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2. Plasma Cell Granuloma of the Thyroid: Review of an Uncommon Entity

Author

Patil, Pallavi A. and DeLellis, Ronald A.

Subjects
Etiology (Medicine) -- Usage, Granuloma -- Care and treatment -- Prognosis, Cell proliferation -- Research, Thyroid diseases -- Risk factors, Signs and symptoms -- Analysis, Health
Abstract

* Plasma cell granuloma (PCG) is characterized by proliferation of polyclonal plasma cells with associated fibrosis and is often considered part of the heterogeneous group of inflammatory myofibroblastic tumors (IMTs). The thyroid is rarely affected by PCG. A patient having PCG associated with Hashimoto thyroiditis (HT) prompted our literature search that revealed 18 cases of PCG, 55% (n = 10) of which occurred together with HT. The etiopathogenesis of PCG is unknown and there is no specific treatment except surgical excision for compressive symptoms. This entity has an excellent prognosis with no evidence of recurrence or metastasis. Lesions of the thyroid with infiltrating plasma cells include HT, fibrous variant of HT, plasmacytoma, plasma cell myeloma, Riedel thyroiditis, IgG4 (immunoglobulin G4)-related disease, IMT, and PCG. Inflammatory myofibroblastic tumor has ALK gene rearrangements and is considered a neoplasm as opposed to PCG, which is a reactive polyclonal plasma cell proliferation. We believe IMT and PCG are distinct entities and consensus definitions are required for avoiding confusion in the literature. doi: 10.5858/arpa.2017-0068-RS, Plasma cell granuloma (PCG) is a pseudotumor-like condition characterized by polyclonal proliferation of plasma cells. Historically, PCGs are considered within the spectrum of inflammatory myofibroblastic tumors (IMTs) and, therefore, we [...]

Published
2018
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5. Endocrine Pathology

Author

DeLellis, Ronald A., Kuta, A. John, Krueger, Gerhard R. F., Krueger, Gerhard R.F., editor, and Buja, L. Maximilian, editor

Published
2013
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15. ColXα1 is a stromal component that colocalizes with elastin in the breast tumor extracellular matrix

Author

Wang, Yihong, Lu, Shaolei, Xiong, Jinjun, Singh, Kamaljeet, Hui, Yiang, Zhao, Chaohui, Brodsky, Alexander S, Yang, Dongfang, Jolly, Grant, Ouseph, Madhu, Schorl, Christoph, DeLellis, Ronald A, and Resnick, Murray B

Subjects
Adult, extracellular matrix, neoadjuvant, Carcinoma, Ductal, Breast, elastin, Breast Neoplasms, Original Articles, Middle Aged, Gene Expression Regulation, Neoplastic, type X collagen α‐1, breast cancer, Carcinoma, Intraductal, Noninfiltrating, Receptors, Estrogen, Biomarkers, Tumor, Tumor Microenvironment, Humans, Original Article, Female, ColXα1, skin and connective tissue diseases, Aged, Collagen Type X
Abstract

The tumor microenvironment regulates tissue development and homeostasis, and its dysregulation contributes to neoplastic progression. Increased expression of type X collagen α‐1 (ColXα1) in tumor‐associated stroma correlates with poor pathologic response to neoadjuvant chemotherapy in estrogen receptor (ER) and human epidermal growth factor receptor 2 (HER2)‐positive breast cancers. Evaluation of ColXα1 expression patterns suggests a potential connection with elastin fibers. To investigate the possible interaction between ColXα1 and elastin, we evaluated the expression of ColXα1 in relation to elastin fibers in normal breast tissue, ductal carcinoma in situ, and invasive breast carcinomas at cellular and subcellular levels. Our findings demonstrate that ColXα1 colocalizes with elastin in invasive breast cancer‐associated stroma by immunohistochemistry, immunofluorescence, and electron microscopy. In 212 invasive breast carcinomas, this complex was aberrantly and selectively expressed in tumor extracellular matrix in 79% of ER+/HER2−, 80% of ER+/HER2+, 76% of ER−/HER2+, and 58% of triple negative breast cancers. In contrast, ColXα1 was generally absent, while elastin was present perivascularly in normal breast tissue. ColXα1 and elastin were coexpressed in 58% of ductal carcinoma in situ (DCIS) in periductal areas. In mass‐forming DCIS with desmoplastic stroma, the complex was intensely expressed in periductal areas as well as within the tumor‐associated stroma in all cases. Our data suggest that the breast carcinoma neoplastic process may involve aberrant expression of ColXα1 and elastin in the tumor microenvironment emerging early at the DCIS stage. Enrichment of these complexes in tumor‐associated stroma may represent a stromal signature indicative of intrinsic differences between breast cancers. These findings shed light on investigation into the role of aberrant collagen complex expression in tumorigenesis and tumor progression which may be leveraged in therapeutic and theranostic applications.

Published
2018

18. Acid-induced p16 hypermethylation contributes to development of esophageal adenocarcinoma via activation of NADPH oxidase NOX5-S

Author

Hong, Jie, Resnick, Murray, Behar, Jose, Wang, Li Juan, Wands, Jack, DeLellis, Ronald A., Souza, Rhonda F., Spechler, Stuart J., and Cao, Weibiao

Subjects
Methylation -- Observations, Adenocarcinoma -- Physiological aspects, Barrett's esophagus -- Physiological aspects, Reactive oxygen species -- Health aspects, Biological sciences
Abstract

Inactivation of tumor suppressor gene p16 may play an important role in the progression from Barrett's esophagus (BE) to esophageal adenocarcinoma (EA). Hypermethylation of p16 gene promoter is an important mechanism inactivating p16. However, the mechanisms of p16 hypermethylation in EA are not known. Therefore, we examined whether acid increases methylation of p16 gene promoter and whether NADPH oxidase NOX5-S mediates acid-induced p16 hypermethylation in a Barrett's cell line BAR-T and an EA cell line OE33. We found that NOX5-S was present in BAR-T and OE33 cells. Acid-induced increase in H202 production and cell proliferation was significantly reduced by knockdown of NOX5-S. Exogenous H202 remarkably increased p16 promoter methylation and cell proliferation. In addition, acid treatment significantly increased p16 promoter methylation and decreased p16 mRNA level. Knockdown of NOX5-S significantly increased p16 mRNA, inhibited acid-induced downregulation of p16 mRNA, and blocked acid-induced increase in p16 methylation and cell proliferation. Conversely, overexpression of NOX5-S significantly decreased p16 mRNA and increased p16 methylation and cell proliferation. In conclusion, NOX5-S is present in BAR-T cells and OE33 cells and mediates acid-induced [H.sub.2][O.sub.2] production and cell proliferation. NOX5-S is also involved in acid-induced hypermethylation of p16 gene promoter and downregulation of p16 mRNA. It is possible that acid reflux present in BE patients may activate NOX5-S and increase production of reactive oxygen species, which in turn increase p16 promoter methylation, downregulate p16 expression, and increase cell proliferation, thereby contributing to the progression from BE to EA. Barrett's esophagus; reactive oxygen species; acid; hydrogen peroxide; cell proliferation doi: 10.1152/ajpgi.00186.2010.

Published
2010

19. Role of a novel bile acid receptor TGR5 in the development of oesophageal adenocarcinoma

Author

Hong, Jie, Behar, Jose, Wands, Jack, Resnick, Murray, Wang, Li Juan, DeLellis, Ronald A., Lambeth, David, Souza, Rhonda F., Spechler, Stuart J., and Cao, Weibiao

Subjects
Esophageal cancer -- Development and progression, Esophageal cancer -- Research, Bile acids -- Physiological aspects, Bile acids -- Research, NADP (Coenzyme) -- Physiological aspects, NADP (Coenzyme) -- Research, Cell proliferation -- Research, Health
Published
2010

21. Contributors

Author

Adams, E. Terence, primary, Adler, Rick, additional, Alden, Carl L., additional, Bartholomew, Phillip M., additional, Basu, Joydeep, additional, Beasley, Val R., additional, Berridge, Brian R., additional, Bertram, Timothy A., additional, Bhang, Hyo-eun, additional, Black, Hugh E., additional, Bolon, Brad, additional, Boorman, Gary A., additional, Bounous, Denise I., additional, Boyce, Rogely Waite, additional, Bracken, William M., additional, Brix, Amy E., additional, Brown, Danielle, additional, Butt, Mark T., additional, Cantor, Glenn H., additional, Car, Bruce D., additional, Castranova, Vincent, additional, Cattley, Russell C., additional, Chan, Curtis, additional, Chapin, Robert E., additional, Cohen, Samuel M., additional, Colegate, Steve, additional, Cook, Daniel, additional, Cooke, Paul S., additional, Crabbs, Torrie A., additional, Creasy, Dianne M., additional, Crissman, James W., additional, Cullen, John M., additional, Danilenko, Dimitry M., additional, Davis, Barbara, additional, Davis, Myrtle A., additional, Davis, T. Zane, additional, DeLellis, Ronald A., additional, Denslow, Nancy D., additional, Diegel, Kelly L., additional, Dorman, David C., additional, Dubielzig, Richard R., additional, Durham, Stephen K., additional, Eldridge, Sandy, additional, Elmore, Susan A., additional, Everitt, Jeffrey I., additional, Fenton, Suzanne, additional, Ferguson, Duncan C., additional, Field, Reuel, additional, Foley, George L., additional, Foster, William R., additional, Frantz, Jerry D., additional, Gabrielson, Kathy, additional, Gad, Shayne C., additional, Galbreath, Elizabeth J., additional, Gardner, Dale R., additional, Garman, Robert H., additional, Gill, Santokh, additional, Glerup, Peter, additional, Goad, Dale L., additional, Pecquet Goad, Mary Elizabeth, additional, Grand, Nanna, additional, Green, Benjamin T., additional, Gropp, Kathryn E., additional, Gundersen, Hans Jørgen G., additional, Gunson, Diane, additional, Gupta, Ramesh C., additional, Gwaltney-Brant, Sharon M., additional, Hall, Jeffery O., additional, Halpern, Wendy, additional, Hard, Gordon C., additional, Hardisty, Jerry F., additional, Harkema, Jack R., additional, Harvey, Philip W., additional, Haschek, Wanda M., additional, Heinz-Taheny, Kathleen, additional, Herbert, Ronald A., additional, Herman, Eugene, additional, Hoenerhoff, Mark, additional, Hubbs, Ann, additional, Hutto, David, additional, Janovitz, Evan B., additional, Khan, Kanwar Nasir M., additional, Keenan, Kevin P., additional, Kerlin, Roy L., additional, Kreeger, John M., additional, Krishnan, Kannan, additional, Kuper, C. Frieke, additional, Lee, Stephen T., additional, Lehman-McKeeman, Lois D., additional, Li, Xiantang, additional, Lombardini, Eric D., additional, Louden, Calvert, additional, Ludlow, John W., additional, Malarkey, David E., additional, Mann, Peter C., additional, Maronpot, Robert R., additional, McDorman, Kevin S., additional, Melanson, Mark A., additional, Mercer, Robert, additional, Mirabile, Rosanna, additional, Moch, Ronald W., additional, Morrison, James P., additional, Morton, Daniel, additional, Morton, Laura Dill, additional, Muthupalani, Sureshkumar, additional, Nikula, Kristen J., additional, Ochoa, Ricardo, additional, Pacheco-Thompson, Michelle E., additional, Pulido, Olga M., additional, Panter, Kip E., additional, Parker, George A., additional, Porter, Dale W., additional, Patterson, Douglas Reid, additional, Pfister, James A., additional, Pinkert, Carl A., additional, Ramaiah, Lila, additional, Rao, Deepa B., additional, Robertson, Donald G., additional, Rojko, Jennifer, additional, Rosol, Thomas J., additional, Rousseaux, Colin G., additional, Rudmann, Daniel G., additional, Ruehl-Fehlert, Christine, additional, Sargent, Linda, additional, Satterwhite, Christina M., additional, Schafer, Kenneth A., additional, Solter, Philip F., additional, Sills, Robert C., additional, Simon, Liz, additional, Skydsgaard, Mikala, additional, Smith, Graham S., additional, Sriram, Krishnan, additional, Stegelmeier, Bryan L., additional, Sullivan, John M., additional, Sutcliffe, Catherine, additional, Swenberg, James A., additional, Sysa-Shah, Polina, additional, Teixeira, Leandro, additional, Tsuchiya, Noriko, additional, Vahle, John L., additional, Van Vleet, John F., additional, Varela, Aurore, additional, Voss, Kenneth A., additional, Walker, Robin M., additional, Wallig, Matthew A., additional, Walter, Gail L., additional, Welch, Kevin D., additional, White, Paul, additional, Winkelmann, Christopher T., additional, Wojcinski, Zbigniew W., additional, and Wolf, Jeffrey C., additional

Published
2013
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22. Endocrine System

Author

Rosol, Thomas J., primary, DeLellis, Ronald A., additional, Harvey, Philip W., additional, and Sutcliffe, Catherine, additional

Published
2013
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34. CONTRIBUTORS

Author

Volkan Adsay, N., primary, Barr, Nancy J., additional, Basturk, Olca, additional, Bhargava, Parul, additional, Bhargava, Rohit, additional, Chivukula, Mamatha, additional, Coffin, Cheryl M., additional, Comstock, Jessica M., additional, Dabbs, David J., additional, Dacic, Sanja, additional, DeLellis, Ronald A., additional, Epstein, Jonathan I., additional, Esposito, Nicole N., additional, Ezyaguirre, Eduardo J., additional, Farris III, Alton B., additional, Goldsmith, Jeffrey D., additional, Hammar, Samuel P., additional, Hornick, Jason L., additional, Hunt, Jennifer L., additional, Kadin, Marshall E., additional, Krasinskas, Alyssa M., additional, Martin, Alvin W., additional, McKeever, Paul E., additional, Netto, George J., additional, Nikiforov, Yuri E., additional, Nikiforova, Marina N., additional, Patterson, James W., additional, Rabban, Joseph T., additional, Shi, Shan-Rong, additional, Shin, Sandra J., additional, Soslow, Robert A., additional, Swanson, Paul E., additional, Taylor, Clive R., additional, Treaba, Diana O., additional, Walker, David H., additional, Wallentine, Jeremy C., additional, Wick, Mark R., additional, Zaki, Sherif R., additional, and Zaloudek, Charles Z., additional

Published
2010
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36. Contributors

Author

Allen, Carl M., primary, Bouquot, Jerry E., additional, Brandwein-Gensler, Margaret S., additional, Crissman, John D., additional, Damm, Douglas D., additional, Davis, Gustave L., additional, DeLellis, Ronald A., additional, El-Mofty, Samir K., additional, Eveson, John, additional, Folpe, Andrew L., additional, Gale, Nina, additional, Gnepp, Douglas R., additional, Guiter, Gerardo E., additional, Henley, John D., additional, Layfield, Lester J., additional, Lin, Pei, additional, Luna, Mario A., additional, Mahadevia, Panna, additional, Medeiros, L. Jeffrey, additional, Muller, Susan, additional, Neville, Brad W., additional, Nikai, Hiromasa, additional, Nikiforov, Yuri E., additional, Perez-Ordonez, Bayardo, additional, Pfaltz, Madeleine, additional, Pisharodi, Latha, additional, Prasad, Manju L., additional, Richardson, Mary, additional, Sakr, Wael A., additional, Simpson, Roderick H.W., additional, Slootweg, Pieter J., additional, and Wick, Mark R., additional

Published
2009
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43. Contributors

Author

Barnes, Leon, primary, Barr, Nancy J, additional, Belchis, Deborah, additional, Bhargava, Parul, additional, Bosler, David S, additional, Bostwick, David G, additional, Cerilli, Lisa A, additional, Coffin, Cheryl, additional, Dabbs, David J, additional, DeLellis, Ronald A, additional, Eyzaguirre, Eduardo J, additional, Gocke, Christopher, additional, Goldstein, Neal S, additional, Hammar, Samuel P, additional, Hunt, Jennifer L, additional, Isacson, Christina, additional, Josefson, Deborah, additional, Kadin, Marshall E, additional, Liu, Lina, additional, Ma, Jun, additional, McKeever, Paul E, additional, Patterson, James W, additional, Qian, Junqi, additional, Shi, Shan-Rong, additional, Shin, Sandra J, additional, Soslow, Robert A, additional, Swanson, Paul E, additional, Taylor, Clive R, additional, Walker, David, additional, Wick, Mark R, additional, Wu, Nancy, additional, Zaki, Sherif R, additional, and Zaloudek, Charles F, additional

Published
2006
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