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492 results on '"Dlugosz, Andrzej A."'

1. Distinct mechanisms for sebaceous gland self-renewal and regeneration provide durability in response to injury.

Author

Veniaminova, Natalia, Jia, Yunlong, Hartigan, Adrien, Huyge, Thomas, Tsai, Shih-Ying, Grachtchouk, Marina, Nakagawa, Seitaro, Dlugosz, Andrzej, Wong, Sunny, and Atwood, Scott

Subjects
CP: Stem cell research, Hair follicle stem cells, K79, Krt79, Pparg, epithelial, infundibulum, sebocyte, skin biology, wound healing, Sebaceous Glands, Cell Differentiation, Skin, Hair Follicle, Epithelial Cells
Abstract

Sebaceous glands (SGs) release oils that protect our skin, but how these glands respond to injury has not been previously examined. Here, we report that SGs are largely self-renewed by dedicated stem cell pools during homeostasis. Using targeted single-cell RNA sequencing, we uncovered both direct and indirect paths by which resident SG progenitors ordinarily differentiate into sebocytes, including transit through a Krt5+PPARγ+ transitional basal cell state. Upon skin injury, however, SG progenitors depart their niche, reepithelialize the wound, and are replaced by hair-follicle-derived stem cells. Furthermore, following targeted genetic ablation of >99% of SGs from dorsal skin, these glands unexpectedly regenerate within weeks. This regenerative process is mediated by alternative stem cells originating from the hair follicle bulge, is dependent upon FGFR2 signaling, and can be accelerated by inducing hair growth. Altogether, our studies demonstrate that stem cell plasticity promotes SG durability following injury.

Published
2023

4. Inhibition of Hedgehog Signaling Alters Fibroblast Composition in Pancreatic CancerHedgehog Signaling in Pancreatic Cancer

Author

Steele, Nina G, Biffi, Giulia, Kemp, Samantha B, Zhang, Yaqing, Drouillard, Donovan, Syu, LiJyun, Hao, Yuan, Oni, Tobiloba E, Brosnan, Erin, Elyada, Ela, Doshi, Abhishek, Hansma, Christa, Espinoza, Carlos, Abbas, Ahmed, The, Stephanie, Irizarry-Negron, Valerie, Halbrook, Christopher J, Franks, Nicole E, Hoffman, Megan T, Brown, Kristee, Carpenter, Eileen S, Nwosu, Zeribe C, Johnson, Craig, Lima, Fatima, Anderson, Michelle A, Park, Youngkyu, Crawford, Howard C, Lyssiotis, Costas A, Frankel, Timothy L, Rao, Arvind, Bednar, Filip, Dlugosz, Andrzej A, Preall, Jonathan B, Tuveson, David A, Allen, Benjamin L, and di Magliano, Marina Pasca

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Pancreatic Cancer, Rare Diseases, Digestive Diseases, Aetiology, 2.1 Biological and endogenous factors, Animals, Cancer-Associated Fibroblasts, Carcinoma, Pancreatic Ductal, Hedgehog Proteins, Humans, Mice, Mice, Inbred C57BL, Pancreatic Neoplasms, Signal Transduction, Tumor Microenvironment, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis
Abstract

PurposePancreatic ductal adenocarcinoma (PDAC) is a deadly disease characterized by an extensive fibroinflammatory stroma, which includes abundant cancer-associated fibroblast (CAF) populations. PDAC CAFs are heterogeneous, but the nature of this heterogeneity is incompletely understood. The Hedgehog pathway functions in PDAC in a paracrine manner, with ligands secreted by cancer cells signaling to stromal cells in the microenvironment. Previous reports investigating the role of Hedgehog signaling in PDAC have been contradictory, with Hedgehog signaling alternately proposed to promote or restrict tumor growth. In light of the newly discovered CAF heterogeneity, we investigated how Hedgehog pathway inhibition reprograms the PDAC microenvironment.Experimental designWe used a combination of pharmacologic inhibition, gain- and loss-of-function genetic experiments, cytometry by time-of-flight, and single-cell RNA sequencing to study the roles of Hedgehog signaling in PDAC.ResultsWe found that Hedgehog signaling is uniquely activated in fibroblasts and differentially elevated in myofibroblastic CAFs (myCAF) compared with inflammatory CAFs (iCAF). Sonic Hedgehog overexpression promotes tumor growth, while Hedgehog pathway inhibition with the smoothened antagonist, LDE225, impairs tumor growth. Furthermore, Hedgehog pathway inhibition reduces myCAF numbers and increases iCAF numbers, which correlates with a decrease in cytotoxic T cells and an expansion in regulatory T cells, consistent with increased immunosuppression.ConclusionsHedgehog pathway inhibition alters fibroblast composition and immune infiltration in the pancreatic cancer microenvironment.

Published
2021

6. Niche-Specific Factors Dynamically Regulate Sebaceous Gland Stem Cells in the Skin.

Author

Veniaminova, Natalia A, Grachtchouk, Marina, Doane, Owen J, Peterson, Jamie K, Quigley, David A, Lull, Madison V, Pyrozhenko, Daryna V, Nair, Raji R, Patrick, Matthew T, Balmain, Allan, Dlugosz, Andrzej A, Tsoi, Lam C, and Wong, Sunny Y

Subjects
Meibomian Glands, Sebaceous Glands, Stem Cells, Skin, Animals, Mice, Knockout, Cell Differentiation, Mutation, Female, Male, Immunoglobulin J Recombination Signal Sequence-Binding Protein, Receptors, Notch, Keratins, Hedgehog Proteins, Stem Cell Niche, K79, Krt79, epithelial stem cells, hair follicles, infundibulum, sebaceous glands, skin biology, Stem Cell Research, Regenerative Medicine, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Oil-secreting sebaceous glands (SGs) are critical for proper skin function; however, it remains unclear how different factors act together to modulate SG stem cells. Here, we provide functional evidence that each SG lobe is serviced by its own dedicated stem cell population. Upon ablating Notch signaling in different skin subcompartments, we find that this pathway exerts dual counteracting effects on SGs. Suppressing Notch in SG progenitors traps them in a hybrid state where stem and differentiation features become intermingled. In contrast, ablating Notch outside of the SG stem cell compartment indirectly drives SG expansion. Finally, we report that a K14:K5→K14:K79 keratin shift occurs during SG differentiation. Deleting K79 destabilizes K14 in sebocytes, and attenuates SGs and eyelid meibomian glands, leading to corneal ulceration. Altogether, our findings demonstrate that SGs integrate diverse signals from different niches and suggest that mutations incurred within one stem cell compartment can indirectly influence another.

Published
2019

10. Predictive modeling provides insight into the clinical heterogeneity associated with TARS1 loss-of-function mutations

Author

Meyer-Schuman, Rebecca, primary, Cale, Allison R, additional, Pierluissi, Jennifer A, additional, Jonatzke, Kira E, additional, Park, Young N, additional, Lenk, Guy M, additional, Oprescu, Stephanie N, additional, Grachtchouk, Marina A, additional, Dlugosz, Andrzej A, additional, Beg, Asim A, additional, Meisler, Miriam H, additional, and Antonellis, Anthony, additional

Published
2024
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14. Corrigendum to “Characterizing the Therapeutic Potential of a Potent BET Degrader in Merkel Cell Carcinoma” [Neoplasia, Volume 21, Issue 3 (2019) 322–330]

Author

Choi, Jae Eun, Verhaegen, Monique E., Yazdani, Sahr, Malik, Rohit, Harms, Paul W., Mangelberger, Doris, Tien, Jean, Cao, Xuhong, Wang, Yuping, Cieślik, Marcin, Gurkan, Jonathan, Yazdani, Mishaal, Jing, Xiaojun, Juckette, Kristin, Su, Fengyun, Wang, Rui, Zhou, Bing, Apel, Ingrid J., Wang, Shaomeng, Dlugosz, Andrzej A., and Chinnaiyan, Arul M.

Published
2024
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17. Direct cellular reprogramming enables development of viral T antigen-driven Merkel cell carcinoma in mice

Author

Verhaegen, Monique E., Harms, Paul W., Van Goor, Julia J., Arche, Jacob, Patrick, Matthew T., Wilbert, Dawn, Zabawa, Haley, Grachtchouk, Marina, Liu, Chia-Jen, Hu, Kevin, Kelly, Michael C., Chen, Ping, Saunders, Thomas L., Weidinger, Stephan, Syu, Li-Jyun, Runge, John S., Gudjonsson, Johann E., Wong, Sunny Y., Brownell, Isaac, Cieslik, Marcin, Udager, Aaron M., Chinnaiyan, Arul M., Tsoi, Lam C., and Dlugosz, Andrzej A.

Subjects
Oncology, Experimental, Merkel cell carcinoma -- Genetic aspects -- Development and progression, Viral antigens -- Genetic aspects, Gene expression -- Research, Cell differentiation -- Research, Tumor antigens -- Genetic aspects, Cancer -- Research, Health care industry
Abstract

Merkel cell carcinoma (MCC) is an aggressive neuroendocrine skin cancer that frequently carries an integrated Merkel cell polyomavirus (MCPyV) genome and expresses viral transforming antigens (TAgs). MCC tumor cells also express signature genes detected in skin-resident, postmitotic Merkel cells, including atonal bHLH transcription factor 1 (ATOH1), which is required for Merkel cell development from epidermal progenitors. We now report the use of in vivo cellular reprogramming, using ATOH1, to drive MCC development from murine epidermis. We generated mice that conditionally expressed MCPyV TAgs and ATOH1 in epidermal cells, yielding microscopic collections of proliferating MCC-like cells arising from hair follicles. Immunostaining of these nascent tumors revealed p53 accumulation and apoptosis, and targeted deletion of transformation related protein 53 (Trp53) led to development of gross skin tumors with classic MCC histology and marker expression. Global transcriptome analysis confirmed the close similarity of mouse and human MCCs, and hierarchical clustering showed conserved upregulation of signature genes. Our data establish that expression of MCPyV TAgs in ATOH1-reprogrammed epidermal cells and their neuroendocrine progeny initiates hair follicle-derived MCC tumorigenesis in adult mice. Moreover, progression to full-blown MCC in this model requires loss of p53, mimicking the functional inhibition of p53 reported in human MCPyV-positive MCCs., Introduction Merkel cell carcinoma (MCC) is an aggressive neuroendocrine skin tumor with a poor prognosis (1), although up to 50% of patients with advanced disease respond to immunotherapy (2). In [...]

Published
2022
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18. Dual and opposing roles of primary cilia in medulloblastoma development.

Author

Han, Young-Goo, Kim, Hong Joo, Dlugosz, Andrzej A, Ellison, David W, Gilbertson, Richard J, and Alvarez-Buylla, Arturo

Subjects
Cilia, Animals, Mice, Transgenic, Humans, Mice, Mice, Mutant Strains, Medulloblastoma, Cerebellar Neoplasms, Glial Fibrillary Acidic Protein, Receptors, G-Protein-Coupled, Nerve Tissue Proteins, Nuclear Proteins, Signal Transduction, Child, Wnt Proteins, Kruppel-Like Transcription Factors, Hedgehog Proteins, Smoothened Receptor, Zinc Finger Protein Gli2, Kinesins, Cancer, Brain Disorders, Brain Cancer, Rare Diseases, Pediatric, Medical and Health Sciences, Immunology
Abstract

Recent work has shown that primary cilia are essential for Hedgehog (Hh) signaling during mammalian development. It is also known that aberrant Hh signaling can lead to cancer, but the role of primary cilia in oncogenesis is not known. Cerebellar granule neuron precursors (GNPs) can give rise to medulloblastomas, the most common malignant brain tumor in children. The primary cilium and Hh signaling are required for GNP proliferation. We asked whether primary cilia in GNPs have a role in medulloblastoma growth in mice. Genetic ablation of primary cilia blocked medulloblastoma formation when this tumor was driven by a constitutively active Smoothened protein (Smo), an upstream activator of Hh signaling. In contrast, removal of cilia was required for medulloblastoma growth by a constitutively active glioma-associated oncogene family zinc finger-2 (GLI2), a downstream transcription factor. Thus, primary cilia are either required for or inhibit medulloblastoma formation, depending on the initiating oncogenic event. Remarkably, the presence or absence of cilia was associated with specific variants of human medulloblastomas; primary cilia were found in medulloblastomas with activation in HH or WNT signaling but not in most medulloblastomas in other distinct molecular subgroups. Primary cilia could serve as a diagnostic tool and provide new insights into the mechanism of tumorigenesis.

Published
2009

20. Common activation of canonical Wnt signaling in pancreatic adenocarcinoma.

Author

Pasca di Magliano, Marina, Biankin, Andrew V, Heiser, Patrick W, Cano, David A, Gutierrez, Pedro JA, Deramaudt, Therese, Segara, Davendra, Dawson, Amanda C, Kench, James G, Henshall, Susan M, Sutherland, Robert L, Dlugosz, Andrzej, Rustgi, Anil K, and Hebrok, Matthias

Subjects
Animals, Humans, Mice, Adenocarcinoma, Pancreatic Neoplasms, Disease Models, Animal, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Wnt Proteins, Hedgehog Proteins, Disease Models, Animal, General Science & Technology
Abstract

Pancreatic ductal adenocarcinoma (PDA) is an extremely aggressive malignancy, which carries a dismal prognosis. Activating mutations of the Kras gene are common to the vast majority of human PDA. In addition, recent studies have demonstrated that embryonic signaling pathway such as Hedgehog and Notch are inappropriately upregulated in this disease. The role of another embryonic signaling pathway, namely the canonical Wnt cascade, is still controversial. Here, we use gene array analysis as a platform to demonstrate general activation of the canonical arm of the Wnt pathway in human PDA. Furthermore, we provide evidence for Wnt activation in mouse models of pancreatic cancer. Our results also indicate that Wnt signaling might be activated downstream of Hedgehog signaling, which is an early event in PDA evolution. Wnt inhibition blocked proliferation and induced apoptosis of cultured adenocarcinoma cells, thereby providing evidence to support the development of novel therapeutical strategies for Wnt inhibition in pancreatic adenocarcinoma.

Published
2007

21. Common Activation of Canonical Wnt Signaling in Pancreatic Adenocarcinoma

Author

di Magliano, Marina Pasca, Biankin, Andrew V, Heiser, Patrick W, Cano, David A, Gutierrez, Pedro JA, Deramaudt, Therese, Segara, Davendra, Dawson, Amanda C, Kench, James G, Henshall, Susan M, Sutherland, Robert L, Dlugosz, Andrzej, Rustgi, Anil K, and Hebrok, Matthias

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Rare Diseases, Digestive Diseases, Pancreatic Cancer, Cancer, Aetiology, 2.1 Biological and endogenous factors, Adenocarcinoma, Animals, Disease Models, Animal, Hedgehog Proteins, Humans, Mice, Pancreatic Neoplasms, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Wnt Proteins, General Science & Technology
Abstract

Pancreatic ductal adenocarcinoma (PDA) is an extremely aggressive malignancy, which carries a dismal prognosis. Activating mutations of the Kras gene are common to the vast majority of human PDA. In addition, recent studies have demonstrated that embryonic signaling pathway such as Hedgehog and Notch are inappropriately upregulated in this disease. The role of another embryonic signaling pathway, namely the canonical Wnt cascade, is still controversial. Here, we use gene array analysis as a platform to demonstrate general activation of the canonical arm of the Wnt pathway in human PDA. Furthermore, we provide evidence for Wnt activation in mouse models of pancreatic cancer. Our results also indicate that Wnt signaling might be activated downstream of Hedgehog signaling, which is an early event in PDA evolution. Wnt inhibition blocked proliferation and induced apoptosis of cultured adenocarcinoma cells, thereby providing evidence to support the development of novel therapeutical strategies for Wnt inhibition in pancreatic adenocarcinoma.

Published
2007

25. SFigure1 from Inhibition of Hedgehog Signaling Alters Fibroblast Composition in Pancreatic Cancer

Author

Steele, Nina G., primary, Biffi, Giulia, primary, Kemp, Samantha B., primary, Zhang, Yaqing, primary, Drouillard, Donovan, primary, Syu, LiJyun, primary, Hao, Yuan, primary, Oni, Tobiloba E., primary, Brosnan, Erin, primary, Elyada, Ela, primary, Doshi, Abhishek, primary, Hansma, Christa, primary, Espinoza, Carlos, primary, Abbas, Ahmed, primary, The, Stephanie, primary, Irizarry-Negron, Valerie, primary, Halbrook, Christopher J., primary, Franks, Nicole E., primary, Hoffman, Megan T., primary, Brown, Kristee, primary, Carpenter, Eileen S., primary, Nwosu, Zeribe C., primary, Johnson, Craig, primary, Lima, Fatima, primary, Anderson, Michelle A., primary, Park, Youngkyu, primary, Crawford, Howard C., primary, Lyssiotis, Costas A., primary, Frankel, Timothy L., primary, Rao, Arvind, primary, Bednar, Filip, primary, Dlugosz, Andrzej A., primary, Preall, Jonathan B., primary, Tuveson, David A., primary, Allen, Benjamin L., primary, and Pasca di Magliano, Marina, primary

Published
2023
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26. Supplementary Table 7 from Cancer-Associated Fibroblasts Promote Aggressive Gastric Cancer Phenotypes via Heat Shock Factor 1–Mediated Secretion of Extracellular Vesicles

Author

Grunberg, Nil, primary, Pevsner-Fischer, Meirav, primary, Goshen-Lago, Tal, primary, Diment, Judith, primary, Stein, Yaniv, primary, Lavon, Hagar, primary, Mayer, Shimrit, primary, Levi-Galibov, Oshrat, primary, Friedman, Gil, primary, Ofir-Birin, Yifat, primary, Syu, Li-Jyun, primary, Migliore, Cristina, primary, Shimoni, Eyal, primary, Stemmer, Salomon M., primary, Brenner, Baruch, primary, Dlugosz, Andrzej A., primary, Lyden, David, primary, Regev-Rudzki, Neta, primary, Ben-Aharon, Irit, primary, and Scherz-Shouval, Ruth, primary

Published
2023
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27. Supplementary Table 9 from Cancer-Associated Fibroblasts Promote Aggressive Gastric Cancer Phenotypes via Heat Shock Factor 1–Mediated Secretion of Extracellular Vesicles

Author

Grunberg, Nil, primary, Pevsner-Fischer, Meirav, primary, Goshen-Lago, Tal, primary, Diment, Judith, primary, Stein, Yaniv, primary, Lavon, Hagar, primary, Mayer, Shimrit, primary, Levi-Galibov, Oshrat, primary, Friedman, Gil, primary, Ofir-Birin, Yifat, primary, Syu, Li-Jyun, primary, Migliore, Cristina, primary, Shimoni, Eyal, primary, Stemmer, Salomon M., primary, Brenner, Baruch, primary, Dlugosz, Andrzej A., primary, Lyden, David, primary, Regev-Rudzki, Neta, primary, Ben-Aharon, Irit, primary, and Scherz-Shouval, Ruth, primary

Published
2023
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29. Supplementary Table 11 from Cancer-Associated Fibroblasts Promote Aggressive Gastric Cancer Phenotypes via Heat Shock Factor 1–Mediated Secretion of Extracellular Vesicles

Author

Grunberg, Nil, primary, Pevsner-Fischer, Meirav, primary, Goshen-Lago, Tal, primary, Diment, Judith, primary, Stein, Yaniv, primary, Lavon, Hagar, primary, Mayer, Shimrit, primary, Levi-Galibov, Oshrat, primary, Friedman, Gil, primary, Ofir-Birin, Yifat, primary, Syu, Li-Jyun, primary, Migliore, Cristina, primary, Shimoni, Eyal, primary, Stemmer, Salomon M., primary, Brenner, Baruch, primary, Dlugosz, Andrzej A., primary, Lyden, David, primary, Regev-Rudzki, Neta, primary, Ben-Aharon, Irit, primary, and Scherz-Shouval, Ruth, primary

Published
2023
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30. Supplementary Materials&Methods and Supplementary Figures 1-6 from Cancer-Associated Fibroblasts Promote Aggressive Gastric Cancer Phenotypes via Heat Shock Factor 1–Mediated Secretion of Extracellular Vesicles

Author

Grunberg, Nil, primary, Pevsner-Fischer, Meirav, primary, Goshen-Lago, Tal, primary, Diment, Judith, primary, Stein, Yaniv, primary, Lavon, Hagar, primary, Mayer, Shimrit, primary, Levi-Galibov, Oshrat, primary, Friedman, Gil, primary, Ofir-Birin, Yifat, primary, Syu, Li-Jyun, primary, Migliore, Cristina, primary, Shimoni, Eyal, primary, Stemmer, Salomon M., primary, Brenner, Baruch, primary, Dlugosz, Andrzej A., primary, Lyden, David, primary, Regev-Rudzki, Neta, primary, Ben-Aharon, Irit, primary, and Scherz-Shouval, Ruth, primary

Published
2023
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31. Supplementary Table 5 from Cancer-Associated Fibroblasts Promote Aggressive Gastric Cancer Phenotypes via Heat Shock Factor 1–Mediated Secretion of Extracellular Vesicles

Author

Grunberg, Nil, primary, Pevsner-Fischer, Meirav, primary, Goshen-Lago, Tal, primary, Diment, Judith, primary, Stein, Yaniv, primary, Lavon, Hagar, primary, Mayer, Shimrit, primary, Levi-Galibov, Oshrat, primary, Friedman, Gil, primary, Ofir-Birin, Yifat, primary, Syu, Li-Jyun, primary, Migliore, Cristina, primary, Shimoni, Eyal, primary, Stemmer, Salomon M., primary, Brenner, Baruch, primary, Dlugosz, Andrzej A., primary, Lyden, David, primary, Regev-Rudzki, Neta, primary, Ben-Aharon, Irit, primary, and Scherz-Shouval, Ruth, primary

Published
2023
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32. Supplementary Table 6 from Cancer-Associated Fibroblasts Promote Aggressive Gastric Cancer Phenotypes via Heat Shock Factor 1–Mediated Secretion of Extracellular Vesicles

Author

Grunberg, Nil, primary, Pevsner-Fischer, Meirav, primary, Goshen-Lago, Tal, primary, Diment, Judith, primary, Stein, Yaniv, primary, Lavon, Hagar, primary, Mayer, Shimrit, primary, Levi-Galibov, Oshrat, primary, Friedman, Gil, primary, Ofir-Birin, Yifat, primary, Syu, Li-Jyun, primary, Migliore, Cristina, primary, Shimoni, Eyal, primary, Stemmer, Salomon M., primary, Brenner, Baruch, primary, Dlugosz, Andrzej A., primary, Lyden, David, primary, Regev-Rudzki, Neta, primary, Ben-Aharon, Irit, primary, and Scherz-Shouval, Ruth, primary

Published
2023
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33. Supplementary Table 4 from Cancer-Associated Fibroblasts Promote Aggressive Gastric Cancer Phenotypes via Heat Shock Factor 1–Mediated Secretion of Extracellular Vesicles

Author

Grunberg, Nil, primary, Pevsner-Fischer, Meirav, primary, Goshen-Lago, Tal, primary, Diment, Judith, primary, Stein, Yaniv, primary, Lavon, Hagar, primary, Mayer, Shimrit, primary, Levi-Galibov, Oshrat, primary, Friedman, Gil, primary, Ofir-Birin, Yifat, primary, Syu, Li-Jyun, primary, Migliore, Cristina, primary, Shimoni, Eyal, primary, Stemmer, Salomon M., primary, Brenner, Baruch, primary, Dlugosz, Andrzej A., primary, Lyden, David, primary, Regev-Rudzki, Neta, primary, Ben-Aharon, Irit, primary, and Scherz-Shouval, Ruth, primary

Published
2023
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34. Data from Cancer-Associated Fibroblasts Promote Aggressive Gastric Cancer Phenotypes via Heat Shock Factor 1–Mediated Secretion of Extracellular Vesicles

Author

Grunberg, Nil, primary, Pevsner-Fischer, Meirav, primary, Goshen-Lago, Tal, primary, Diment, Judith, primary, Stein, Yaniv, primary, Lavon, Hagar, primary, Mayer, Shimrit, primary, Levi-Galibov, Oshrat, primary, Friedman, Gil, primary, Ofir-Birin, Yifat, primary, Syu, Li-Jyun, primary, Migliore, Cristina, primary, Shimoni, Eyal, primary, Stemmer, Salomon M., primary, Brenner, Baruch, primary, Dlugosz, Andrzej A., primary, Lyden, David, primary, Regev-Rudzki, Neta, primary, Ben-Aharon, Irit, primary, and Scherz-Shouval, Ruth, primary

Published
2023
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35. Supplementary Data from Inhibition of Hedgehog Signaling Alters Fibroblast Composition in Pancreatic Cancer

Author

Steele, Nina G., primary, Biffi, Giulia, primary, Kemp, Samantha B., primary, Zhang, Yaqing, primary, Drouillard, Donovan, primary, Syu, LiJyun, primary, Hao, Yuan, primary, Oni, Tobiloba E., primary, Brosnan, Erin, primary, Elyada, Ela, primary, Doshi, Abhishek, primary, Hansma, Christa, primary, Espinoza, Carlos, primary, Abbas, Ahmed, primary, The, Stephanie, primary, Irizarry-Negron, Valerie, primary, Halbrook, Christopher J., primary, Franks, Nicole E., primary, Hoffman, Megan T., primary, Brown, Kristee, primary, Carpenter, Eileen S., primary, Nwosu, Zeribe C., primary, Johnson, Craig, primary, Lima, Fatima, primary, Anderson, Michelle A., primary, Park, Youngkyu, primary, Crawford, Howard C., primary, Lyssiotis, Costas A., primary, Frankel, Timothy L., primary, Rao, Arvind, primary, Bednar, Filip, primary, Dlugosz, Andrzej A., primary, Preall, Jonathan B., primary, Tuveson, David A., primary, Allen, Benjamin L., primary, and Pasca di Magliano, Marina, primary

Published
2023
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36. Supplementary Figures S1-S2 and Supplementary Tables S1-S2 from Merkel Cell Polyomavirus Small T Antigen Initiates Merkel Cell Carcinoma-like Tumor Development in Mice

Author

Verhaegen, Monique E., primary, Mangelberger, Doris, primary, Harms, Paul W., primary, Eberl, Markus, primary, Wilbert, Dawn M., primary, Meireles, Julia, primary, Bichakjian, Christopher K., primary, Saunders, Thomas L., primary, Wong, Sunny Y., primary, and Dlugosz, Andrzej A., primary

Published
2023
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37. Supplementary Table 8 from Cancer-Associated Fibroblasts Promote Aggressive Gastric Cancer Phenotypes via Heat Shock Factor 1–Mediated Secretion of Extracellular Vesicles

Author

Grunberg, Nil, primary, Pevsner-Fischer, Meirav, primary, Goshen-Lago, Tal, primary, Diment, Judith, primary, Stein, Yaniv, primary, Lavon, Hagar, primary, Mayer, Shimrit, primary, Levi-Galibov, Oshrat, primary, Friedman, Gil, primary, Ofir-Birin, Yifat, primary, Syu, Li-Jyun, primary, Migliore, Cristina, primary, Shimoni, Eyal, primary, Stemmer, Salomon M., primary, Brenner, Baruch, primary, Dlugosz, Andrzej A., primary, Lyden, David, primary, Regev-Rudzki, Neta, primary, Ben-Aharon, Irit, primary, and Scherz-Shouval, Ruth, primary

Published
2023
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38. Supplementary Table 3 from Cancer-Associated Fibroblasts Promote Aggressive Gastric Cancer Phenotypes via Heat Shock Factor 1–Mediated Secretion of Extracellular Vesicles

Author

Grunberg, Nil, primary, Pevsner-Fischer, Meirav, primary, Goshen-Lago, Tal, primary, Diment, Judith, primary, Stein, Yaniv, primary, Lavon, Hagar, primary, Mayer, Shimrit, primary, Levi-Galibov, Oshrat, primary, Friedman, Gil, primary, Ofir-Birin, Yifat, primary, Syu, Li-Jyun, primary, Migliore, Cristina, primary, Shimoni, Eyal, primary, Stemmer, Salomon M., primary, Brenner, Baruch, primary, Dlugosz, Andrzej A., primary, Lyden, David, primary, Regev-Rudzki, Neta, primary, Ben-Aharon, Irit, primary, and Scherz-Shouval, Ruth, primary

Published
2023
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39. Data from The Distinctive Mutational Spectra of Polyomavirus-Negative Merkel Cell Carcinoma

Author

Harms, Paul William, primary, Vats, Pankaj, primary, Verhaegen, Monique Elise, primary, Robinson, Dan R., primary, Wu, Yi-Mi, primary, Dhanasekaran, Saravana Mohan, primary, Palanisamy, Nallasivam, primary, Siddiqui, Javed, primary, Cao, Xuhong, primary, Su, Fengyun, primary, Wang, Rui, primary, Xiao, Hong, primary, Kunju, Lakshmi P., primary, Mehra, Rohit, primary, Tomlins, Scott A., primary, Fullen, Douglas Randall, primary, Bichakjian, Christopher Keram, primary, Johnson, Timothy M., primary, Dlugosz, Andrzej Antoni, primary, and Chinnaiyan, Arul M., primary

Published
2023
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40. Supplemental Figure Legends from The Distinctive Mutational Spectra of Polyomavirus-Negative Merkel Cell Carcinoma

Author

Harms, Paul William, primary, Vats, Pankaj, primary, Verhaegen, Monique Elise, primary, Robinson, Dan R., primary, Wu, Yi-Mi, primary, Dhanasekaran, Saravana Mohan, primary, Palanisamy, Nallasivam, primary, Siddiqui, Javed, primary, Cao, Xuhong, primary, Su, Fengyun, primary, Wang, Rui, primary, Xiao, Hong, primary, Kunju, Lakshmi P., primary, Mehra, Rohit, primary, Tomlins, Scott A., primary, Fullen, Douglas Randall, primary, Bichakjian, Christopher Keram, primary, Johnson, Timothy M., primary, Dlugosz, Andrzej Antoni, primary, and Chinnaiyan, Arul M., primary

Published
2023
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41. Supplemental Table S4 from The Distinctive Mutational Spectra of Polyomavirus-Negative Merkel Cell Carcinoma

Author

Harms, Paul William, primary, Vats, Pankaj, primary, Verhaegen, Monique Elise, primary, Robinson, Dan R., primary, Wu, Yi-Mi, primary, Dhanasekaran, Saravana Mohan, primary, Palanisamy, Nallasivam, primary, Siddiqui, Javed, primary, Cao, Xuhong, primary, Su, Fengyun, primary, Wang, Rui, primary, Xiao, Hong, primary, Kunju, Lakshmi P., primary, Mehra, Rohit, primary, Tomlins, Scott A., primary, Fullen, Douglas Randall, primary, Bichakjian, Christopher Keram, primary, Johnson, Timothy M., primary, Dlugosz, Andrzej Antoni, primary, and Chinnaiyan, Arul M., primary

Published
2023
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42. Supplemental Table S7 A. from The Distinctive Mutational Spectra of Polyomavirus-Negative Merkel Cell Carcinoma

Author

Harms, Paul William, primary, Vats, Pankaj, primary, Verhaegen, Monique Elise, primary, Robinson, Dan R., primary, Wu, Yi-Mi, primary, Dhanasekaran, Saravana Mohan, primary, Palanisamy, Nallasivam, primary, Siddiqui, Javed, primary, Cao, Xuhong, primary, Su, Fengyun, primary, Wang, Rui, primary, Xiao, Hong, primary, Kunju, Lakshmi P., primary, Mehra, Rohit, primary, Tomlins, Scott A., primary, Fullen, Douglas Randall, primary, Bichakjian, Christopher Keram, primary, Johnson, Timothy M., primary, Dlugosz, Andrzej Antoni, primary, and Chinnaiyan, Arul M., primary

Published
2023
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43. Supplemental Figure S4 from The Distinctive Mutational Spectra of Polyomavirus-Negative Merkel Cell Carcinoma

Author

Harms, Paul William, primary, Vats, Pankaj, primary, Verhaegen, Monique Elise, primary, Robinson, Dan R., primary, Wu, Yi-Mi, primary, Dhanasekaran, Saravana Mohan, primary, Palanisamy, Nallasivam, primary, Siddiqui, Javed, primary, Cao, Xuhong, primary, Su, Fengyun, primary, Wang, Rui, primary, Xiao, Hong, primary, Kunju, Lakshmi P., primary, Mehra, Rohit, primary, Tomlins, Scott A., primary, Fullen, Douglas Randall, primary, Bichakjian, Christopher Keram, primary, Johnson, Timothy M., primary, Dlugosz, Andrzej Antoni, primary, and Chinnaiyan, Arul M., primary

Published
2023
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47. Gli2 and Gli3 Regulate Horizontal Basal Cell-Mediated Regeneration of the Olfactory Epithelium

Author

Shirazyan, Anna, primary, Park, Haeyoung, additional, Joiner, Ariell M, additional, Ra, Justine, additional, Kim, Melissa S, additional, Kumari, Archana, additional, Franks, Nicole E, additional, PENG, TIEN, additional, Bradley, Robert M, additional, Mistretta, Charlotte M, additional, Dlugosz, Andrzej A, additional, and Allen, Benjamin L, additional

Published
2022
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48. Reciprocal interplay between thyroid hormone and microRNA-21 regulates hedgehog pathway-driven skin tumorigenesis

Author

Di Girolamo, Daniela, Ambrosio, Raffaele, De Stefano, Maria A., Mancino, Giuseppina, Porcelli, Tommaso, Luongo, Cristina, Di Cicco, Emery, Scalia, Giulia, Del Vecchio, Luigi, Colao, Annamaria, Dlugosz, Andrzej A., Missero, Caterina, Salvatore, Domenico, and Dentice, Monica

Subjects
Thyroid hormones -- Analysis, MicroRNA -- Analysis, Basal cell carcinoma -- Diagnosis, Health care industry
Abstract

The thyroid hormone-inactivating (TH-inactivating) enzyme type 3 iodothyronine deiodinase (D3) is an oncofetal protein that is rarely expressed in adult life but has been shown to be reactivated in the context of proliferation and neoplasms. D3 terminates TH action within the tumor microenvironment, thereby enhancing cancer cell proliferation. However, the pathological role of D3 and the contribution of TH metabolism in cancer have yet to be fully explored. Here, we describe a reciprocal regulation between TH action and the cancer-associated microRNA-21 (miR21) in basal cell carcinoma (BCC) skin tumors. We found that, besides being negatively regulated by TH at the transcriptional level, miR21 attenuates the TH signal by increasing D3 levels. The ability of miR21 to positively regulate D3 was mediated by the tumor suppressor gene GRHL3, a hitherto unrecognized D3 transcriptional inhibitor. Finally, in a BCC mouse model, keratinocyte-specific D3 depletion markedly reduced tumor growth. Together, our results establish TH action as a critical hub of multiple oncogenic pathways and provide functional and mechanistic evidence of the involvement of TH metabolism in BCC tumorigenesis. Moreover, our results identify a miR21/GRHL3/D3 axis that reduces TH in the tumor microenvironment and has potential to be targeted as a therapeutic approach to BCC., Introduction Basal cell carcinoma (BCC) is the most frequently diagnosed human cancer and accounts for approximately 80% of all nonmelanoma skin cancers. BCC formation is based on a combination of [...]

Published
2016
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49. Basal cell carcinomas acquire secondary mutations to overcome dormancy and progress from microscopic to macroscopic disease

Author

Trieu, Kenneth G., primary, Tsai, Shih-Ying, additional, Eberl, Markus, additional, Ju, Virginia, additional, Ford, Noah C., additional, Doane, Owen J., additional, Peterson, Jamie K., additional, Veniaminova, Natalia A., additional, Grachtchouk, Marina, additional, Harms, Paul W., additional, Swartling, Fredrik J., additional, Dlugosz, Andrzej A., additional, and Wong, Sunny Y., additional

Published
2022
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50. Hedgehog (HH) pathway endogenous antagonist HHIP: unique lingual expression in filiform papillae during homeostasis and ectopic in fungiform papillae during HH signaling inhibition

Author

Kumari, Archana, Li, Libo, Ermilov, Alexandre N., Franks, Nicole E., Dlugosz, Andrzej A., Allen, Benjamin L., and Mistretta, Charlotte M.

Subjects
Tongue, Homeostasis, Hedgehog Proteins, Taste Buds, Article, Ectopic Gene Expression
Abstract

BACKGROUND: Hedgehog (HH) signaling is essential for homeostasis in gustatory fungiform papillae (FP) and taste buds. However, activities of HH antagonists in these tissues remain unexplored. We investigated a potential role for HH-interacting protein (HHIP), an endogenous pathway antagonist, in regulating HH signaling during taste organ homeostasis. We found a restricted pattern of Hhip-expressing cells in the anterior epithelium of each nongustatory filiform papilla (FILIF) only. To test for roles in antagonism of HH signaling, we investigated HHIP after pathway inhibition with SMO inhibition via sonidegib and Smo deletion, Gli2 deletion/suppression, or with chorda tympani/lingual nerve cut. RESULTS: In all approaches, the HHIP expression pattern was retained in FILIF suggesting HH-independent regulation of HHIP. Remarkably, after pathway inhibition, HHIP expression was detected also in the conical, FILIF-like atypical FP. We found a close association of de novo expression of HHIP in atypical FP with loss of Gli1+, HH-responding cells. Further, we report that PTCH1 is another potential HH antagonist in FILIF that co-localizes with HHIP. CONCLUSIONS: After HH pathway inhibition the ectopic expression of HHIP correlates with a FILIF-like morphology in atypical FP and we propose that localized expression of the HH antagonist HHIP regulates pathway inhibition to maintain FILIF during tongue homeostasis.

Published
2022

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