George F Murphy

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

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Publications (203)1154.47 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: In 2009 the revised 7(th) staging system for melanoma recommended the use of mitotic count to separate stage T1a from T1b. However, careful scrutiny of cases may lead to an inadvertent selection effect, with consequent increased reporting of mitotic counts. We investigated whether there is a significant increase in mitotic counts reported since 2009 for melanomas with a Breslow thickness of 1.0 mm or less. We conducted a retrospective, case-controlled study examining invasive melanoma cases at a large academic center. Mitotic counts were compared between pathology reports before 2009 (n = 61) and after 2009 (n = 125), with a subset of slides re-examined in a blinded fashion. Before the 2009 staging guidelines, 51% of cases had one or more mitosis reported compared to 38% after 2009 (p = 0.113). Blinded re-counting did not yield a significant difference when compared with the original pathology reports in either group. There was not a significant difference in the number of mitoses reported after the implementation of the new guidelines. This article is protected by copyright. All rights reserved.
    Journal of Cutaneous Pathology 04/2015; DOI:10.1111/cup.12517 · 1.56 Impact Factor
  • Leigh A. Compton, George F. Murphy, Christine G. Lian
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    ABSTRACT: Immunohistochemistry (IHC) is an important adjunct in the diagnosis of neoplastic skin diseases. In addition to the many established IHC markers currently in use, new markers continue to emerge, although their general acceptance and routine application requires robust validation. Here, we summarize the most well-established and commonly used biomarkers along with an array of newer ones reported in the past several decades that either demonstrate or hold high clinical promise in the field of cutaneous pathology. We also highlight recent applications of novel IHC markers in melanoma diagnosis including genetic mutation status markers [e.g. BRAF (v-raf murine sarcoma viral oncogene homolog B) and NRAS (neuroblastoma RAS viral oncogene homolog)] and an epigenetic alteration marker (e.g. 5-hydroxymethylcytosine). We specifically focus on the role of IHC in the differential diagnosis of cutaneous lesions that fall under the following categories: melanoma, epidermal tumors with an intraepidermal epitheliomatous pattern, spindle cell lesions of the dermis, small round blue cell tumors of the dermis, and cutaneous adnexal tumors. While IHC is a valuable tool in diagnostic dermatopathology, marker selection and interpretation must be highly informed by clinical context and the histologic differential diagnosis. With rapid progress in our understanding of the genetic and epigenetic mechanisms of tumorigenesis, new IHC markers will continue to emerge in the field of diagnostic dermatopathology.
    03/2015; 2(1):15-42. DOI:10.1159/000377698
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    ABSTRACT: Metastatic melanoma is a highly aggressive skin cancer with a poor prognosis. Despite a complete response in fewer than 5% of patients, the chemotherapeutic agent dacarbazine (DTIC) remains the reference drug after almost 40 years. More recently, FDA-approved drugs have shown promise but patient outcome remains modest, predominantly due to drug resistance. As such, combinatorial targeting has received increased attention, and will advance with the identification of new molecular targets. One attractive target for improving melanoma therapy is the growth factor Nodal, whose normal expression is largely restricted to embryonic development, but is reactivated in metastatic melanoma. In this study, we sought to determine how Nodal-positive human melanoma cells respond to DTIC treatment and to ascertain whether targeting Nodal in combination with DTIC would be more effective than monotherapy. A single treatment with DTIC inhibited cell growth but did not induce apoptosis. Rather than reducing Nodal expression, DTIC increased the size of the Nodal-positive subpopulation, an observation coincident with increased cellular invasion. Importantly, clinical tissue specimens from patients with melanomas refractory to DTIC therapy stained positive for Nodal expression, both in pre- and post-DTIC tumors, underscoring the value of targeting Nodal. In vitro, anti-Nodal antibodies alone had some adverse effects on proliferation and apoptosis, but combining DTIC treatment with anti-Nodal antibodies decreased cell growth and increased apoptosis synergistically, at concentrations incapable of producing meaningful effects as monotherapy. Targeting Nodal in combination with DTIC therapy holds promise for the treatment of metastatic melanoma. Mol Cancer Res; 1-11. ©2015 AACR. ©2015 American Association for Cancer Research.
    Molecular Cancer Research 03/2015; 13(4). DOI:10.1158/1541-7786.MCR-14-0077 · 4.50 Impact Factor
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    ABSTRACT: Galectin-1 (Gal-1)-binding to Gal-1 ligands on immune and endothelial cells can influence melanoma development through dampening anti-tumor immune responses and promoting angiogenesis. However, whether Gal-1 ligands are functionally expressed on melanoma cells to help control intrinsic malignant features remains poorly understood. Here, we analyzed expression, identity and function of Gal-1 ligands in melanoma progression. Immunofluorescent analysis of benign and malignant human melanocytic neoplasms revealed that Gal-1 ligands were abundant in severely-dysplastic nevi as well as in primary and metastatic melanomas. Biochemical assessments indicated that melanoma cell adhesion molecule (MCAM) was a major Gal-1 ligand on melanoma cells that was largely dependent on its N-glycans. Other melanoma cell Gal-1 ligand activity conferred by O-glycans was negatively regulated by α2,6 sialyltransferase ST6GalNAc2. In Gal-1-deficient mice, MCAM-silenced (MCAM(KD)) or ST6GalNAc2-overexpressing (ST6(O/E)) melanoma cells exhibited slower growth rates, underscoring a key role for melanoma cell Gal-1 ligands and host Gal-1 in melanoma growth. Further analysis of MCAM(KD) or ST6(O/E) melanoma cells in cell migration assays indicated that Gal-1 ligand-dependent melanoma cell migration was severely inhibited. These findings provide a refined perspective on Gal-1 - melanoma cell Gal-1 ligand interactions as contributors to melanoma malignancy.Journal of Investigative Dermatology accepted article preview online, 10 March 2015. doi:10.1038/jid.2015.95.
    Journal of Investigative Dermatology 03/2015; DOI:10.1038/jid.2015.95 · 6.37 Impact Factor
  • Plastic &amp Reconstructive Surgery 01/2015; 135:1219. DOI:10.1097/01.prs.0000463340.84041.3a · 3.33 Impact Factor
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    ABSTRACT: BACKGROUND: Severe facial injuries can compromise the upper airway by reducing airway volume, obstructing or obliterating the nasal passage, and interfering with oral airflow. Besides the significant impact on quality of life, upper airway impairments can have life-threatening or life-altering consequences. The authors evaluated improvements in functional airway after face transplantation. METHODS: Between 2009 and 2011, four patients underwent face transplantation at the authors' institution, the Brigham and Women's Hospital. Patients were examined preoperatively and postoperatively and their records reviewed for upper airway infections and sleeping disorders. The nasal mucosa was biopsied after face transplantation and analyzed using scanning electron microscopy. Volumetric imaging software was used to evaluate computed tomographic scans of the upper airway and assess airway volume changes before and after transplantation. RESULTS: Before transplantation, two patients presented an exposed naked nasal cavity and two suffered from occlusion of the nasal passage. Two patients required tracheostomy tubes and one had a prosthetic nose. Sleeping disorders were seen in three patients, and chronic cough was diagnosed in one. After transplantation, there was no significant improvement in sleeping disorders. The incidence of sinusitis increased because of mechanical interference of the donor septum and disappeared after surgical correction. All patients were decannulated after transplantation and were capable of nose breathing. Scanning electron micrographs of the respiratory mucosa revealed viable tissue capable of mucin production. Airway volume significantly increased in all patients. CONCLUSIONS: Face transplantation successfully restored the upper airway in four patients. Unhindered nasal breathing, viable respiratory mucosa, and a significant increase in airway volume contributed to tracheostomy decannulation. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, IV.
    Plastic &amp Reconstructive Surgery 12/2014; 134:946e-54e. DOI:10.1097/PRS.0000000000000752 · 3.33 Impact Factor
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    ABSTRACT: Purpose of review: The field of vascularized composite allograft (VCA) to achieve its full potential will require induction of tolerance. This review will introduce a new method of potential inducing tolerance in hand transplantation. Recent findings: Hand transplantation is never a life-extending transplant. This fact resulted in considerable debate both for and against the use of immunosuppression for nonlife-extending transplants. There is considerable debate about the ethics of hand transplantation. There is now consensus that nonlife-extending transplants are acceptable in properly selected patients. However, ideally, hand transplants should not receive life-long immunosuppression. Therefore, attempts to achieve drug-free tolerance through nonlife-endangering therapies are warranted. To this end, we propose implementation of tolerizing therapy long after periinflammation has subsided and drug minimization has proven successful. Evidence that short-term treatment with low doses of IL-2 or a long-lived IL-2 immunoglobulin (Ig) can tilt the balance of immunity from tissue destructive to tolerance come from preclinical demonstrations in mouse and nonhuman primate models of autoimmunity and/or transplantation and even more recent clinical trials. Summary: We believe that with the proper use of low-dose IL-2 given at an opportune time in the inflammatory process of transplant that reduce immunosuppression and even tolerance can be induced in hand transplantation. We propose that tolerance can be inducted after a long period of conventional treatment to avoid 'tolerance-hindering' adverse inflammation that occurs in the posttransplant period. With abatement of posttransplant inflammation and with time, we will institute low-dose IL-2-based therapy to support the proliferation, viability and functional phenotype of regulatory T cells.
    Current Opinion in Organ Transplantation 12/2014; 19(6):545-51. DOI:10.1097/MOT.0000000000000138 · 2.38 Impact Factor
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    ABSTRACT: Inflammatory vitiligo with raised borders (IVRB) is a rare subtype of vitiligo described as having a rim of raised erythema at the periphery of the depigmented patches. The etiology is poorly understood, and there are few reports of successful treatment of the condition in the literature. We report a 38-year-old South Asian male who presented with diffuse depigmented macules and patches surrounded by blue-gray rims involving a large body surface area. Light microscopy revealed inflammatory vitiligo. He was treated with 2 courses of oral prednisone and whole-body narrow-band ultraviolet B (NB-UVB) therapy, which resulted in cessation of disease spread as well as substantial repigmentation. Our observation suggests that early and aggressive treatment can lead to significant and rapid improvement in patients with IVRB. © 2014 S. Karger AG, Basel.
    Dermatology 11/2014; 230(1). DOI:10.1159/000366197 · 1.69 Impact Factor
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    ABSTRACT: Matrix metalloproteinases (MMPs) are key biological mediators of processes as diverse as wound healing, embryogenesis, and cancer progression. Although MMPs may be induced through multiple signaling pathways, the precise mechanisms for their regulation in cancer are incompletely understood. Because cytoskeletal changes are known to accompany MMP expression, we sought to examine the potential role of the poorly understood cytoskeletal protein, nestin, in modulating melanoma MMPs. Nestin knockdown (KD) upregulated the expression of specific MMPs and MMP-dependent invasion both through extracellular matrix barriers in vitro and in peritumoral connective tissue of xenografts in vivo. The development of three-dimensional melanospheres that in vitro partially recapitulate noninvasive tumorigenic melanoma growth was inhibited by nestin KD, although ECM invasion by aberrant melanospheres that did form was enhanced. Mechanistically, nestin KD-dependent melanoma invasion was associated with intracellular redistribution of phosphorylated focal adhesion kinase and increased melanoma cell responsiveness to transforming growth factor-beta, both implicated in pathways of melanoma invasion. The results suggest that the heretofore poorly understood intermediate filament, nestin, may serve as a novel mediator of MMPs critical to melanoma virulence.Laboratory Investigation advance online publication, 3 November 2014; doi:10.1038/labinvest.2014.130.
    Laboratory Investigation 11/2014; DOI:10.1038/labinvest.2014.130 · 3.83 Impact Factor
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    ABSTRACT: Purpose of review Acute rejection is the most common complication after vascularized composite allotransplantation (VCA). This review provides a state-of-the-art analysis of prevention, diagnosis and treatment of acute rejection episodes and highlights recent findings with the potential to improve patient care and enhance understanding of the underlying biologic processes. Recent findings Recent reports suggest that maintenance immunosuppression dose reduction and steroid withdrawal are realistic goals in VCA, despite the known high immunogenicity of the skin component. It appears that utilization of sentinel flaps, in-depth histological analyses and application of novel biomarkers have facilitated early diagnosis and characterization of acute rejection episodes, leading to timely institution of appropriate therapy. The successful management of the first highly sensitized face transplant recipient suggests the possibility of carefully considering these high-risk VCA candidates for transplantation. Summary Acute rejection is higher in VCA than in any other organ in the field of transplantation, although most episodes are controlled by high-dose steroids and optimization of maintenance immunosuppression. Because of limitations in patient number and the duration of follow-up, the long-term safety and effectiveness of VCA remain unclear. Moreover, the tests currently used to diagnose acute rejection are of limited value. Better diagnostic tools and a better understanding of the immunologic events during acute rejection are therefore needed to improve diagnosis, treatment and outcomes of this life-changing restorative surgery.
    Current opinion in organ transplantation 10/2014; DOI:10.1097/MOT.0000000000000140 · 2.38 Impact Factor
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    ABSTRACT: Atg16L1 mediates the cellular degradative process of autophagy and is considered a critical regulator of inflammation based on its genetic association with inflammatory bowel disease. Here we find that Atg16L1 deficiency leads to an exacerbated graft-versus-host disease (GVHD) in a mouse model of allogeneic hematopoietic stem cell transplantation (allo-HSCT). Atg16L1-deficient allo-HSCT recipients with GVHD displayed increased T cell proliferation due to increased dendritic cell (DC) numbers and costimulatory molecule expression. Reduced autophagy within DCs was associated with lysosomal abnormalities and decreased amounts of A20, a negative regulator of DC activation. These results broaden the function of Atg16L1 and the autophagy pathway to include a role in limiting a DC-mediated response during inflammatory disease, such as GVHD.
    Immunity 10/2014; DOI:10.1016/j.immuni.2014.09.011 · 19.75 Impact Factor
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    ABSTRACT: Skin biopsies are critical for histological evaluation of rejection and proper treatment after facial allotransplantation (FAT). Many facial allografts provide only limited skin area and frequent biopsies may additionally compromise aesthetic outcome. Sentinel flaps (SFs), recovered as free fasciocutanous radial forearm flaps, have been employed for remote site rejection monitoring. They maintain their axial blood supply similar to facial allografts. The correlation between FAT and SF in cases of rejection is presented.
    Plastic &amp Reconstructive Surgery 09/2014; DOI:10.1097/PRS.0000000000000797 · 3.33 Impact Factor
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    ABSTRACT: IMPORTANCE Port-wine stains (PWSs) are common congenital cutaneous capillary malformations. A somatic GNAQ mutation was recently identified in patients with sporadic PWSs and Sturge-Weber syndrome. However, subsequent studies to confirm or extend this observation are lacking. OBSERVATIONS We report a long-standing, unilateral facial PWS of a man in his early 70s confirmed by histopathological analysis. Staged surgical excision of the vascular malformation was performed, and genomic DNA was extracted from the vascular malformation specimen and normal skin. Targeted next-generation sequencing of the coding sequence of 275 known cancer genes including GNAQ was performed in both specimens. A single-nucleotide variant (c.548G>A, p.Arg183Gln) in GNAQ was identified in the PWS-affected tissue but not in the normal skin sample. In addition, this sequencing approach uncovered several additional novel somatic mutations in the genes SMARCA4, EPHA3, MYB, PDGFR-beta, and PIK3CA. CONCLUSIONS AND RELEVANCE Our findings confirm the presence of somatic mutations in GNAQ in the affected skin of a patient with congenital PWS, as well as alterations in several other novel genes of possible importance in the pathogenesis of PWS that may also offer substantial therapeutic targets.
    JAMA Dermatology 09/2014; 150(12). DOI:10.1001/jamadermatol.2014.1244 · 4.30 Impact Factor
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    ABSTRACT: Merkel cell carcinoma (MCC) is a highly virulent cutaneous neoplasm that, like melanoma, is a frequent cause of patient morbidity and mortality. The cellular mechanisms responsible for the aggressive behavior of MCC remain unknown. Vasculogenic mimicry (VM) is a phenomenon associated with cancer virulence, including in melanoma, whereby anastomosing laminin networks form in association with tumor cells that express certain endothelial genes. To determine whether VM is a factor in MCC, we employed a relevant xenograft model using two independent human MCC lines. Experimentally induced tumors were remarkably similar histologically to patient MCC, and both contained laminin networks associated with vascular endothelial-cadherin (CD144) and vascular endothelial growth factor receptor 1, as well as Nodal expression typical of VM in melanoma. Moreover, two established chemotherapeutic agents utilized for human MCC, etoposide and carboplatin, induced necrosis in xenografts on systemic administration while enriching for laminin networks in apparently resistant viable tumor regions that persisted. These findings for the first time establish VM-like laminin networks as a biomarker in MCC, demonstrate the experimental utility of the MCC xenograft model, and suggest that VM-rich regions of MCC may be refractory to conventional chemotherapeutic agents.Laboratory Investigation advance online publication, 11 August 2014; doi:10.1038/labinvest.2014.99.
    Laboratory Investigation 08/2014; 94(10). DOI:10.1038/labinvest.2014.99 · 3.83 Impact Factor
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    ABSTRACT: Sentinel lymph node biopsies are conducted to stage patients with newly diagnosed melanomas that have histopathological attributes conferring defined levels of metastatic potential. Because benign nevic cells may also form 'deposits' in lymph nodes (nodal nevus), the pathological evaluation for metastatic melanoma within sentinel lymph nodes can be challenging. Twenty-eight sentinel lymph node biopsy cases containing either metastatic melanoma (N=18) or nodal nevi (N=10) were retrieved from the archives of the Brigham and Women's Hospital, Department of Pathology (2011-2014). In addition, two sentinel lymph node cases that were favored to represent metastatic disease but whose histopathological features were viewed as equivocal, with melanoma favored, were also included. Dual labeling for the melanocyte lineage marker, MART-1, and the epigenetic marker, 5-hydroxymethylcytosine, a functionally significant indicator that has been shown to distinguish benign nevi from melanoma, was performed on all cases using immunohistochemistry and/or direct immunofluorescence. All (18 of 18) metastatic melanoma cases showed complete loss of 5-hydroxymethylcytosine nuclear staining in MART-1-positive cells, and all (10 of 10) nodal nevus cases demonstrated 5-hydroxymethylcytosine nuclear staining in MART-1-positive cells. In addition, 5-hydroxymethylcytosine staining confirmed the favored diagnoses of metastatic melanoma in the two 'equivocal' cases. Thus, 5-hydroxymethylcytosine may be a useful adjunctive marker to distinguish between benign nodal nevi and metastatic melanoma during the evaluation of sentinel lymph node biopsies for metastatic melanoma.Modern Pathology advance online publication, 1 August 2014; doi:10.1038/modpathol.2014.99.
    Modern Pathology 08/2014; 28(2). DOI:10.1038/modpathol.2014.99 · 6.36 Impact Factor
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    ABSTRACT: The level of 5-hydroxymethylcytosine (5-hmC) converted by ten-eleven translocation (TET) family is decreased in cancers. However, whether 5-hmC level is perturbed in early stages of carcinogenesis caused by genotoxic carcinogens is not defined. 5-hmC levels and TET2 expression were measured in liver of rats treated with genotoxic carcinogens, riddelliine, or aristolochic acid. Levels of 5-hmC and TET2 expression decreased in the liver of the carcinogens-treated rats. Loss of 5-hmC correlates well with documented induction of genetic mutations by the carcinogens, suggesting that TET2-mediated 5-hydroxymethylation plays an epigenetic role in early state of carcinogenesis. © 2014 Wiley Periodicals, Inc.
    Molecular Carcinogenesis 08/2014; DOI:10.1002/mc.22201 · 4.77 Impact Factor
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    ABSTRACT: Background The chondrogenic potential of adipose-derived stem cells (ASCs) has been previously demonstrated, although several reports have indicated that ASCs produce less cartilage specific matrix than bone marrow derived mesencymal stem cells (BMSCs). In this study, we intended to improve chondrogenic phenotypes of ASCs using hydrostatic pressure (HP), without utilizing any growth factors other than TGF-β1. Methods Human ASCs (CD13+, 44+, 90+, 14-, 31-, 34-) were harvested and cultured. After 3 passages, the cells were suspended in 0.3% neutralized collagen type I solution and injected into semi-permeable membrane tubes from which 60 pouches were constructed. After a day of incubation, the 60 pouches were divided into three groups; Group HP1: Pouches were incubated for one week with treatment of cyclic HP at 0-0.5 MPa (4.93 atm), 0.5 Hz, with a medium replenishment rate of 0.1 ml/min at 37˚C, 3% O2, and 5% CO2 in air using a bioprocessor. This was followed by 3 weeks with no HP and without pouches. Group HP2: Pouches were incubated for the first and third week (two total weeks) with the same condition of Group HP1. No HP was applied in the second and fourth week. Group AP: Pouches with one end opened were incubated without HP. We evaluated the cell constructs histologically and immunohistochemically, as well as for specific gene expression. Resutls Accumulation of the matrix in the HP1 and HP2 groups was much denser than AP groups, particularly after 2 weeks. Cell numbers in the HP groups increased gradually in the middle zone, and peaked at one week after incubation, maintaining their numbers for the entire course on the surface layer of the construct. In the genomic study results, COL 2A1, COL 10A1, ACAN, SOX9, MMP3, and MMP13 were up-regulated and COL 1A1, ITGB1, and PCNA were down-regulated by HP. However, there were no significant differences between HP1 and HP2 groups in all genes. Conclusion It was suggested that HP is especially beneficial in the early stage of chondrogenesis of ASCs. Moreover, the expression profile of genes related to chondrocyte differentiation/proliferation was significantly enhanced by HP loading compared with the AP control.
    Tissue Engineering Part A 07/2014; 21(1-2). DOI:10.1089/ten.TEA.2013.0525 · 4.70 Impact Factor
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    ABSTRACT: Corneal epithelial homeostasis and regeneration are sustained by limbal stem cells (LSCs), and LSC deficiency is a major cause of blindness worldwide. Transplantation is often the only therapeutic option available to patients with LSC deficiency. However, while transplant success depends foremost on LSC frequency within grafts, a gene allowing for prospective LSC enrichment has not been identified so far. Here we show that ATP-binding cassette, sub-family B, member 5 (ABCB5) marks LSCs and is required for LSC maintenance, corneal development and repair. Furthermore, we demonstrate that prospectively isolated human or murine ABCB5-positive LSCs possess the exclusive capacity to fully restore the cornea upon grafting to LSC-deficient mice in xenogeneic or syngeneic transplantation models. ABCB5 is preferentially expressed on label-retaining LSCs in mice and p63α-positive LSCs in humans. Consistent with these findings, ABCB5-positive LSC frequency is reduced in LSC-deficient patients. Abcb5 loss of function in Abcb5 knockout mice causes depletion of quiescent LSCs due to enhanced proliferation and apoptosis, and results in defective corneal differentiation and wound healing. Our results from gene knockout studies, LSC tracing and transplantation models, as well as phenotypic and functional analyses of human biopsy specimens, provide converging lines of evidence that ABCB5 identifies mammalian LSCs. Identification and prospective isolation of molecularly defined LSCs with essential functions in corneal development and repair has important implications for the treatment of corneal disease, particularly corneal blindness due to LSC deficiency.
    Nature 07/2014; 511(7509):353-7. DOI:10.1038/nature13426 · 42.35 Impact Factor
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Publication Stats

5k Citations
1,154.47 Total Impact Points

Institutions

  • 1983–2015
    • Brigham and Women's Hospital
      • • Department of Pathology
      • • Division of Genetics
      Boston, Massachusetts, United States
  • 2014
    • Ruhr-Universität Bochum
      Bochum, North Rhine-Westphalia, Germany
  • 1982–2014
    • Harvard Medical School
      • • Department of Pathology
      • • Department of Dermatology
      Boston, Massachusetts, United States
    • Beth Israel Deaconess Medical Center
      • Department of Dermatology
      Boston, Massachusetts, United States
  • 1981–2014
    • Harvard University
      Cambridge, Massachusetts, United States
  • 2013
    • Stanford University
      • Division of Plastic and Reconstructive Surgery
      Palo Alto, California, United States
  • 2003–2013
    • Memorial Sloan-Kettering Cancer Center
      • • Department of Medicine
      • • Department of Pediatrics
      New York City, New York, United States
  • 1983–2013
    • Massachusetts General Hospital
      • • Transplantation Biology Research Center
      • • Department of Pathology
      Boston, Massachusetts, United States
  • 2012
    • Fudan University
      • Department of Immunology
      Shanghai, Shanghai Shi, China
  • 1986–2012
    • Dana-Farber Cancer Institute
      • • Center for Melanoma Oncology
      • • Department of Pediatric Oncology
      Boston, Massachusetts, United States
  • 2011
    • Huazhong University of Science and Technology
      Wu-han-shih, Hubei, China
  • 2010
    • Charité Universitätsmedizin Berlin
      • Department of Pediatrics, Division of Oncology and Hematology
      Berlin, Land Berlin, Germany
  • 1998–2004
    • Thomas Jefferson University
      • • Department of Pathology, Anatomy & Cell Biology
      • • Department of Microbiology & Immunology
      Philadelphia, Pennsylvania, United States
  • 1997–2004
    • Jefferson College
      Хиллсборо, Missouri, United States
  • 2002
    • Johns Hopkins Medicine
      • Department of Dermatology
      Baltimore, Maryland, United States
  • 1997–1999
    • Thomas Jefferson University Hospitals
      • Department of Pathology, Anatomy and Cell Biology
      Philadelphia, Pennsylvania, United States
  • 1989–1996
    • University of Pennsylvania
      • Department of Dermatology
      Philadelphia, Pennsylvania, United States
    • William Penn University
      Filadelfia, Pennsylvania, United States
  • 1995
    • Hospital of the University of Pennsylvania
      • Department of Dermatology
      Philadelphia, Pennsylvania, United States
  • 1993
    • Showa University
      Shinagawa, Tōkyō, Japan
    • Wistar Institute
      Philadelphia, Pennsylvania, United States
  • 1992
    • Philadelphia University
      Philadelphia, Pennsylvania, United States
  • 1985–1986
    • Beverly Hospital, Boston MA
      BVY, Massachusetts, United States