatment of high-risk prostate cancer with radical prostatectomy or radiation improves survival. We assessed whether racial disparities in the receipt of definitive therapy for prostate cancer vary by regional income.
    Urologic oncology. 10/2014;
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    ABSTRACT: OBJECTIVE. The purpose of this study was to investigate whether retroperitoneal craniocaudal nodal length or nodal volume predicts relapse risk in stage I testicular cancer. MATERIALS AND METHODS. We retrospectively reviewed 826 testicular cancer patients. Of these 826 patients, 118 had stage I disease and either less than 2 years of surveillance or retroperitoneal lymph node dissection with no adjuvant chemotherapy. These patients formed our analytic cohort, and 3D nodal volumes and craniocaudal nodal length were measured. Association between relapse risk and craniocaudal nodal length and nodal volume was evaluated using univariable or multivariable logistic regression models adjusted for known prognostic factors. RESULTS. Sixty-six (56%) of 118 patients had nonseminomatous germ cell tumor and 52 (44%) had seminomatous germ cell tumor. Craniocaudal nodal length proved to be an independent risk factor in nonseminomatous germ cell tumors using a multivariable logistic regression model adjusting for other potential known risk factors of embryonal predominance and lymphovascular invasion. For every 3-mm increase in craniocaudal nodal length, the risk of relapse increased by 52% (odds ratio [OR], 1.52; 95% CI, 1.03-2.25). For patients with seminomas, only primary tumor size was an independent risk factor for relapse (1.34, 1.02-1.75). CONCLUSION. In nonseminomatous germ cell tumors, craniocaudal nodal length was shown to be associated with increased risk of relapse independently of other known risk factors. If validated in an independent cohort, craniocaudal nodal length could provide important additional information to inform management decisions in these patients.
    AJR. American journal of roentgenology. 10/2014; 203(4):W415-W420.
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    ABSTRACT: Cabozantinib (XL184), an oral inhibitor of multiple receptor tyrosine kinases such as MET and VEGFR2, was evaluated in a phase II nonrandomized expansion study in castration-resistant prostate cancer (CRPC).
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 09/2014;
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    ABSTRACT: Objectives To determine if androgen deprivation therapy (ADT) is associated with excess cardiac-specific mortality (CSM) in men with prostate cancer and no cardiovascular comorbidity, coronary artery disease risk factors, or congestive heart failure (CHF) or past myocardial infarction (MI).Subjects/patients and methodsFive thousand seventy-seven men (median age, 69.5 years) with cT1c-T3N0M0 prostate cancer were treated with brachytherapy with or without neoadjuvant ADT (median duration, four months) between 1997 and 2006. Fine and Gray's competing risks analysis evaluated the association of ADT with CSM, adjusting for age, year of brachytherapy, and ADT treatment propensity score among men in groups defined by cardiac comorbidity.ResultsAfter a median follow-up of 4.8 years, no association was detected between ADT and CSM in men with no cardiac risk factors (1.08% at 5 years for ADT vs 1.27% at five years for no ADT, adjusted hazard ratio (AHR) 0.83; 95% confidence interval (CI), 0.39-1.78; P=0.64; n=2653) or in men with diabetes mellitus, hypertension, or hypercholesterolemia (2.09% vs 1.97%, AHR, 1.33; 95% CI, 0.70-2.53; P=0.39; n=2168). However, ADT was associated with significantly increased CSM in men with CHF or MI (AHR 3.28; 95% CI 1.01-10.64; P=0.048; n=256). In this subgroup, the five-year cumulative incidence of CSM was 7.01% (95% CI 2.82-13.82%) for ADT vs 2.01% (95% CI 0.38-6.45%) for no ADT.ConclusionADT was associated with a five percent absolute excess risk of CSM at five years in men with CHF or prior MI, suggesting that administering ADT to 20 men in this potentially vulnerable subgroup could result in one cardiac death.
    BJU International 08/2014; · 3.05 Impact Factor
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    ABSTRACT: Background:The Affordable Care Act (ACA) aims to expand health insurance coverage to over 30 million previously uninsured Americans. To help evaluate the potential impact of the ACA on prostate cancer care, we examined the associations between insurance coverage and prostate cancer outcomes among men <65 years old who are not yet eligible for Medicare.Methods:The Surveillance, Epidemiology and End Results Program was used to identify 85 203 men aged <65 years diagnosed with prostate cancer from 2007 to 2010. Multivariable logistic regression modeled the association between insurance status and stage at presentation. Among men with high-risk disease, the associations between insurance status and receipt of definitive therapy, prostate cancer-specific mortality (PCSM) and all-cause mortality were determined using multivariable logistic, Fine and Gray competing-risks and Cox regression models, respectively.Results:Uninsured patients were more likely to be non-white and come from regions of rural residence, lower median household income and lower education level (P<0.001 for all cases). Insured men were less likely to present with metastatic disease (adjusted odds ratio (AOR) 0.23; 95% confidence interval (CI) 0.20-0.27; P<0.001). Among men with high-risk disease, insured men were more likely to receive definitive treatment (AOR 2.29; 95% CI 1.81-2.89; P<0.001), and had decreased PCSM (adjusted hazard ratio 0.56; 95% CI 0.31-0.98; P=0.04) and all-cause mortality (adjusted hazard ratio 0.60; 0.39-0.91; P=0.01).Conclusions:Insured men with prostate cancer are less likely to present with metastatic disease, more likely to be treated if they develop high-risk disease and are more likely to survive their cancer, suggesting that expanding health coverage under the ACA may significantly improve outcomes for men with prostate cancer who are not yet eligible for Medicare.Prostate Cancer and Prostatic Disease advance online publication, 1 July 2014; doi:10.1038/pcan.2014.23.
    Prostate cancer and prostatic diseases. 07/2014;
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    ABSTRACT: To determine whether African Americans (AAs) with intermediate- to high-risk prostate cancer (PCa) receive similar treatment as white patients and whether any observed disparities are narrowing with time.
    Urology 06/2014; · 2.42 Impact Factor
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    ABSTRACT: To evaluate the relationship between age and race on the receipt of definitive therapy among men with high-risk prostate cancer (CaP).
    Journal of Geriatric Oncology 05/2014; · 1.12 Impact Factor
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    ABSTRACT: In advanced urothelial cancer, treatment with dose-dense methotrexate, vinblastine, doxorubicin, and cisplatin (ddMVAC) results in a high response rate, less toxicity, and few dosing delays. We explored the efficacy and safety of neoadjuvant ddMVAC with pegfilgrastim support in muscle-invasive urothelial cancer (MIUC). Patients with cT2-cT4, N0-1, M0 MIUC were enrolled. Four cycles of ddMVAC were administered, followed by radical cystectomy. The primary end point was pathologic response (PaR) defined by pathologic downstaging to ≤ pT1N0M0. The study used Simon's optimal two-stage design to evaluate null and alternative hypotheses of PaR rate of 35% versus 55%. Secondary end points included toxicity, disease-free survival (DFS), radiologic response (RaR), and biomarker correlates, including ERCC1. Between December 2008 and April 2012, 39 patients (cT2N0, 33%; cT3N0, 18%; cT4N0, 3%; cT2-4N1, 43%; unspecified, 3%) were enrolled. Median follow-up was 2 years. Overall, 49% (80% CI, 38 to 61) achieved PaR of ≤ pT1N0M0, and we concluded this regimen was effective. High-grade (grade ≥ 3) toxicities were observed in 10% of patients, with no neutropenic fevers or treatment-related death. One-year DFS was 89% versus 67% for patients who achieved PaR compared with those who did not (hazard ratio [HR], 2.6; 95% CI, 0.8 to 8.1; P = .08) and 86% versus 62% for patients who achieved RaR compared with those who did not (HR, 4.1; 95% CI, 1.3 to 12.5; P = .009). We found no association between serum tumor markers or ERCC1 expression with response or survival. In patients with MIUC, neoadjuvant ddMVAC was well tolerated and resulted in significant pathologic and radiologic downstaging.
    Journal of Clinical Oncology 05/2014; · 18.04 Impact Factor
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    ABSTRACT: The androgen receptor (AR) is a key factor that regulates the behavior and fate of prostate cancer cells. The AR-regulated network is activated when AR binds enhancer elements and modulates specific enhancer-promoter looping. Kallikrein-related peptidase 3 (KLK3), which codes for prostate-specific antigen (PSA), is a well-known AR-regulated gene and its upstream enhancers produce bidirectional enhancer RNAs (eRNAs), termed KLK3e. Here, we demonstrate that KLK3e facilitates the spatial interaction of the KLK3 enhancer and the KLK2 promoter and enhances long-distance KLK2 transcriptional activation. KLK3e carries the core enhancer element derived from the androgen response element III (ARE III), which is required for the interaction of AR and Mediator 1 (Med1). Furthermore, we show that KLK3e processes RNA-dependent enhancer activity depending on the integrity of core enhancer elements. The transcription of KLK3e was detectable and its expression is significantly correlated with KLK3 (R(2) = 0.6213, P < 5 × 10(-11)) and KLK2 (R(2) = 0.5893, P < 5 × 10(-10)) in human prostate tissues. Interestingly, RNAi silencing of KLK3e resulted in a modest negative effect on prostate cancer cell proliferation. Accordingly, we report that an androgen-induced eRNA scaffolds the AR-associated protein complex that modulates chromosomal architecture and selectively enhances AR-dependent gene expression.
    Proceedings of the National Academy of Sciences 04/2014; · 9.81 Impact Factor
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    ABSTRACT: To identify factors associated with weight gain at 1 year from initiation of androgen deprivation therapy (ADT). A retrospective review assessed weight change among 118 men with nonmetastatic prostate cancer treated with ADT for at least 6 months. Outcome associations were tested using 2-tailed t tests and linear regression. Men in our cohort had significant weight gain (+1.32 kg, P = .0005) in the 1 year after ADT initiation. Three risk factors for weight gain on ADT were identified as follows: age <65 years (2.72 kg gained, P = .001), body mass index (BMI) <30 (1.98 kg gained, P = .00002), and nondiabetic status (1.56 kg gained, P = .0003). Multivariable regression found both age <65 years (beta = 4.01, P = .02) and BMI <30 (beta = 3.57, P = .03) to be independently predictive of weight gain, whereas nondiabetic status was nonsignificantly predictive of weight gain (beta = 2.14, P = .29). Weight change was further stratified by the total number of risk factors present (risk score): scores of 0, 1, 2, and 3 risk factors corresponded to weight changes of -1.10, +0.41, +1.34, and +3.79 kg, respectively (P-trend = .0005). Age <65 years and BMI <30 were both independently associated with weight gain 1 year after starting ADT. Increasing weight gain was also strongly associated with increasing number of baseline risk factors present. Despite traditional concerns about ADT in unhealthy men, these data suggest younger, healthier patients may be at higher risk for gaining weight on ADT and should be counseled accordingly.
    Urology 04/2014; · 2.42 Impact Factor
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    ABSTRACT: Chemokines and cytokines have been implicated in progression to castration-resistant prostate cancer (CRPC). Retrospective data were accessed from 122 men with serum samples drawn at a median of 0.5 months after starting ADT for metastatic prostate cancer. MCP-1, IL-1-β, IL-2, IL-8, IL-6, and TNF-α levels were measured by multiplex electrochemiluminescence assays. A multivariable Cox model assessed the association of time to CRPC and overall survival by the protein levels and adjusted for clinical variables (age and prostate specific antigen (PSA) levels at start of ADT, race, ECOG status, and extent of metastases). Associations were reported as hazard ratio (HR) with 95% confidence interval (CI). Median follow-up and overall survival were 44 and 42.2 months, respectively. ECOG performance status (≥1 vs. 0) was negatively associated with overall survival [HR = 2.8 (1.1-7.0), P = 0.03], and PSA nadir < 0.2 was predictive of longer time to development of CRPC [HR = 0.3 (0.2-0.5), P < 0.0001]. The HR for time to CRPC by protein above the median was 1.4 (95% CI: 0.9, 2.2, P = 0.13) for IL-8; 1.3 (95% CI: 0.8, 2, P = 0.18) for TNF-α; 1.0 (95% CI: 0.7, 1.6, P = 0.95) for MCP-1. The HR for median overall survival for protein levels above the median was: 1.9 (95% CI: 1.0, 3.5, P = 0.04) for IL-8; 2.0 (95% CI: 1.1, 3.5, P = 0.02) for TNF-α; 1.7 (95% CI: 1.7, 3.0, P = 0.08) for MCP-1. There was no association with IL-1-β, IL-2, or IL-6. Higher levels of inflammation-associated cytokines correlate with poorer prostate cancer outcomes and may guide strategies to improve prostate cancer therapy. Prostate © 2014 Wiley Periodicals, Inc.
    The Prostate 03/2014; · 3.84 Impact Factor
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    ABSTRACT: Pain negatively affects quality of life for cancer patients. Preliminary data in metastatic castration-resistant prostate cancer (mCRPC) suggested a benefit of the oral tyrosine kinase inhibitor cabozantinib to pain palliation. Prospective evaluation of cabozantinib's benefits on pain and narcotic use in mCRPC. This was a nonrandomized expansion (NRE) cohort (n=144) of a phase 2 randomized discontinuation trial in docetaxel-refractory mCRPC patients. Pain and interference of symptoms with sleep and general activity were electronically self-reported daily for 7-d intervals at baseline and regularly scheduled throughout the study. Mean per-patient scores were calculated for each interval. Narcotic use was recorded daily during the same intervals. Open-label cabozantinib (100mg or 40mg). The following stringent response definition was used: clinically meaningful pain reduction (≥30% improvement in mean scores from baseline) confirmed at a later interval without concomitant increases in narcotics. Only patients with moderate or severe baseline pain were analyzed. Sixty-five patients with moderate or severe baseline pain were evaluable. Of these, 27 (42%) experienced pain palliation according to the stringent response definition. Thirty-seven patients (57%) had clinically meaningful pain relief at two consecutive intervals, reported ≥6 wk apart in the majority. Forty-four patients (68%) had palliation at one or more intervals; 36 (55%) decreased narcotics use during one or more intervals. Clinically meaningful pain reduction was associated with significant (p ≤ 0.001) improvements in sleep quality and general activity. A limitation of this study was its open-label design. Cabozantinib demonstrated clinically meaningful pain palliation, reduced or eliminated patients' narcotic use, and improved patient functioning, thus meriting prospective validation in phase 3 studies. We evaluated the potential of cabozantinib to improve symptoms in patients with metastatic prostate cancer that no longer responds to standard therapies. We saw a promising reduction in pain and reduced need for narcotic painkillers. Larger, well-controlled trials are necessary to confirm these findings.
    European Urology 02/2014; · 10.48 Impact Factor
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    ABSTRACT: Objective To identify factors associated with weight gain at 1 year from initiation of androgen deprivation therapy (ADT). Methods A retrospective review assessed weight change among 118 men with nonmetastatic prostate cancer treated with ADT for at least 6 months. Outcome associations were tested using 2-tailed t tests and linear regression. Results Men in our cohort had significant weight gain (+1.32 kg, P = .0005) in the 1 year after ADT initiation. Three risk factors for weight gain on ADT were identified as follows: age <65 years (2.72 kg gained, P = .001), body mass index (BMI) <30 (1.98 kg gained, P = .00002), and nondiabetic status (1.56 kg gained, P = .0003). Multivariable regression found both age <65 years (beta = 4.01, P = .02) and BMI <30 (beta = 3.57, P = .03) to be independently predictive of weight gain, whereas nondiabetic status was nonsignificantly predictive of weight gain (beta = 2.14, P = .29). Weight change was further stratified by the total number of risk factors present (risk score): scores of 0, 1, 2, and 3 risk factors corresponded to weight changes of −1.10, +0.41, +1.34, and +3.79 kg, respectively (P-trend = .0005). Conclusion Age <65 years and BMI <30 were both independently associated with weight gain 1 year after starting ADT. Increasing weight gain was also strongly associated with increasing number of baseline risk factors present. Despite traditional concerns about ADT in unhealthy men, these data suggest younger, healthier patients may be at higher risk for gaining weight on ADT and should be counseled accordingly.
    Urology 01/2014; · 2.42 Impact Factor
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    ABSTRACT: Background Men with low-risk prostate cancer (CaP) are considered unlikely to die of CaP and have the option of active surveillance. We evaluated whether African Americans (AA) who present with low-risk disease are at higher risk for death from CaP than white patients. Patients and Methods We identified 56,045 men with low-risk CaP (T1-T2a, Gleason score <6, PSA <10) diagnosed between 2004-2009 using the Surveillance, Epidemiology and End Results (SEER) database. We used Fine and Gray’s competing-risks regression analyses to analyze the impact of race on prostate cancer-specific mortality (PCSM) after adjusting for known prognostic and sociodemographic factors in 51,315 (43,792 white; 7,523 AA) patients with clinical follow-up information available. Results After a median follow-up of 46 months, 258 (209 [0.48%] white and 49 [0.65%] AA men) patients died from CaP. Both AA race (Adjusted Hazard Ratio [AHR] 1.45; 95% Confidence Interval [CI] 1.03-2.05; P = 0.032) and non-curative management (AHR 1.49; 95% CI 1.15-1.95; P = 0.003) were significantly associated with an increased risk of PCSM. When analyzing only patients who underwent curative treatment, AA race (AHR 1.62; 95% CI 1.04-2.53; P = 0.034) remained significantly associated with increased PCSM. Conclusion Among men with low-risk prostate cancer, AA compared to white race was associated with a higher risk of PCSM, raising the possibility that clinicians may need to exercise caution when recommending active surveillance for AA men with low-risk disease. Further studies are needed to ultimately determine whether guidelines for active surveillance should take race into account.
    Clinical Genitourinary Cancer 01/2014; · 1.43 Impact Factor
  • Article: Preface.
    Christopher J Sweeney
    Hematology/oncology clinics of North America 12/2013; 27(6):xi-xii. · 2.05 Impact Factor
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    ABSTRACT: Insulin-like growth factor (IGF) and adipokines have been implicated in prostate cancer carcinogenesis. Data from 122 men with serum samples drawn within 3 months of starting ADT for metastatic prostate cancer was accessed retrospectively. IGF-1, IGF binding protein (BP)-1, leptin, and adiponectin levels were measured by multiplex electrochemiluminescence assays. A multivariable Cox model assessed the association of time to castration resistant prostate cancer (CRPC) and overall survival by the protein levels, adjusted for clinical variables, age and prostate specific antigen (PSA) levels at start of ADT, race, ECOG status, extent of metastases and were reported as hazard ratio (HR) with 95% confidence interval (CI). Median follow-up and overall survival were 44 and 42.2 months, respectively. ECOG performance status (≥1 vs. 0) was negatively associated with overall survival [HR = 2.8 (1.1-7.0), P = 0.03], and PSA nadir <0.2 was predictive of longer time to CRPC [HR = 0.3 (0.2-0.5), P < 0.0001]. The median time to CRPC by low, middle, and top IGFBP-1 tertile distribution was 20.7, 18.1, and 12.4 months, respectively, with HR for middle versus low tertile levels 3.1 (1.7-5), P = 0.0003, and for top versus low tertile levels was 2.4 (1.3-4.2), P = 0.003. The median overall survival by low, middle and top tertile IGFBP-1 level was 48.5, 46.4, and 32.8 months, respectively, with HR for top versus low tertile 2.5 (1.2-5.1), P = 0.01. There was no association with IGF-1, adiponectin and leptin. Elevated IGFBP-1 appears to be associated with shorter time to CRPC and lower overall survival in men with metastatic prostate cancer. Prostate © 2013 Wiley Periodicals, Inc.
    The Prostate 10/2013; · 3.84 Impact Factor
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    ABSTRACT: Elevated markers of bone turnover are prognostic for shorter survival in castration-resistant prostate cancer. We aimed to determine the prognostic value of bone turnover markers in metastatic hormone-sensitive prostate cancer. Markers of bone turnover (urine deoxypyridinoline [DPD] and N-telopeptide, serum bone alkaline phosphatase (AP), and osteocalcin [OC]) from baseline and after 6 months of study were assessed in men enrolled in a prospective metastatic prostate cancer trial with androgen deprivation therapy (ADT) with or without risedronate (ClinicalTrials.gov, NCT00216060). Serum samples were collected from 63 patients with bone involvement and a median follow-up of 39.7 months. A multivariate model using Cox regression-which included prostate-specific antigen (PSA) nadir, bisphosphonate treatment, and extent of metastases-showed that suppression of bone turnover markers after 6 months of therapy compared with baseline was significantly associated with longer skeletal-related event (SRE)-free survival. ADT without bisphosphonate therapy was also associated with a decline in markers of bone turnover, presumably resulting from direct anticancer activity. Elevated baseline bone turnover markers were not prognostic. Failure to suppress bone turnover while receiving ADT, even when otherwise responding to therapy, may identify patients with hormone-sensitive metastatic prostate cancer who are destined for a shorter time to SREs and progression.
    Clinical Genitourinary Cancer 10/2013; · 1.43 Impact Factor
  • Journal of Clinical Oncology 09/2013; · 18.04 Impact Factor
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    ABSTRACT: Hormone-sensitive prostate cancer typically progresses to castration resistant prostate cancer (CRPC) after the androgen deprivation therapy. We investigated the impact of microRNAs (miRs) in the transition of prostate cancer to CRPC. MiR-221/-222 was highly expressed in bone metastatic CRPC tumor specimens. We previously demonstrated that transient overexpression of miR-221/-222 in LNCaP promoted the development of the CRPC phenotype. In current study, we show that stably overexpressing miR-221 confers androgen independent (AI) cell growth in LNCaP by rescuing LNCaP cells from growth arrest at G1 phase due to the lack of androgen. Overexpressing of miR-221 in LNCaP reduced the transcription of a subgroup of androgen-responsive genes without affecting the androgen receptor (AR) or AR-androgen integrity. By performing systematic biochemical and bioinformatical analyses, we identified two miR-221 targets, HECTD2 and RAB1A, which could mediate the development of CRPC phenotype in multiple prostate cancer cell lines. Downregulation of HECTD2 significantly affected the androgen-induced and AR-mediated transcription, and downregulation of HECTD2 or RAB1A enhances AI cell growth. As a result of the elevated expression of miR-221, expression of many cell cycle genes was altered and pathways promoting epithelial to mesenchymal transition/tumor metastasis were activated. We hypothesize that a major biological consequence of upregulation of miR-221 is reprogramming of AR signaling, which in turn may mediate the transition to the CRPC phenotype.Oncogene advance online publication, 17 June 2013; doi:10.1038/onc.2013.230.
    Oncogene 06/2013; · 8.56 Impact Factor

Publication Stats

3k Citations
620.98 Total Impact Points

Institutions

  • 2013–2014
    • Harvard Medical School
      • Department of Radiation Oncology
      Boston, Massachusetts, United States
  • 2011–2014
    • Dana-Farber Cancer Institute
      Boston, Massachusetts, United States
  • 1999–2011
    • Indiana University-Purdue University Indianapolis
      • • Department of Medicine
      • • Department of Surgery
      • • Department of Urology
      • • Department of Pathology and Laboratory Medicine
      Indianapolis, IN, United States
  • 2010
    • Royal Adelaide Hospital
      • Department of Medicine
      Tarndarnya, South Australia, Australia
    • Harvard University
      Cambridge, Massachusetts, United States
  • 2009
    • Indiana University-Purdue University School of Medicine
      • Department of Medicine
      Indianapolis, IN, United States