Garron J Solomon

Weill Cornell Medical College, New York City, New York, United States

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Publications (5)20.71 Total impact

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    ABSTRACT: The borderline melanocytic tumor (BMT) is a morphologically and biologically indeterminate melanocytic proliferation manifesting worrisome architectural features and cytologic atypia exceeding that encountered in melanocytic nevi yet insufficient to warrant designation as melanoma. The criteria that define the BMT are not well defined nor is the concept widely recognized. The purpose of this study is to provide a practical framework for the approach to the dermal BMT. Thirty-two patients with BMTs extending into the reticular dermis and at a depth of 0.75 mm or more underwent local excision and sentinel lymph node biopsy between 2000 and 2006. Four categories of BMT were recognized: (1) nevoid BMT (BNM); (2) the atypical Spitz tumor (AST); (3) pigmented epithelioid melanocytoma (PEM); and (4) BMT arising in a deep penetrating nevus (B-DPN). Four patients were in the BNM category (male/female ratio [M:F] = 1:3; mean age = 27 years, range = 15-36), 14 in the AST category (M:F = 7:7; mean age = 20.9, range = 3-58), 7 in the PEM category (M:F = 4:3; mean age = 23.5, range = 3-39), and 7 in the B-DPN category (M:F = 5:2; mean age = 22.3, range = 14-36). The percentages of patients with positive sentinel nodes in each category were 25% (1/4), 35% (5/14), 14% (1/7), and 57% (4/7), respectively. The average time of follow-up was approximately 4.2 years. One patient, a 36-year-old man, died of disease, while the others are alive and well. In the one death attributable to widespread metastatic disease, the lesion was initially interpreted as a deep penetrating nevus; however, retrospective review revealed features compatible with a B-DPN; the review was prompted by a recurrence that was morphologically compatible with a Clark level V malignant melanoma, reflecting clinical and morphologic progression. The mean follow-up was less than 5 years. Molecular studies to further explore the biologic commonality with melanoma were not performed. The dermal variant of BMT is a tumor of younger adults and children that can be associated with lymph node disease and a potential for morphologic and biologic progression when inadequately treated.
    Journal of the American Academy of Dermatology 03/2010; 62(3):469-79. · 4.91 Impact Factor
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    HSS Journal 08/2009; 5(2):169-77.
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    ABSTRACT: The light microscopic distinction between complex atypical hyperplasia (CAH) and invasive endometrioid carcinoma (UEC) on endometrial sampling is problematic and often has significant clinical implications. Using mouse models of endometrial tumorigenesis based on two of the most common molecular alterations found in primary human UEC we sought to characterize the transition from CAH to carcinoma to identify clinically useful biomarkers. We used the previously described Pten(+/-); Mlh1(-/-) mouse model. DNA was isolated from microdissected lesions (CAH and carcinoma) and analyzed for LOH and mutations of Pten and additional candidate genes. To identify novel candidate genes associated with invasion, global gene expression profiles were compared from uteri with extensive CAH and carcinoma. The majority of CAHs and carcinomas, arising in this model showed biallelic inactivation of Pten mediated through LOH or intragenic mutation of the wild-type allele suggesting that complete loss of Pten is insufficient for the development of carcinoma. The global gene expression studies detected increased expression of oviduct-specific glycoprotein (OGP) in carcinoma as compared with CAHs. This finding was validated using immunohistochemical staining in a collection of primary human UECs and CAHs. Our studies identify a molecular marker for invasive endometrial cancer that may have clinical significance, and highlight the usefulness of this mouse model in not only understanding the genetic underpinnings of endometrial carcinoma, but as a tool to develop clinically relevant biomarkers.
    International Journal of Cancer 10/2008; 124(6):1349-57. · 6.20 Impact Factor
  • Garron J Solomon, Cynthia M Magro
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    ABSTRACT: The primary function of regulatory T cells (Treg cells) is to regulate the function and proliferation of immunologically responsive T cells; the transcription factor Foxp3 is expressed by this cell populace and is held to be the standard marker for Treg cells. A variety of cutaneous T-cell lymphocytic infiltrates were evaluated for Foxp3 expression. Of the 95 cases, 33 (35%) were reactive, 40 (42%) were prelymphomatous cutaneous T-cell dyscrasia and 22 were (23%) T-cell lymphoma. The reactive category included dermatomyositis, lupus erythematosus, hypersensitivity reactions and graft-vs.-host disease. The prelymphomatous dyscrasia category was represented chiefly by pityriasis lichenoides chronica (PLC) and pigmented purpuric dermatosis (PPD). The Foxp3 reactivity was less than 10% for cases of dermatomyositis and lupus erythematosus, 23% for hypersensitivity cases, 0% for graft-vs.-host disease, 16% for the dyscrasias and 11% for the lymphomas. Intermediate grade and aggressive lymphomas had very few Foxp3+ cells (< 5%). There were fewer numbers of Foxp3+ T cells in the monoclonal variants of PLC and PPD. T-reg cells may play a role in controlling the extent of T-cell proliferations in the skin with a lack of T-regulatory function permissive to the development of various T-cell disorders.
    Journal of Cutaneous Pathology 09/2008; 35(11):1032-9. · 1.77 Impact Factor
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    ABSTRACT: The tumor suppressor PTEN gene and the PIK3CA oncogene are frequently mutated in uterine endometrioid carcinoma (UEC). PTEN mutations are also common in complex atypical hyperplasia (CAH), the precursor lesion of UEC. The status of PIK3CA has not yet been explored in CAH. In this study, we evaluated both CAH and UEC for PTEN and PIK3CA mutations. Neoplastic tissue was microdissected, and DNA was extracted from 29 cases of CAH. DNA was available from 44 UEC cases previously characterized for PTEN mutations. Direct DNA sequencing of exons 9 and 20 of the PIK3CA gene was done on all 73 cases. In addition, CAH cases were analyzed for PTEN mutations. Statistical analyses were done using the Fisher's exact test. Two (7%) of 29 CAH and 17 (39%) of 44 UEC cases contained a PIK3CA mutation (P = 0.003). Fourteen (48%) of 29 CAH cases had a PTEN mutation, but none contained both a PTEN and PIK3CA mutation. Twenty-five (57%) of 44 UEC cases had a PTEN mutation, and 12 (48%) of these 25 cases also contained a PIK3CA mutation. Coexistent PIK3CA and PTEN mutations were significantly correlated with UEC compared with CAH (P = 0.002), but the association in UEC did not reach statistical significance (P = 0.21). PIK3CA is the most commonly mutated oncogene in UEC; however, mutations are uncommon in CAH. Thus, mutations in PIK3CA, unlike PTEN mutations, are associated with invasion. These findings suggest that mutations in PIK3CA may serve as a marker of invasion with potential clinical use. Furthermore, PIK3CA and PTEN mutations may play distinct roles in endometrial tumorigenesis.
    Clinical Cancer Research 11/2006; 12(20 Pt 1):5932-5. · 7.84 Impact Factor

Publication Stats

113 Citations
20.71 Total Impact Points

Institutions

  • 2008–2010
    • Weill Cornell Medical College
      • Department of Pathology and Laboratory Medicine
      New York City, New York, United States
    • Cornell University
      • Department of Pathology and Laboratory Medicine
      Ithaca, NY, United States