George F Murphy

Brigham and Women's Hospital , Boston, Massachusetts, United States

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Publications (183)1051.35 Total impact

  • Plastic and reconstructive surgery 04/2014; 133(4 Suppl):1021. · 2.74 Impact Factor
  • Journal of Clinical Oncology 03/2014; · 18.04 Impact Factor
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    ABSTRACT: Preventing unfavorable graft-versus-host disease (GVHD) without inducing broad suppression of the immune system presents a major challenge of allogeneic hematopoietic stem cell transplantation. We developed a novel strategy to ameliorate GVHD while preserving graft-versus-tumor (GVT) activity by small molecule-based inhibition of the NF-κB family member c-Rel. Underlying mechanisms included reduced alloactivation, defective gut homing, and impaired negative feedback on IL-2 production resulting in optimal IL-2 levels, which, in the absence of competition by effector T-cells, translated into expansion of regulatory T-cells. c-Rel activity was dispensable for antigen-specific T-cell receptor activation, allowing c-Rel-deficient T-cells to display normal GVT activity. In addition, inhibition of c-Rel activity reduced alloactivation without compromising antigen-specific cytotoxicity of human T-cells. Finally, we were able to demonstrate feasibility and efficacy of systemic c-Rel inhibitor administration. Our findings validate c-Rel as a promising target for immunomodulatory therapy and demonstrate feasibility and efficacy of pharmaceutical inhibition of c-Rel activity.
    Cancer Discovery 02/2014; · 10.14 Impact Factor
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    ABSTRACT: We previously established a mast cell (MC)-dependent thermal injury model in mice with ulceration and scar formation that depended on nonredundant functions of mouse MC protease (mMCP)4 and mMCP5. We hypothesized that MC activation is an early event and now find by histology that exocytosis of granule contents occurred by 2 min after thermal injury in wild-type (WT) C57BL/6 mice and in the mMCP4- or mMCP5-deficient mice. The degranulation was equivalent for MCs in the dermis and hypodermis of all three strains, but only the WT mice showed an appreciable increase in epidermal thickness. There was no loss of total MCs, partially degranulated plus intact, during the 4 h of observation. By electron microscopy, MCs in all strains showed early zonal degranulation at 30 s with marked progression in magnitude by 120 s and no mitochondrial injury or cellular necrosis. Concomitantly there was an increase in intercellular spaces indicative of tight junction (TJ) disruption in WT mice but not in the mMCP4- or mMCP5-deficient strains. The desmosomes were intact in all strains. Immunodetection of the TJ protein claudin 4 in WT and mMCP5-deficient mice indicated a significant reduction after scald injury whereas mMCP4(-/-) mice showed no significant changes. Taken together, these findings reveal that a second-degree burn injury can initiate an immediate novel zonal degranulation of MCs throughout all skin layers and a disruption of the epidermal TJs dependent on the nonredundant presence of mMCP4 and mMCP5.
    The Journal of Immunology 02/2014; · 5.52 Impact Factor
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    ABSTRACT: Of more than 150 000 published studies evaluating new biomarkers, fewer than 100 biomarkers have been implemented for patient care. One reason for this is lack of rigorous testing by the medical community to validate claims for biomarker clinical relevance, and potential reluctance to publish negative results when confirmation is not obtained. Here we sought to determine the utility and reproducibility of immunohistochemical detection of hepatocyte growth factor (HGF) in melanoma tissue, an approach of potential assistance in defining patients with innate resistance to BRAF inhibitor therapy. To this end, a published and a revised method that retained sensitivity but with greater specificity for HGF detection, were evaluated in cells known to endogenously express HGF, and in models where HGF is upregulated via cytokine induction and via overexpression by gene transfection. Consequent patient evaluation in collaboration with the Melanoma Institute Australia of a cohort of 41 melanoma specimens with extensive clinical annotation failed to validate HGF immunohistochemistry as a predictor of response to BRAF inhibitors. Targeted therapies for advanced melanoma and other cancers show great promise, and rigorous validation studies are thus indicated for approaches that seek to personalize such therapies to maximize therapeutic efficacy.Modern Pathology advance online publication, 17 January 2014; doi:10.1038/modpathol.2013.226.
    Modern Pathology 01/2014; · 5.25 Impact Factor
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    ABSTRACT: This series of 113 sequential biopsies of full facial transplants provides findings of potential translational significance as well as biological insights that could prompt reexamination of conventional paradigms of effector pathways in skin allograft rejection. Serial biopsies before, during, and after rejection episodes were evaluated for clinicopathological assessment that in selected cases included specific biomarkers for donor-versus-recipient T cells. Histologic evidence of rejection included lymphocyte-associated injury to epidermal rete ridges, follicular infundibula, and dermal microvessels. Surprisingly, during active rejection, immune cells spatially associated with target cell injury consisted abundantly or predominantly of lymphocytes of donor origin with an immunophenotype typical of the resident memory T-cell subset. Current dogma assumes that skin allograft rejection is mediated by recipient T cells that attack epidermal targets, and the association of donor T cells with sites of target cell injury raises questions regarding the potential complexity of immune cell interactions in the rejection process. A more histopathologically refined and immune-based biomarker approach to assessment of rejection of facial transplants is now indicated.Modern Pathology advance online publication, 17 January 2014; doi:10.1038/modpathol.2013.249.
    Modern Pathology 01/2014; · 5.25 Impact Factor
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    ABSTRACT: DNA methylation is the most well-studied epigenetic modification in cancer biology. 5-hydroxymethylcytosine is an epigenetic mark that can be converted from 5-methylcytosine by the ten-eleven translocation gene family. We recently reported the loss of 5-hydroxymethylcytosine in melanoma compared with benign nevi and suggested that loss of this epigenetic marker is correlated with tumor virulence based on its association with a worse prognosis. In this study, we further characterize the immunoreactivity patterns of 5-hydroxymethylcytosine in the full spectrum of melanocytic lesions to further validate the potential practical application of this epigenetic marker. One hundred and seventy-five cases were evaluated: 18 benign nevi, 20 dysplastic nevi (10 low-grade and 10 high-grade lesions), 10 atypical Spitz nevi, 20 borderline tumors, 5 melanomas arising within nevi, and 102 primary melanomas. Progressive loss of 5-hydroxymethylcytosine from benign dermal nevi to high-grade dysplastic nevi to borderline melanocytic neoplasms to melanoma was observed. In addition, an analysis of the relationship of nuclear diameter with 5-hydroxymethylcytosine staining intensity within lesional cells revealed a significant correlation between larger nuclear diameter and decreased levels of 5-hydroxymethylcytosine. Furthermore, borderline lesions uniquely exhibited a diverse spectrum of staining of each individual case. This study further substantiates the association of 5-hydroxymethylcytosine loss with dysplastic cytomorphologic features and tumor progression and supports the classification of borderline lesions as a biologically distinct category of melanocytic lesions.Modern Pathology advance online publication, 3 January 2014; doi:10.1038/modpathol.2013.224.
    Modern Pathology 01/2014; · 5.25 Impact Factor
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    ABSTRACT: Melanoma is a tumor where virulence is conferred on transition from flat (radial) to three-dimensional (tumorigenic) growth. Virulence of tumorigenic growth is governed by numerous attributes, including presence of self-renewing stem-like cells and related formation of patterned networks associated with the melanoma mitogen, laminin, a phenomenon known as vasculogenic mimicry. Vasculogenic mimicry is posited to contribute to melanoma perfusion and nutrition in vivo; we hypothesized that it may also play a role in stem cell-driven spheroid formation in vitro. Using a model of melanoma in vitro tumorigenesis, laminin-associated networks developed in association with three-dimensional melanoma spheroids. Real-time PCR analysis of laminin subunits showed that spheroids formed from anchorage-independent melanoma cells expressed increased α4 and β1 laminin chains and α4 laminin expression was confirmed by in situ hybridization. Association of laminin networks with melanoma stem cell-associated nestin and vascular endothelial growth factor receptor-1 also was documented. Moreover, knockdown of nestin gene expression impaired laminin expression and network formation within spheroids. Laminin networks were remarkably similar to those observed in melanoma xenografts in mice and to those seen in patient melanomas. These data indicate that vasculogenic mimicry-like laminin networks, in addition to their genesis in vivo, are integral to the extracellular architecture of melanoma spheroids in vitro, where they may serve as stimulatory scaffolds to support three-dimensional growth.
    American Journal Of Pathology 01/2014; 184(1):71-78. · 4.52 Impact Factor
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    ABSTRACT: To compare American Joint Committee on Cancer (AJCC), International Union Against Cancer (UICC), and Brigham and Women's Hospital (BWH) tumor (T) staging systems for cutaneous squamous cell carcinoma and validate BWH staging against prior data. Primary tumors diagnosed from 2000 to 2009 at BWH (n = 1,818) were analyzed. Poor outcomes (local recurrence [LR], nodal metastasis [NM], and disease-specific death [DSD]) were analyzed by T stage with regard to each staging system's distinctiveness (outcome differences between stages), homogeneity (outcome similarity within stages), and monotonicity (outcome worsening with increasing stage). AJCC and UICC T3 and T4 were indistinct with overlapping 95% CIs for 10-year cumulative incidences of poor outcomes, but all four BWH stages were distinct. AJCC and UICC high-stage tumors (T3/T4) were rare at 0.3% and 3% of the cohort, respectively. Most poor outcomes occurred in low stages (T1/T2; AJCC: 86% [95% CI, 77% to 91%]; UICC: 70% [61% to 79%]) resulting in heterogeneous outcomes in T1/T2. Conversely, in BWH staging, only 5% of tumors were high stage (T2b/T3), but they accounted for 60% (95% CI, 50% to 69%) of poor outcomes (70% of NMs and 83% of DSDs) indicating superior homogeneity and monotonicity as previously defined. Cumulative incidences of poor outcomes were low for BWH low-stage (T1/T2a) tumors (LR, 1.4% [95% CI, 1% to 2%]; NM, 0.6% [95% CI, 0% to 1%]; DSD, 0.2% [95% CI, 0% to 0.5%]) and higher for high-stage (T2b/T3) tumors (LR, 24% [95% CI, 16% to 34%]; NM, 24% [95% CI, 16% to 34%]; and DSD, 16% [95% CI, 10% to 25%], which validated an earlier study of an alternative staging system. BWH staging offers improved distinctiveness, homogeneity, and monotonicity over AJCC and UICC staging. Population-based validation is needed. BWH T2b/T3 tumors define a high-risk group requiring further study for optimal management.
    Journal of Clinical Oncology 12/2013; · 18.04 Impact Factor
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    ABSTRACT: ATP-binding cassette (ABC) transporters in placenta protectively transport drugs and xenobiotics. ABCB5 [subfamily B (MDR/TAP)] is a novel ABC multidrug-resistance transporter that also mediates cell fusion, stem cell function, and vasculogenic plasticity. Immunohistochemistry and double-labeling immunofluorescence staining for ABCB5 and ABCB5/CD200, respectively, was performed on formalin-fixed, paraffin-embedded placental tissue from 5 first trimester, 5 second trimester, and 5 term pregnancies as well as 5 partial moles, and 5 complete moles. In addition, tumor cells from 5 choriocarcinoma and 5 placental site trophoblastic tumor cases were examined. ABCB5 staining was observed in villous trophoblasts in 100% (5/5) of first trimester placentas (with progressive decrease in term placentas); 100% of partial moles (5/5); and 100% of complete moles (5/5). Notably, reactivity was discretely restricted to the inner trophoblast layer, with no staining of overlying syncytiotrophoblast. Antibody specificity and localization was confirmed further by in situ hybridization. ABCB5 expression was retained in 20% of choriocarcinomas (1/5) and 40% of placental site trophoblastic tumors (2/5). Prior studies have localized expression of multidrug-resistance-1, also known as ABCB1, within the syncytiotrophoblast of early placentas, where it serves a protective function as an efflux transporter. Our results show that ABCB5 is preferentially expressed in the cytotrophoblast layer of placental villi. The expression of this novel biomarker at the maternal-fetal interface raises questions on its role in placental structure and function as well as on its potential contribution to the protective efflux provided by other P-glycoprotein transporters.
    International journal of gynecological pathology: official journal of the International Society of Gynecological Pathologists 12/2013; · 2.07 Impact Factor
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    ABSTRACT: Background Pattern (androgenetic) alopecia is commonly encountered in scalp biopsies obtained for non-scarring hair loss. Prostaglandin D-synthase is known to be elevated in bald versus non-alopetic scalp of patients with androgenetic alopecia. We hypothesized that this difference in pattern of prostaglandin D-synthase expression may constitute a developmental pattern inherent to normal as well as alopecic scalp skin, thus defining a ‘field’ vulnerable to acquired hair loss. Methods We immunohistochemically mapped prostaglandin D-synthase expression from supra-auricular to vertex scalp skin of 11 cadavers. ResultsWe found significantly more dermal mast cells immunoreactive for prostaglandin D-synthase in the vertex compared to the lateral aspects of the scalp, with a decrement that spatially approximated the pattern of androgenetic alopecia. This difference was present in both balding and non-balding scalps and was independent of gender. Dual labeling established dermal cells expressing prostaglandin D-synthase as mast cells. Conclusions These data indicate that scalp is spatially programmed via mast cell prostaglandin D-synthase distribution in a manner reminiscent of the pattern seen in androgenetic alopecia.
    Journal of Cutaneous Pathology 12/2013; · 1.77 Impact Factor
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    ABSTRACT: Genetic predisposition plays a major role in the etiology of melanoma, but known genetic markers only account for a limited fraction of family-history-associated melanoma cases. Expression microarrays have offered the opportunity to identify further genomic profiles correlated with family history of melanoma. We aimed to distinguish mRNA expression signatures between melanoma cases with and without a family history of melanoma. Based on the Nurses' Health Study, family history was defined as having one or more first-degree family members diagnosed with melanoma. Melanoma diagnosis was confirmed by reviewing pathology reports, and tumor blocks were collected by mail from across the USA. Genomic interrogation was accomplished through evaluating expression profiling of formalin-fixed paraffin-embedded tissues from 78 primary cutaneous invasive melanoma cases, on either a 6K or whole-genome (24K) Illumina gene chip. Gene set enrichment analysis was performed for each batch to determine the differentially enriched pathways and key contributing genes. The CXC chemokine receptor 4 (CXCR4) pathway was consistently up-regulated within cases of familial melanoma in both platforms. Leading edge analysis showed four genes from the CXCR4 pathway, including MAPK1, PLCG1, CRK, and PTK2, were among the core members that contributed to the enrichment of this pathway. There was no association between the enrichment of CXCR4 pathway and NRAS, BRAF mutation, or Breslow thickness of the primary melanoma cases. We found that the CXCR4 pathway might constitute a novel susceptibility pathway associated with family history of melanoma in first-degree relatives.
    Cancer Causes and Control 10/2013; · 3.20 Impact Factor
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    ABSTRACT: Melanoma stem cells, also known as malignant melanoma-initiating cells, are identifiable through expression of specific biomarkers such as ABCB5 (ATP-binding cassette, sub-family B (MDR/TAP), member 5), NGFR (nerve growth factor receptor, CD271) and ALDH (aldehyde dehydrogenase), and drive melanoma initiation and progression based on prolonged self-renewal capacity, vasculogenic differentiation and immune evasion. As we will review here, specific roles of these aggressive subpopulations have been documented in tumorigenic growth, metastatic dissemination, therapeutic resistance, and malignant recurrence. Moreover, recent findings have provided pre-clinical proof-of-concept for the potential therapeutic utility of the melanoma stem cell concept. Therefore, melanoma stem cell-directed therapeutic approaches represent promising novel strategies to improve therapy of this arguably most virulent human cancer.
    Molecular Aspects of Medicine 10/2013; · 10.38 Impact Factor
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    ABSTRACT: Efforts to limit graft-versus-host disease (GVHD) mediated by alloreactive donor T cells after allogeneic bone marrow transplantation (allo-BMT) are limited by a concomitant decrease in graft-versus-tumor (GVT) activity and increased possibilities of tumor relapse. Using a novel approach, we adoptively transferred conventional T cells expressing the transcription factor promyelocytic leukemia zinc finger (PLZF), which confers effector properties resembling invariant natural killer T cells (iNKT cells), such as copious production of cytokines under suboptimal stimulation. PLZF expression in T cell allografts attenuates expansion of alloreactive T cells, leading to lower GVHD. Intact alloreactivity-driven antitumor cytokine responses result in preserved GVT effects leading to improved survival. Our findings suggest that therapy with PLZF-overexpressing T cells would result in overall improved outcomes due to less GVHD and intact GVT effects.
    Cancer Research 06/2013; · 8.65 Impact Factor
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    ABSTRACT: Current strategies to suppress graft-versus-host disease (GVHD) also compromise graft-versus-tumor (GVT) responses. Furthermore, most experimental strategies to separate GVHD and GVT responses merely spare GVT function without actually enhancing it. We have previously shown that endogenously expressed TNF-related apoptosis-inducing ligand (TRAIL) is required for optimal GVT activity against certain malignancies in recipients of allogeneic hematopoietic stem cell transplantation (allo-HSCT). In order to model a donor-derived cellular therapy, we genetically engineered T cells to overexpress TRAIL and adoptively transferred donor-type unsorted TRAIL+ T cells into mouse models of allo-HSCT. We found that murine TRAIL+ T cells induced apoptosis of alloreactive T cells, thereby reducing GVHD in a DR5-dependent manner. Furthermore, murine TRAIL+ T cells mediated enhanced in vitro and in vivo antilymphoma GVT response. Moreover, human TRAIL+ T cells mediated enhanced in vitro cytotoxicity against both human leukemia cell lines and against freshly isolated chronic lymphocytic leukemia (CLL) cells. Finally, as a model of off-the-shelf, donor-unrestricted antitumor cellular therapy, in vitro-generated TRAIL+ precursor T cells from third-party donors also mediated enhanced GVT response in the absence of GVHD. These data indicate that TRAIL-overexpressing donor T cells could potentially enhance the curative potential of allo-HSCT by increasing GVT response and suppressing GVHD.
    The Journal of clinical investigation 05/2013; · 15.39 Impact Factor
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    ABSTRACT: : Two cases of a pseudoherpetic variant of Grover disease are presented. The first patient was a 60-year-old woman who had high fevers in combination with right lower lobe pneumonia. She developed an itchy papulovesicular rash on her back and upper abdomen. The second patient was a 68-year-old woman who while bedridden developed an itchy papulovesicular rash on her back. Vesiculobullous forms of dermatitis were clinically suspected in both cases, and herpetic vesicles were the lead diagnosis in one case. Pathologically, lesions from both patients revealed intraepidermal fluid-filled vesicles that at scanning magnification raised the suspicion of herpetic lesions. At higher magnification, acantholytic cells, some seemingly multinucleated, could be ppreciated. However, immunohistochemistry for herpes simplex virus and varicella zoster virus antigens proved negative. Moreover, some of the lesional cells revealed dyskeratosis more typical of the spongiotic/vesicular variant of Grover disease, and accordingly, this diagnosis was eventually established in both patients. Recognition of the pseudoherpetic variant of spongiotic/vesicular Grover disease is important in determining correct treatment, and therefore, subtle clues to its diagnosis should be sought in evaluation of such lesions.
    The American Journal of dermatopathology 05/2013; · 1.30 Impact Factor
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    ABSTRACT: : Chronic wounds are biochemically complex and are associated with insufficient cell proliferation, angiogenesis, and extracellular matrix remodeling. The mechanisms by which pulsed radiofrequency energy modulates wound healing are still unclear. : Db/db mice were wounded and exposed to pulsed radiofrequency energy. Gross closure, cell proliferation, and morphometric analysis of CD31-stained wound cross-sections were assessed. The mRNA expression of profibrotic factors (transforming growth factor-β and platelet-derived growth factor-A), angiogenetic factors (vascular endothelial growth factor and basic fibroblast growth factor), and extracellular matrix components (collagen I and α-smooth muscle actin) were evaluated by quantitative reverse-transcriptase polymerase chain reaction. Collagen protein level of the wound was determined by Western blot analysis. To test the effect of pulsed radiofrequency energy on cell movement in wound healing, cell migration was monitored in monolayer dermal fibroblast cultures. The degree of collagen alignment and gelation time was quantitatively assessed using image analysis techniques. : Pulsed radiofrequency energy-treated wounds were characterized by dermal cell proliferation and increased collagen synthesis. By contrast, the CD31 density and the mRNA expression of vascular endothelial growth factor and basic fibroblast growth factor showed no significant difference between the pulsed radiofrequency energy-treated wounds and the sham group. The pulsed radiofrequency energy-treated dermal fibroblast cultures expressed a significantly longer gelation time compared with the sham-exposed cultures. : Exposing wounds to pulsed radiofrequency accelerated wound healing in this diabetic mouse model by means of significantly increasing dermal cell proliferation and collagen synthesis. A cellular mechanism behind these observations has been proposed.
    Plastic and reconstructive surgery 04/2013; 131(4):490e-8e. · 2.74 Impact Factor
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    ABSTRACT: PURPOSE: To evaluate the effects BRAF inhibition on the tumor microenvironment in patients with metastatic melanoma. EXPERIMENTAL DESIGN: Thirty-five biopsies were collected from 16 patients with metastatic melanoma pretreatment (day 0) and at 10-14 days after initiation of treatment with either BRAF inhibitor alone (vemurafenib) or BRAF + MEK inhibition (dabrafenib + trametinib), and were also taken at time of progression. Biopsies were analyzed for melanoma antigens, T cell markers, and immunomodulatory cytokines. RESULTS: Treatment with either BRAF inhibitor alone or BRAF + MEK inhibitor was associated with an increased expression of melanoma antigens and an increase in CD8+ T cell infiltrate. This was also associated with a decrease in immunosuppressive cytokines (IL-6 & IL-8) and an increase in markers of T cell cytotoxicity. Interestingly, expression of exhaustion markers TIM-3 and PD1 and the immunosuppressive ligand PDL1 were increased on treatment. A decrease in melanoma antigen expression and CD8 T cell infiltrate was noted at time of progression on BRAF inhibitor alone, and was reversed with combined BRAF and MEK inhibition. CONCLUSIONS: Together, this data suggests that treatment with BRAF inhibition enhances melanoma antigen expression and facilitates T cell cytotoxicity and a more favorable tumor microenvironment, providing support for potential synergy of BRAF-targeted therapy and immunotherapy. Interestingly, markers of T cell exhaustion and the immunosuppressive ligand PDL1 are also increased with BRAF inhibition, further implying that immune checkpoint blockade may be critical in augmenting responses to BRAF-targeted therapy in patients with melanoma.
    Clinical Cancer Research 01/2013; · 7.84 Impact Factor
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    ABSTRACT: Scratching triggers skin flares in atopic dermatitis. We demonstrate that scratching of human skin and tape stripping of mouse skin cause neutrophil influx. In mice, this influx was largely dependent on the generation of leukotriene B4 (LTB4) by neutrophils and their expression of the LTB4 receptor BLT1. Allergic skin inflammation in response to epicutaneous (EC) application of ovalbumin to tape-stripped skin was severely impaired in Ltb4r1(-/-) mice and required expression of BLT1 on both T cells and non-T cells. Cotransfer of wild-type (WT) neutrophils, but not neutrophils deficient in BLT1 or the LTB4-synthesizing enzyme LTA4H, restored the ability of WT CD4(+) effector T cells to transfer allergic skin inflammation to Ltb4r1(-/-) recipients. Pharmacologic blockade of LTB4 synthesis inhibited allergic skin inflammation elicited by cutaneous antigen challenge in previously EC-sensitized mice. Our results demonstrate that a neutrophil-T cell axis reliant on LTB4-BLT1 interaction is required for allergic skin inflammation.
    Immunity 10/2012; 37(4):747-58. · 19.80 Impact Factor
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    ABSTRACT: DNA methylation at the 5 position of cytosine (5-mC) is a key epigenetic mark that is critical for various biological and pathological processes. 5-mC can be converted to 5-hydroxymethylcytosine (5-hmC) by the ten-eleven translocation (TET) family of DNA hydroxylases. Here, we report that "loss of 5-hmC" is an epigenetic hallmark of melanoma, with diagnostic and prognostic implications. Genome-wide mapping of 5-hmC reveals loss of the 5-hmC landscape in the melanoma epigenome. We show that downregulation of isocitrate dehydrogenase 2 (IDH2) and TET family enzymes is likely one of the mechanisms underlying 5-hmC loss in melanoma. Rebuilding the 5-hmC landscape in melanoma cells by reintroducing active TET2 or IDH2 suppresses melanoma growth and increases tumor-free survival in animal models. Thus, our study reveals a critical function of 5-hmC in melanoma development and directly links the IDH and TET activity-dependent epigenetic pathway to 5-hmC-mediated suppression of melanoma progression, suggesting a new strategy for epigenetic cancer therapy.
    Cell 09/2012; 150(6):1135-46. · 31.96 Impact Factor

Publication Stats

5k Citations
543 Downloads
1,051.35 Total Impact Points

Institutions

  • 2004–2014
    • Brigham and Women's Hospital
      • • Department of Pathology
      • • Department of Medicine
      Boston, Massachusetts, United States
  • 2003–2013
    • Memorial Sloan-Kettering Cancer Center
      • • Department of Medicine
      • • Division of Immunology
      • • Department of Pediatrics
      New York City, New York, United States
  • 1987–2013
    • Harvard Medical School
      • • Department of Pathology
      • • Division of Immunology
      • • Department of Dermatology
      Boston, Massachusetts, United States
  • 2012
    • Dana-Farber Cancer Institute
      • Center for Melanoma Oncology
      Boston, Massachusetts, United States
  • 2010–2012
    • Boston Children's Hospital
      Boston, Massachusetts, United States
    • Charité Universitätsmedizin Berlin
      • Department of Pediatrics, Division of Oncology and Hematology
      Berlin, Land Berlin, Germany
  • 2008
    • Partners HealthCare
      Boston, Massachusetts, United States
  • 1994–2007
    • Thomas Jefferson University
      • • Department of Microbiology & Immunology
      • • Division of Hospital Medicine
      Philadelphia, PA, United States
  • 1997–1999
    • King's College London
      • School of Biomedical Sciences
      Londinium, England, United Kingdom
    • Yale-New Haven Hospital
      New Haven, Connecticut, United States
    • Thomas Jefferson University Hospitals
      Philadelphia, Pennsylvania, United States
  • 1988–1999
    • Hospital of the University of Pennsylvania
      • • Department of Dermatology
      • • Department of Medicine
      Philadelphia, Pennsylvania, United States
  • 1997–1998
    • Dong-Pusan College
      Tsau-liang-hai, Busan, South Korea
  • 1990–1997
    • University of Pennsylvania
      • • School of Veterinary Medicine
      • • Department of Dermatology
      Philadelphia, PA, United States
  • 1996
    • Plano Cancer Institute
      Plano, Texas, United States
  • 1990–1993
    • Wistar Institute
      Philadelphia, Pennsylvania, United States
  • 1992
    • University of Queensland 
      • School of Dentistry
      Brisbane, Queensland, Australia
  • 1988–1989
    • University of Massachusetts Boston
      Boston, Massachusetts, United States