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1. Polypoid amelanotic melanoma: a diagnostic challenge

Author

Milani-Nejad, Nima, Scarbrough, Chase, Mauzo, Shakuntala H, Peters, Sara B, Bechtel, Mark A, and Carr, David

Subjects
melanoma, amelanotic, metastasis
Abstract

Melanoma is a highly aggressive cutaneous malignancy with considerable risk for metastasis. These malignant tumors are typically pigmented given that they arise from melanocytes capable of producing melanin. Amelanotic melanomas are a rare variant and there is often a delay in diagnosis owing to lack of pigmentation. Although there are various presentations of amelanotic melanoma, a solitary polypoid nodule is unusual and warrants further reporting. Herein, we present a patient with a 3-year history of a tender firm, skin-to-pink colored polypoid nodule. Excisional biopsy and work up showed an aggressive amelanotic melanoma with depth of 20mm and nodal metastasis consistent with stage IIIC disease. This case highlights the necessity of recognition and prompt management of this rare subtype of melanoma.

Published
2018

2. Allele‐specific imbalance mapping identifies HDAC9 as a candidate gene for cutaneous squamous cell carcinoma

Author

Fleming, Jessica L, Dworkin, Amy M, Allain, Dawn C, Fernandez, Soledad, Wei, Lai, Peters, Sara B, Iwenofu, O Hans, Ridd, Katie, Bastian, Boris C, and Toland, Amanda Ewart

Subjects
Prevention, Cancer, Genetics, Biotechnology, Human Genome, 2.1 Biological and endogenous factors, Aetiology, Allelic Imbalance, Carcinoma, Squamous Cell, Chromosome Mapping, Genotype, Histone Deacetylases, Humans, Polymorphism, Single Nucleotide, Repressor Proteins, Skin Neoplasms, HDAC9, cutaneous squamous cell carcinoma, allelic-specific imbalance, Skts5, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

More than 3.5 million nonmelanoma skin cancers were treated in 2006; of these 700,000 were cutaneous squamous cell carcinomas (cSCCs). Despite clear environmental causes for cSCC, studies also suggest genetic risk factors. A cSCC susceptibility locus, Skts5, was identified on mouse chromosome 12 by linkage analysis. The orthologous locus to Skts5 in humans maps to 7p21 and 7q31. These loci show copy number increases in ∼10% of cSCC tumors. Here, we show that an additional 15-22% of tumors exhibit copy-neutral loss of heterozygosity. Furthermore, our previous data identified microsatellite markers on 7p21 and 7q31 that demonstrate preferential allelic imbalance (PAI) in cSCC tumors. On the basis of these results, we hypothesized that the human orthologous locus to Skts5 would house a gene important in human cSCC development and that tumors would demonstrate allele-specific somatic alterations. To test this hypothesis, we performed quantitative genotyping of 108 single nucleotide polymorphisms (SNPs) mapping to candidate genes at human SKTS5 in paired normal and tumor DNAs. Nine SNPs in HDAC9 (rs801540, rs1178108, rs1178112, rs1726610, rs10243618, rs11764116, rs1178355, rs10269422 and rs12540872) showed PAI in tumors. These data suggest that HDAC9 variants may be selected for during cSCC tumorigenesis.

Published
2014

4. Contributors

Author

Abderrahman, Balkees, primary, Aebi, Stefan, additional, Alluri, Prasanna, additional, Anderson, Benjamin O., additional, Arciero, Cletus A., additional, Ashfaq, Raheela, additional, Aversano, Thomas, additional, Axilbund, Jennifer, additional, Azizi, Ebrahim, additional, Banderudrappagari, Rajesh, additional, Barrio, Andrea V., additional, Bassett, Lawrence W., additional, Bedrosian, Isabelle, additional, Berkowitz, Alyssa, additional, Bevers, Therese B., additional, Bland, Kirby I., additional, Boneti, Cristiano, additional, Bostanci, Zeynep, additional, Brown-Glaberman, Ursa, additional, Brufsky, Adam, additional, Bryant-Smith, Gwendolyn, additional, Cahlon, Oren, additional, Calhoun, Benjamin C., additional, Calhoun, Kristine E., additional, Carr, Ryan J., additional, Chang, Helena R., additional, Chen, Steven L., additional, Chung, Alice, additional, Chung, Maureen A., additional, Cody, Hiram S., additional, Copeland, Edward M., additional, Costa, Ricardo, additional, de la Torre, Jorge I., additional, Degnim, Amy C., additional, Disis, Mary L., additional, Dupont, William D., additional, Epstein, Melinda S., additional, Esteva, Francisco J., additional, Euhus, David M., additional, Evans, Suzanne, additional, Fayanju, Oluwadamilola M., additional, Freedman, Gary M., additional, Garvey, Patrick Bryan, additional, Geletzke, Abby, additional, Gemignani, Mary L., additional, Giuliano, Armando E., additional, Golshan, Mehra, additional, Gradishar, William J., additional, Granger, Jill, additional, Greenberg, Caprice C., additional, Grimm, Lars J., additional, Grobmyer, Stephen R., additional, Hansen, Nora, additional, Harouaka, Ramdane, additional, Harris, Eleanor E., additional, Hartmann, Lynn C., additional, Hieken, Tina J., additional, Higgins, Susan, additional, Holmes, Dennis, additional, Hunt, Kelly K., additional, Hwang, E. Shelley, additional, Jagsi, Reshma, additional, Jain, Sarika, additional, Jasra, Bharti, additional, Jeruss, Jacqueline S., additional, Jimenez, Rafael E., additional, Jones, Veronica, additional, Jordan, V. Craig, additional, Joshi, Himanshu, additional, Kaklamani, Virginia, additional, Karlin, Nina J., additional, Karuturi, Meghan S., additional, Kass, Rena B., additional, Kern, Kenneth, additional, Khan, Seema A., additional, Klemp, Jennifer R., additional, Klimberg, V. Suzanne, additional, Korourian, Soheila, additional, Kuerer, Henry M., additional, Kumarapeli, Asangi R., additional, Kumthekar, Priya, additional, Kwa, Maryann, additional, Lagios, Michael D., additional, Landercasper, Jeffrey, additional, Lathrop, Kate I., additional, Lee, Gordon K., additional, Lee-Felker, Stephanie, additional, Leitch, A. Marilyn, additional, Lind, D. Scott, additional, Loprinzi, Charles L., additional, Lucci, Anthony, additional, Luther, Tahra Kaur, additional, Majithia, Neil, additional, Makhoul, Issam, additional, Mallory, Melissa Anne, additional, Mancino, Anne T., additional, Maraboyina, Sanjay, additional, Mathew, Aju, additional, McCartan, Damian, additional, McCloskey, Susan A., additional, McCormick, Beryl, additional, Mehra, Karishma, additional, Mendez, Jane E., additional, Mhatre, Priya V., additional, Mix, Michael D., additional, Moran, Meena S., additional, Moravek, Molly, additional, Neumayer, Leigh, additional, Obeng-Gyasi, Samilia, additional, Odele, Patience, additional, O'Donnell, Maureen, additional, O'Kelly Priddy, Colleen M., additional, O'Regan, Ruth M., additional, Oza, Sonal, additional, Pederson, Holly J., additional, Pennisi, Angela, additional, Peters, Margot S., additional, Peters, Sara B., additional, Petersen, Lindsay F., additional, Pilewskie, Melissa, additional, Prati, Raquel, additional, Press, Michael F., additional, Ramos, Erik, additional, Rivere, Amy E., additional, Rosenbloom, Arlan L., additional, Ruddy, Kathryn J., additional, Salerno, Kilian E., additional, Sanders, Melinda E., additional, Sanft, Tara, additional, Santa-Maria, Cesar A., additional, Sasaki, Jennifer, additional, Savalia, Nirav B., additional, Shah, Chirag, additional, Shahpar, Samman, additional, Shyr, Yu, additional, Silverstein, Melvin J., additional, Simpson, Jean F., additional, Sledge, George W., additional, Smith, Karen Lisa, additional, Smith, Stephen M., additional, Somlo, George, additional, Stanton, Sasha E., additional, Stearns, Vered, additional, Steliga, Matthew A., additional, Stopeck, Alison T., additional, Styblo, Toncred M., additional, Sun, Susie X., additional, Telli, Melinda L., additional, Tevaarwerk, Amye J., additional, Thomas, Parijatham S., additional, Tingquist, Nicholas D., additional, Tsai, Jacqueline, additional, Valente, Stephanie A., additional, Van den Bruele, Astrid Botty, additional, Vasconez, Luis O., additional, Causa, Doctor Honoris, additional, Vicini, Frank A., additional, Viscusi, Rebecca K., additional, Visscher, Daniel W., additional, Vogel, Victor G., additional, Waks, Adrienne G., additional, Wapnir, Irene L., additional, Wells, Thomas, additional, White, Julia, additional, Wicha, Max S., additional, Winer, Eric P., additional, Wisinski, Kari B., additional, Wong, Debra A., additional, Woodruff, Teresa K., additional, Wright, Eric J., additional, Young, Melissa, additional, and Young, Zachary T., additional

Published
2018
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6. Contributors

Author

Agnese, Doreen, primary, Allen, Kathleen Gardiner, additional, Ashfaq, Raheela, additional, Aversano, Thomas R., additional, Barsky, Sanford H., additional, Bassett, Lawrence W., additional, Beahm, Elisabeth K., additional, Beenken, Samuel W., additional, Bermas, Honnie R., additional, Bevers, Therese B., additional, Birru, Mehret, additional, Bland, Kirby I., additional, Brewster, Abenaa M., additional, Brinton, Louise A., additional, Brock, Malcolm V., additional, Brooks, Mai N., additional, Buchholz, Thomas A., additional, Chang, Helena R., additional, Chera, Bhishamjit S., additional, Ching, C. Denise, additional, Chung, Maureen A., additional, Cody, Hiram S., additional, Copeland, Edward M., additional, Cox, Charles E., additional, Cristofanilli, Massimo, additional, Curiel, David T., additional, Cuttino, Laurie W., additional, de la Torre, Jorge I., additional, De Los Santos, Jennifer F., additional, Diab, Mohammad S., additional, Disis, Mary L., additional, Dooley, William C., additional, DuPont, William D., additional, Dutt, Philip L., additional, Eberlein, Timothy J., additional, Edgerton, Mary, additional, El-Tamer, Mahmoud, additional, Farrar, William B., additional, Fearmonti, Regina M., additional, Folkman, M. Judah, additional, Freedman, Gary M., additional, Frykberg, Eric R., additional, Gaskin, Thomas A., additional, Gemignani, Mary, additional, Gillanders, William E., additional, Giuliano, Armando E., additional, Goedegebuure, Peter S., additional, Gold, Julie, additional, Golshan, Mehra, additional, Gradishar, William J., additional, Grobmyer, Stephen R., additional, Grube, Baiba J., additional, Harichand-Herdt, Seema, additional, Harper, J. Garrett, additional, Hasan, Yasmin, additional, Hohenhaus, Mary H., additional, Hortobagyi, Gabriel N., additional, Howard, J. Harrison, additional, Hsu, Christopher P., additional, Hudson, Alana G., additional, Hunt, Kelly K., additional, Ioan, Anamaria, additional, Jimenez, Rafael E., additional, Johnson, Joyce E., additional, Kaklamani, Virginia G., additional, Karam, Amer, additional, Karlin, Nina J., additional, Kass, Rena B., additional, Kaur, Paramjeet, additional, Kern, Kenneth A., additional, Khan, Seema A., additional, Kiluk, John V., additional, Kim, Paula, additional, Kirwan, Jessica, additional, Klimberg, V. Suzanne, additional, Klobocista, Merieme, additional, Kort, Kara C., additional, Krontiras, Helen, additional, Kruse, E. James, additional, Kuerer, Henry, additional, Lee, Jane W., additional, Leitch, A. Marilyn, additional, Le-Petross, Huong T., additional, Lightsey, Judith L., additional, Ligibel, Jennifer A., additional, Lind, D. Scott, additional, Lipkowitz, Stanley, additional, Long, James N., additional, Love, Richard, additional, Lu, Hailing, additional, Lynch, Henry T., additional, Lynch, Jane, additional, Mahoney, Mary, additional, Mancino, Anne T., additional, Marcus, Joseph N., additional, Marks, Lawrence B., additional, Masood, Shahla, additional, Massoll, Nicole, additional, McCraw, John B., additional, McLoughlin, James, additional, Meguid, Michael M., additional, Mendenhall, Nancy P., additional, Mendenhall, William M., additional, Mendez, Jane, additional, Middleton, Lavinia P., additional, Miller, Michael J., additional, Moore-Higgs, Giselle J., additional, Moulton, Anne W., additional, Mrozek, Ewa, additional, Nabell, Lisle, additional, Nam, Jiho, additional, Niederhuber, John E., additional, Numann, Patricia J., additional, Oler, Albert, additional, O'Regan, Ruth, additional, Page, David L., additional, Palazzo, Juan P., additional, Partridge, Ann H., additional, Peters, Sara B., additional, Hoang Pham, John Dung, additional, Phan, Vy, additional, Pollock, Raphael E., additional, Port, Elisa R., additional, Potter, David, additional, Povoski, Stephen P., additional, Prati, Raquel, additional, Press, Michael F., additional, Price, Janet E., additional, Puleo, Christopher A., additional, Recht, Abram, additional, Reeves, Katherine W., additional, Reuben, James M., additional, Romrell, Lynn J., additional, Rosenbloom, Arlan L., additional, Rubinstein, Wendy S., additional, Ruddy, Kathryn J., additional, Sanfilippo, Kristen, additional, Santillan, Alfredo A., additional, Schwartz, Gordon F., additional, Shah, Heather, additional, Shapiro, Charles, additional, Shen, Angela, additional, Shirazi, Sherin, additional, Shyr, Yu, additional, Silverstein, Melvin J., additional, Simpson, Jean F., additional, Singletary, S. Eva, additional, Smith, Benjamin D., additional, Snead, Felicia E., additional, Snyder, Carrie L., additional, Strong, Theresa V., additional, Styblo, Toncred M., additional, Urist, Marshall M., additional, Uttarwar, Mohan, additional, Vasconez, Luis O., additional, Vicini, Frank A., additional, Vogel, Victor G., additional, Wakely, Paul E., additional, Wall, Terry J., additional, Wicha, Max, additional, Winchester, David J., additional, Winchester, David P., additional, Winer, Eric P., additional, Wood, William C., additional, Yee, Douglas, additional, Yung, Rex C.W., additional, and Zelnak, Amelia, additional

Published
2009
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13. Case reports: telepathology in Mohs micrographic surgery

Author

Lambert, David R. and Peters, Sara B.

Subjects
Mohs surgery -- Health aspects, Mohs surgery -- Research, Skin cancer -- Risk factors, Skin cancer -- Diagnosis, Skin cancer -- Care and treatment, Skin cancer -- Patient outcomes, Skin cancer -- Case studies, Health, Pharmaceuticals and cosmetics industries
Abstract

Intraoperative histopathology consultation during Mohs micrographic surgery (MMS) with a dermatopathologist is advantageous in some cases requiring a clarification of a diagnosis but may be difficult because in comparison to [...]

Published
2008

15. Thyroid carcinoma in children and adolescents in Ukraine after the Chernobyl nuclear accident: statistical data and clinicomorphologic characteristics

Author

Tronko, Mykola D., Bogdanova, Tetyana I., Komissarenko, Igor V., Epstein, Ovsiy, Oliynyk, V., Kovalenko, A., Likhtarev, Ilya A., Kairo, I., Peters, Sara B., and LiVolsi, Virginia A.

Subjects
Chernobyl, Ukraine -- Accidents, Thyroid cancer -- Demographic aspects, Radioactivity -- Health aspects, Cancer in children -- Development and progression, Health
Published
1999

16. Differential mutation frequencies in metastatic cutaneous squamous cell carcinomas versus primary tumors

Author

Yilmaz, Ayse Selen, Ozer, Hatice Gulcin, Gillespie, Jessica, Allain, Dawn C., Bernhardt, Madison N., Furlan, Karina Colossi, Castro, Leticia Tambasco, Peters, Sara B., Nagarajan, Priyadharsini, Kang, Stephen, Iwenofu, O. Hans, Olencki, Thomas, Teknos, Theodoros N., and Toland, Amanda Ewart

Subjects
Aged, 80 and over, Male, Skin Neoplasms, DNA Mutational Analysis, High-Throughput Nucleotide Sequencing, Middle Aged, Article, Gene Expression Regulation, Neoplastic, Mutation Rate, Mutation, Biomarkers, Tumor, Carcinoma, Squamous Cell, Humans, Female, Neoplasm Grading, Neoplasm Metastasis, Aged, Neoplasm Staging
Abstract

Exome and targeted sequencing studies have identified potential driver mutations for a variety of tumor types. Cutaneous squamous cell carcinoma (cSCC) is one of the most highly mutated cancers but typically is associated with low rates of metastasis and high survival rates. Nevertheless, metastatic cSCC is a significant health threat; up to 8800 individuals die each year of this disease.Because it is difficult to predict which cSCCs are more likely to metastasize, and because to the best of the authors' knowledge there are no targeted therapies specifically designated for patients with metastatic cSCC, exome and/or targeted sequencing of 18 metastatic and 10 primary cSCCs was performed to identify mutations that were more frequent in metastatic tumors and might be targeted for therapeutic benefit. The authors compared their results with published sequencing results of an additional 223 primary tumors and 68 metastatic cSCCs.The authors identified genes demonstrating higher mutation frequencies in metastatic cSCC compared with primary tumors, including the chromatin remodeling gene lysine methyltransferase 2D (KMT2D) and the classic skin tumor suppressor tumor protein p53 (TP53), which was found to be mutated in 54% of primary tumors compared with 85% of metastatic tumors (P.0001).These studies appear to uncover potential pathways that are important in metastatic cSCC and that broaden understanding of the biology contributing to aggressive tumor behavior. These results may lead to new therapeutic strategies. Cancer 2017;123:1184-1193. © 2016 American Cancer Society.

Published
2016

17. Differential mutation frequencies in metastatic cutaneous squamous cell carcinomas versus primary tumors

Author

Yilmaz, Ayse Selen, primary, Ozer, Hatice Gulcin, additional, Gillespie, Jessica L., additional, Allain, Dawn C., additional, Bernhardt, Madison N., additional, Furlan, Karina Colossi, additional, Castro, Leticia T. F., additional, Peters, Sara B., additional, Nagarajan, Priyadharsini, additional, Kang, Stephen Y., additional, Iwenofu, O. Hans, additional, Olencki, Thomas, additional, Teknos, Theodoros N., additional, and Toland, Amanda Ewart, additional

Published
2016
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18. Global microRNA profiling for diagnostic appraisal of melanocytic Spitz tumors

Author

Latchana, Nicholas, primary, Regan, Kelly, additional, Howard, John Harrison, additional, Aldrink, Jennifer H., additional, Ranalli, Mark A., additional, Peters, Sara B., additional, Zhang, Xiaoli, additional, Gru, Alejandro, additional, Payne, Philip R.O., additional, Suarez-Kelly, Lorena P., additional, and Carson, William E., additional

Published
2016
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19. Classification of Indeterminate Melanocytic Lesions by MicroRNA Profiling

Author

Latchana, Nicholas, primary, del Campo, Sara E. Martin, additional, Grignol, Valerie P., additional, Clark, Jennifer R., additional, Albert, Scott P., additional, Zhang, Jie, additional, Wei, Lai, additional, Aldrink, Jennifer H., additional, Nicol, Kathleen K., additional, Ranalli, Mark A., additional, Peters, Sara B., additional, Gru, Alejandro, additional, Trihka, Prashant, additional, Payne, Philip R. O., additional, Howard, J. Harrison, additional, and Carson, William E., additional

Published
2016
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21. Eccrine carcinoma masquerading as metastatic breast cancer.

Author

Merrill, Andrea L., Smith, Stephen M., Peters, Sara B., and Agnese, Doreen M.

Subjects
BIOPSY, BREAST tumors, COMPUTED tomography, DIFFERENTIAL diagnosis, DIAGNOSTIC errors, IMMUNOHISTOCHEMISTRY, MAGNETIC resonance imaging, METASTASIS, SKIN tumors
Abstract

Case studies for 67‐year‐old female with a pimple‐like lesion on scalp for 3 years, and a 77‐year‐old female with a right axillary skin lesion for less than one year. Differential diagnosis for both included primary eccrine carcinoma versus metastasis from a mucinous adenocarcinoma. Given the absence of breast abnormalities, a diagnosis of eccrine carcinoma was favored in both.

Published
2020
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22. Differential mutation frequencies in metastatic cutaneous squamous cell carcinomas versus primary tumors.

Author

Yilmaz, Ayse Selen, Ozer, Hatice Gulcin, Gillespie, Jessica L., Allain, Dawn C., Bernhardt, Madison N., Furlan, Karina Colossi, Castro, Leticia T. F., Peters, Sara B., Nagarajan, Priyadharsini, Kang, Stephen Y., Iwenofu, O. Hans, Olencki, Thomas, Teknos, Theodoros N., and Toland, Amanda Ewart

Subjects
SQUAMOUS cell carcinoma, CARCINOMA, GENETIC mutation, CANCER invasiveness, METASTASIS
Abstract

BACKGROUND Exome and targeted sequencing studies have identified potential driver mutations for a variety of tumor types. Cutaneous squamous cell carcinoma (cSCC) is one of the most highly mutated cancers but typically is associated with low rates of metastasis and high survival rates. Nevertheless, metastatic cSCC is a significant health threat; up to 8800 individuals die each year of this disease. METHODS Because it is difficult to predict which cSCCs are more likely to metastasize, and because to the best of the authors' knowledge there are no targeted therapies specifically designated for patients with metastatic cSCC, exome and/or targeted sequencing of 18 metastatic and 10 primary cSCCs was performed to identify mutations that were more frequent in metastatic tumors and might be targeted for therapeutic benefit. The authors compared their results with published sequencing results of an additional 223 primary tumors and 68 metastatic cSCCs. RESULTS The authors identified genes demonstrating higher mutation frequencies in metastatic cSCC compared with primary tumors, including the chromatin remodeling gene lysine methyltransferase 2D ( KMT2D) and the classic skin tumor suppressor tumor protein p53 ( TP53), which was found to be mutated in 54% of primary tumors compared with 85% of metastatic tumors ( P<.0001). CONCLUSIONS These studies appear to uncover potential pathways that are important in metastatic cSCC and that broaden understanding of the biology contributing to aggressive tumor behavior. These results may lead to new therapeutic strategies. Cancer 2017;123:1184-1193. © 2016 American Cancer Society. [ABSTRACT FROM AUTHOR]

Published
2017
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24. PRMT5 Is Upregulated in Malignant and Metastatic Melanoma and Regulates Expression of MITF and p27Kip1

Author

Nicholas, Courtney, primary, Yang, Jennifer, additional, Peters, Sara B., additional, Bill, Matthew A., additional, Baiocchi, Robert A., additional, Yan, Fengting, additional, Sïf, Saïd, additional, Tae, Sookil, additional, Gaudio, Eugenio, additional, Wu, Xin, additional, Grever, Michael R., additional, Young, Gregory S., additional, and Lesinski, Gregory B., additional

Published
2013
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38. PRMT5 Is Upregulated in Malignant and Metastatic Melanoma and Regulates Expression of MITF and p27Kip1.

Author

Nicholas, Courtney, Yang, Jennifer, Peters, Sara B., Bill, Matthew A., Baiocchi, Robert A., Yan, Fengting, Sïf, Saïd, Tae, Sookil, Gaudio, Eugenio, Wu, Xin, Grever, Michael R., Young, Gregory S., and Lesinski, Gregory B.

Subjects
PROTEIN arginine methyltransferases, MELANOMA, GENE expression, CYTOPLASM, ENZYMATIC analysis, CELL lines
Abstract

Protein arginine methyltransferase-5 (PRMT5) is a Type II arginine methyltransferase that regulates various cellular functions. We hypothesized that PRMT5 plays a role in regulating the growth of human melanoma cells. Immunohistochemical analysis indicated significant upregulation of PRMT5 in human melanocytic nevi, malignant melanomas and metastatic melanomas as compared to normal epidermis. Furthermore, nuclear PRMT5 was significantly decreased in metastatic melanomas as compared to primary cutaneous melanomas. In human metastatic melanoma cell lines, PRMT5 was predominantly cytoplasmic, and associated with its enzymatic cofactor Mep50, but not STAT3 or cyclin D1. However, histologic examination of tumor xenografts from athymic mice revealed heterogeneous nuclear and cytoplasmic PRMT5 expression. Depletion of PRMT5 via siRNA inhibited proliferation in a subset of melanoma cell lines, while it accelerated growth of others. Loss of PRMT5 also led to reduced expression of MITF (microphthalmia-associated transcription factor), a melanocyte-lineage specific oncogene, and increased expression of the cell cycle regulator p27Kip1. These results are the first to report elevated PRMT5 expression in human melanoma specimens and indicate this protein may regulate MITF and p27Kip1 expression in human melanoma cells. [ABSTRACT FROM AUTHOR]

Published
2013
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40. Immunophenotypic diagnosis of primary cutaneous lymphomas: a review for the practicing dermatologist.

Author

Campbell, Shannon M, Peters, Sara B, Zirwas, Matthew J, and Wong, Henry K

Abstract

The application of CD markers to medicine has advanced our understanding of several dermatological diseases, most notably primary cutaneous lymphomas. CD markers are monoclonal antibodies that target cell surface molecules on leukocytes and antigens from other cells. T-cell processes are typically CD3+, CD20-, CD45+ while B-cell processes are typically CD3-, CD20+, and CD45+. Other CD markers are used to further delineate cutaneous lymphomas. Although an imperfect system, CD markers empower dermatologists to synthesize immunophenotyping with clinical findings and formulate an appropriate diagnosis. [ABSTRACT FROM AUTHOR]

Published
2010

41. Contributors

Author

Agnese, Doreen, Allen, Kathleen Gardiner, Ashfaq, Raheela, Aversano, Thomas R., Barsky, Sanford H., Bassett, Lawrence W., Beahm, Elisabeth K., Beenken, Samuel W., Bermas, Honnie R., Bevers, Therese B., Birru, Mehret, Bland, Kirby I., Brewster, Abenaa M., Brinton, Louise A., Brock, Malcolm V., Brooks, Mai N., Buchholz, Thomas A., Chang, Helena R., Chera, Bhishamjit S., Ching, C. Denise, Chung, Maureen A., Cody, Hiram S., III, Copeland, Edward M., III, Cox, Charles E., Cristofanilli, Massimo, Curiel, David T., Cuttino, Laurie W., de la Torre, Jorge I., De Los Santos, Jennifer F., Diab, Mohammad S., Disis, Mary L., Dooley, William C., DuPont, William D., Dutt, Philip L., Eberlein, Timothy J., Edgerton, Mary, El-Tamer, Mahmoud, Farrar, William B., Fearmonti, Regina M., Folkman, M. Judah, Freedman, Gary M., Frykberg, Eric R., Gaskin, Thomas A., III, Gemignani, Mary, Gillanders, William E., Giuliano, Armando E., Goedegebuure, Peter S., Gold, Julie, Golshan, Mehra, Gradishar, William J., Grobmyer, Stephen R., Grube, Baiba J., Harichand-Herdt, Seema, Harper, J. Garrett, Hasan, Yasmin, Hohenhaus, Mary H., Hortobagyi, Gabriel N., Howard, J. Harrison, Hsu, Christopher P., Hudson, Alana G., Hunt, Kelly K., Ioan, Anamaria, Jimenez, Rafael E., Johnson, Joyce E., Kaklamani, Virginia G., Karam, Amer, Karlin, Nina J., Kass, Rena B., Kaur, Paramjeet, Kern, Kenneth A., Khan, Seema A., Kiluk, John V., Kim, Paula, Kirwan, Jessica, Klimberg, V. Suzanne, Klobocista, Merieme, Kort, Kara C., Krontiras, Helen, Kruse, E. James, Kuerer, Henry, Lee, Jane W., Leitch, A. Marilyn, Le-Petross, Huong T., Lightsey, Judith L., Ligibel, Jennifer A., Lind, D. Scott, Lipkowitz, Stanley, Long, James N., Love, Richard, Lu, Hailing, Lynch, Henry T., Lynch, Jane, Mahoney, Mary, Mancino, Anne T., Marcus, Joseph N., Marks, Lawrence B., Masood, Shahla, Massoll, Nicole, McCraw, John B., McLoughlin, James, Meguid, Michael M., Mendenhall, Nancy P., Mendenhall, William M., Mendez, Jane, Middleton, Lavinia P., Miller, Michael J., Moore-Higgs, Giselle J., Moulton, Anne W., Mrozek, Ewa, Nabell, Lisle, Nam, Jiho, Niederhuber, John E., Numann, Patricia J., Oler, Albert, O'Regan, Ruth, Page, David L., Palazzo, Juan P., Partridge, Ann H., Peters, Sara B., Hoang Pham, John Dung, Phan, Vy, Pollock, Raphael E., Port, Elisa R., Potter, David, Povoski, Stephen P., Prati, Raquel, Press, Michael F., Price, Janet E., Puleo, Christopher A., Recht, Abram, Reeves, Katherine W., Reuben, James M., Romrell, Lynn J., Rosenbloom, Arlan L., Rubinstein, Wendy S., Ruddy, Kathryn J., Sanfilippo, Kristen, Santillan, Alfredo A., Schwartz, Gordon F., Shah, Heather, Shapiro, Charles, Shen, Angela, Shirazi, Sherin, Shyr, Yu, Silverstein, Melvin J., Simpson, Jean F., Singletary, S. Eva, Smith, Benjamin D., Snead, Felicia E., Snyder, Carrie L., Strong, Theresa V., Styblo, Toncred M., Urist, Marshall M., Uttarwar, Mohan, Vasconez, Luis O., Vicini, Frank A., Vogel, Victor G., Wakely, Paul E., Jr, Wall, Terry J., Wicha, Max, Winchester, David J., Winchester, David P., Winer, Eric P., Wood, William C., Yee, Douglas, Yung, Rex C.W., and Zelnak, Amelia

Published
2010
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42. PRMT5 Is Upregulated in Malignant and Metastatic Melanoma and Regulates Expression of MITF and p27Kip1.

Author

Nicholas, Courtney, Yang, Jennifer, Peters, Sara B., Bill, Matthew A., Baiocchi, Robert A., Yan, Fengting, Sïf, Saïd, Tae, Sookil, Gaudio, Eugenio, Wu, Xin, Grever, Michael R., Young, Gregory S., and Lesinski, Gregory B.

Subjects
*PROTEIN arginine methyltransferases, *MELANOMA, *GENE expression, *CYTOPLASM, *ENZYMATIC analysis, *CELL lines
Abstract

Protein arginine methyltransferase-5 (PRMT5) is a Type II arginine methyltransferase that regulates various cellular functions. We hypothesized that PRMT5 plays a role in regulating the growth of human melanoma cells. Immunohistochemical analysis indicated significant upregulation of PRMT5 in human melanocytic nevi, malignant melanomas and metastatic melanomas as compared to normal epidermis. Furthermore, nuclear PRMT5 was significantly decreased in metastatic melanomas as compared to primary cutaneous melanomas. In human metastatic melanoma cell lines, PRMT5 was predominantly cytoplasmic, and associated with its enzymatic cofactor Mep50, but not STAT3 or cyclin D1. However, histologic examination of tumor xenografts from athymic mice revealed heterogeneous nuclear and cytoplasmic PRMT5 expression. Depletion of PRMT5 via siRNA inhibited proliferation in a subset of melanoma cell lines, while it accelerated growth of others. Loss of PRMT5 also led to reduced expression of MITF (microphthalmia-associated transcription factor), a melanocyte-lineage specific oncogene, and increased expression of the cell cycle regulator p27Kip1. These results are the first to report elevated PRMT5 expression in human melanoma specimens and indicate this protein may regulate MITF and p27Kip1 expression in human melanoma cells. [ABSTRACT FROM AUTHOR]

Published
2013
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43. Unusual presentation of erythema elevatum diutinum with underlying hepatitis B infection.

Author

Hoy JV, Kikam A, Tyler K, Peters SB, and Kaffenberger BH

Subjects
Diagnosis, Differential, Hepatitis B complications, Humans, Male, Middle Aged, Vasculitis, Leukocytoclastic, Cutaneous etiology, Hepatitis B diagnosis, Vasculitis, Leukocytoclastic, Cutaneous diagnosis
Abstract

Erythema elevatum diutinum (EED) is a rare, chronic, cutaneous small vessel vasculitis of unclear pathogenesis. Classically, lesions present as symmetric red to purple plaques, papules, and nodules overlying joints. First-line therapy is dapsone. We present a case of EED with widespread lesions involving the hands, extensor arms and legs, and trunk. Multiple biopsies showed concentric intradermal perivascular inflammation with dermal fibrosis and leukocytoclastic vasculitis (LCV) suggesting EED in various stages of evolution. An extensive workup was positive for underlying hepatitis B infection. Our case represents the clinicopathologic spectrum that EED can present and emphasizes the importance of searching for an underlying etiology.

Published
2018

44. Telepathology in Mohs micrographic surgery.

Author

Lambert DR and Peters SB

Subjects
Adult, Carcinoma in Situ pathology, Carcinoma, Squamous Cell pathology, Humans, Male, Referral and Consultation, Skin Neoplasms pathology, Carcinoma in Situ surgery, Carcinoma, Squamous Cell surgery, Mohs Surgery, Skin Neoplasms surgery, Telepathology
Abstract

Intraoperative histopathology consultation during Mohs micrographic surgery (MMS) with a dermatopathologist is advantageous in some cases requiring a clarification of a diagnosis but may be difficult because in comparison to the Mohs laboratory, the dermatopathology facility can be remote. Telepathology technology provides a time-efficient means of consultation during MMS via the electronic transmission of pathology images, which can foster case discussions, and expedite the confirmation of diagnosis and treatment decisions.

Published
2008

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