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2. Spatial metabolomics reveals glycogen as an actionable target for pulmonary fibrosis

Author

Conroy, Lindsey R., Clarke, Harrison A., Allison, Derek B., Valenca, Samuel Santos, Sun, Qi, Hawkinson, Tara R., Young, Lyndsay E. A., Ferreira, Juanita E., Hammonds, Autumn V., Dunne, Jaclyn B., McDonald, Robert J., Absher, Kimberly J., Dong, Brittany E., Bruntz, Ronald C., Markussen, Kia H., Juras, Jelena A., Alilain, Warren J., Liu, Jinze, Gentry, Matthew S., Angel, Peggi M., Waters, Christopher M., and Sun, Ramon C.

Published
2023
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7. Single-cell analysis identifies PLK1 as a driver of immunosuppressive tumor microenvironment in LUAD.

Author

Kong, Yifan, Li, Chaohao, Liu, Jinpeng, Wu, Sai, Zhang, Min, Allison, Derek B., Hassan, Faisal, He, Daheng, Wang, Xinyi, Mao, Fengyi, Zhang, Qiongsi, Zhang, Yanquan, Li, Zhiguo, Wang, Chi, and Liu, Xiaoqi

Subjects
TUMOR microenvironment, IMMUNOREGULATION, ANTIGEN presentation, MAJOR histocompatibility complex, IMMUNE system, T cell receptors
Abstract

PLK1 (Polo-like kinase 1) plays a critical role in the progression of lung adenocarcinoma (LUAD). Recent studies have unveiled that targeting PLK1 improves the efficacy of immunotherapy, highlighting its important role in the regulation of tumor immunity. Nevertheless, our understanding of the intricate interplay between PLK1 and the tumor microenvironment (TME) remains incomplete. Here, using genetically engineered mouse model and single-cell RNA-seq analysis, we report that PLK1 promotes an immunosuppressive TME in LUAD, characterized with enhanced M2 polarization of tumor associated macrophages (TAM) and dampened antigen presentation process. Mechanistically, elevated PLK1 coincides with increased secretion of CXCL2 cytokine, which promotes M2 polarization of TAM and diminishes expression of class II major histocompatibility complex (MHC-II) in professional antigen-presenting cells. Furthermore, PLK1 negatively regulates MHC-II expression in cancer cells, which has been shown to be associated with compromised tumor immunity and unfavorable patient outcomes. Taken together, our results reveal PLK1 as a novel modulator of TME in LUAD and provide possible therapeutic interventions. Author summary: Our research has pinpointed a vital protein, PLK1, in the development of lung cancer. Through the use of mouse models simulating the onset of lung cancer and genetic sequencing analysis, we've discovered that high level of PLK1 hinders the immune response, making it challenging for the patient's immune system to effectively eliminate lung cancer. Elevated PLK1 level specifically increases the presence of M2 macrophages, a type of immune cell, which, in turn, prevents the immune system from recognizing and attacking lung cancer cells. We've identified that this immune-suppressing effect is linked to PLK1's role in secreting a specific molecule called CXCL2. This molecule promotes the presence of M2 macrophages and hampers the recognition of cancer cells by decreasing the machinery that presents the cancer cells' signature to the immune system, known as MHC-II. These findings suggest that drugs targeting PLK1 could be a promising strategy for treating lung cancer patients. [ABSTRACT FROM AUTHOR]

Published
2024
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8. Phosphorylation of AHR by PLK1 promotes metastasis of LUAD via DIO2-TH signaling

Author

Li, Chaohao, primary, Allison, Derek B., additional, He, Daheng, additional, Mao, Fengyi, additional, Wang, Xinyi, additional, Rychahou, Piotr, additional, Imam, Ibrahim A., additional, Kong, Yifan, additional, Zhang, Qiongsi, additional, Zhang, Yanquan, additional, Liu, Jinghui, additional, Wang, Ruixin, additional, Rao, Xiongjian, additional, Wu, Sai, additional, Evers, B. Mark, additional, Shao, Qing, additional, Wang, Chi, additional, Li, Zhiguo, additional, and Liu, Xiaoqi, additional

Published
2023
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13. A Phase I Dose Escalation and Expansion Study of Epidiolex (Cannabidiol) in Patients with Biochemically Recurrent Prostate Cancer

Author

Myint, Zin W., primary, St. Clair, William H., additional, Strup, Stephen E., additional, Yan, Donglin, additional, Li, Ning, additional, Allison, Derek B., additional, McLouth, Laurie E., additional, Ellis, Carleton S., additional, Wang, Peng, additional, James, Andrew C., additional, Hensley, Patrick J., additional, Otto, Danielle E., additional, Arnold, Susanne M., additional, DiPaola, Robert S., additional, and Kolesar, Jill M., additional

Published
2023
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14. Abstract 4840: Dysregulation of mitochondrial function by PLK1-mediated PDHA1 phosphorylation promotes Cr(VI)-associated lung cancer progression

Author

Zhang, Qiongsi, primary, Li, Zhiguo, additional, Rao, Xiongjian, additional, Allison, Derek B., additional, Qiao, Qi, additional, Zhang, Zhuangzhuang, additional, Kong, Yifan, additional, Wang, Ruixin, additional, Fan, Teresa W., additional, Higashi, Richard M., additional, Lane, Andrew N., additional, and Liu, Xiaoqi, additional

Published
2023
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15. Abstract 4992: Taxol-elevated PLK1 overcomes BETi-resistant in prostate cancer via triggering phosphorylation-dependent degradation of BRD4

Author

Zhang, Yanquan, primary, Fong, Ka Will, additional, Mao, Fengyi, additional, Wang, Ruixin, additional, Kong, Yifan, additional, Li, Chaohao, additional, Liu, Jinghui, additional, Li, Zhiguo, additional, Allison, Derek B., additional, Napier, Dana, additional, Li, Daheng, additional, Liu, Jinpeng, additional, Wang, Chi, additional, Zhang, Yeqing, additional, Li, Guangbing, additional, and Liu, Xiaoqi, additional

Published
2023
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16. Abstract 3673: Plk1 phosphorylation of PHGDH to regulate serine metabolism

Author

Rao, Xiongjian, primary, Allison, Derek B., additional, Flight, Robert M., additional, Wu, Yuanyuan, additional, Scott, Timothy, additional, He, Daheng, additional, Wang, RuiXing, additional, Li, Zhiguo, additional, Li, Chaohao, additional, Kong, Yifan, additional, Mao, Fengyi, additional, Wang, Chi, additional, Higashi, Richard M., additional, Lane, Andrew N., additional, Moseley, Hunter NB, additional, and Liu, Xiaoqi, additional

Published
2023
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20. In situ mass spectrometry imaging reveals heterogeneous glycogen stores in human normal and cancerous tissues

Author

Young, Lyndsay E A, primary, Conroy, Lindsey R, additional, Clarke, Harrison A, additional, Hawkinson, Tara R, additional, Bolton, Kayli E, additional, Sanders, William C, additional, Chang, Josephine E, additional, Webb, Madison B, additional, Alilain, Warren J, additional, Vander Kooi, Craig W, additional, Drake, Richard R, additional, Andres, Douglas A, additional, Badgett, Tom C, additional, Wagner, Lars M, additional, Allison, Derek B, additional, Sun, Ramon C, additional, and Gentry, Matthew S, additional

Published
2022
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21. Targeting Plk1 Sensitizes Pancreatic Cancer to Immune Checkpoint Therapy

Author

Zhang, Zhuangzhuang, primary, Cheng, Lijun, additional, Li, Jie, additional, Qiao, Qi, additional, Karki, Anju, additional, Allison, Derek B., additional, Shaker, Nuha, additional, Li, Kunyu, additional, Utturkar, Sagar M., additional, Atallah Lanman, Nadia M., additional, Rao, Xiongjian, additional, Rychahou, Piotr, additional, He, Daheng, additional, Konieczny, Stephen F., additional, Wang, Chi, additional, Shao, Qing, additional, Evers, B. Mark, additional, and Liu, Xiaoqi, additional

Published
2022
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24. High-dimensionality reduction clustering of complex carbohydrates to study lung cancer metabolic heterogeneity

Author

Conroy, Lindsey R., Chang, Josephine E., Sun, Qi, Clarke, Harrison A., Buoncristiani, Michael D., Young, Lyndsay E.A., McDonald, Robert J., Liu, Jinze, Gentry, Matthew S., Allison, Derek B., and Sun, Ramon C.

Subjects
Lung Neoplasms, Polysaccharides, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization, Tumor Microenvironment, Cluster Analysis, Humans, Article
Abstract

The tumor microenvironment contains a heterogeneous population of stromal and cancer cells that engage in metabolic crosstalk to ultimately promote tumor growth and contribute to progression. Due to heterogeneity within solid tumors, pooled mass spectrometry workflows are less sensitive at delineating unique metabolic perturbations between stromal and immune cell populations. Two critical, but understudied, facets of glucose metabolism are anabolic pathways for glycogen and N-linked glycan biosynthesis. Together, these complex carbohydrates modulate bioenergetics and protein-structure function, and create functional microanatomy in distinct cell populations within the tumor heterogeneity. Herein, we combine high-dimensionality reduction and clustering (HDRC) analysis with matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) and demonstrate its ability for the comprehensive assessment of tissue histopathology and metabolic heterogeneity in human FFPE sections. In human lung adenocarcinoma (LUAD) tumor tissues, HDRC accurately clusters distinct regions and cell populations within the tumor microenvironment, including tumor cells, tumor-infiltrating lymphocytes, cancer-associated fibroblasts, and necrotic regions. In-depth pathway enrichment analyses revealed unique metabolic pathways are associated with each distinct pathological region. Further, we highlight the potential of HDRC analysis to study complex carbohydrate metabolism in a case study of lung cancer disparity. Collectively, our results demonstrate the promising potentials of HDRC of pixel-based carbohydrate analysis to study cell-type and regional-specific stromal signaling within the tumor microenvironment.

Published
2022

33. Alternative lengthening of telomeres and ATRX/DAXX loss can reliably be detected in fine needle aspirates of pancreatic neuroendocrine tumors

Author

VandenBussche, Christopher J., Allison, Derek B., Graham, Mindy K., Charu, Vivek, Lennon, Anne Marie, Wolfgang, Christopher L., Hruban, Ralph H., and Heaphy, Christopher M.

Subjects
Adult, Male, X-linked Nuclear Protein, Biopsy, Fine-Needle, DNA Helicases, Nuclear Proteins, Telomere Homeostasis, Middle Aged, Immunohistochemistry, Article, Cohort Studies, Gene Expression Regulation, Neoplastic, Pancreatic Neoplasms, Survival Rate, Neuroendocrine Tumors, Humans, Female, Co-Repressor Proteins, In Situ Hybridization, Fluorescence, Adaptor Proteins, Signal Transducing, Aged, Molecular Chaperones, Proportional Hazards Models, Retrospective Studies
Abstract

Pancreatic neuroendocrine tumors (PanNETs) frequently use the alternative lengthening of telomeres (ALT) pathway for telomere maintenance. ALT is strongly correlated with α thalassemia-mental retardation, X linked (ATRX), and death domain-associated protein 6 (DAXX) alterations and a poor prognosis in patients with primary PanNET. Because fine-needle aspiration (FNA) is a noninvasive way to sample tumors, the authors evaluated whether they could accurately detect ALT and loss of ATRX/DAXX in a primary PanNET cohort of FNAs.All preoperative FNA cytology cases (2005-2016) with adequate remnant FNA cell block material were assessed for ALT by telomere-specific fluorescence in situ hybridization and for ATRX and DAXX protein expression by immunohistochemistry. For 21 patients who underwent tumor resection, the resected specimen also was assessed to determine the concordance between the FNA and surgical specimens.In the primary PanNET cohort of 65 FNAs, ALT was detected in 15 specimens (23%). Although all ATRX-negative and DAXX-negative tumors were ALT-positive, 3 of 14 (21%) ALT-positive tumors did not exhibit nuclear loss of either ATRX or DAXX. The ALT-positive tumors were associated with larger radiographic size (4.9 vs 2.4 cm, on average; P.05) and higher grade (P.05). Overall, there was 100% concordance in ALT status and ATRX/DAXX immunohistochemistry results between the FNA and surgical specimens.Both ALT and loss of ATRX/DAXX can be accurately performed on FNA specimens with adequate material. Because ALT is a fundamental mechanism of pathogenesis, the ability to determine ALT in small biospecimens has implications for the design of clinical trials. Cancer Cytopathol 2017;125:544-51. © 2017 American Cancer Society.

Published
2017

36. POU2F3: A new IHC marker for small cell lung cancer with low neuroendocrine marker expression.

Author

Obid, Randa H., Reynolds, Jordan P., and Allison, Derek B.

Subjects
*SMALL cell lung cancer, *YAP signaling proteins
Abstract

A recent article in CAP Today discusses the use of POU2F3 as a new immunohistochemical (IHC) marker for small cell lung cancer (SCLC) with low neuroendocrine marker expression. Traditionally, SCLC is characterized by strong expression of neuroendocrine markers, but up to 20% of cases show low or no expression of these markers. POU2F3 has been found to be a highly sensitive and specific IHC marker for these NE-low/negative SCLCs. However, caution should be exercised when using POU2F3 as a diagnostic marker for other tumor types, as its specificity for SCLC of pulmonary origin is not yet established. [Extracted from the article]

Published
2024

39. Immunological and microbial shifts in the aging rhesus macaque lung during nontuberculous mycobacterial infection.

Author

Cinco IR, Napier EG, Rhoades NS, Davies MH, Allison DB, Kohama SG, Bermudez L, Winthrop K, Fuss C, Spindel ER, and Messaoudi I

Subjects
Animals, Male, Female, Age Factors, Tomography, X-Ray Computed, Transcriptome, Microbiota physiology, Mycobacterium Infections, Nontuberculous diagnostic imaging, Mycobacterium Infections, Nontuberculous immunology, Mycobacterium Infections, Nontuberculous microbiology, Lung diagnostic imaging, Lung immunology, Lung microbiology, Macaca mulatta
Abstract

Nontuberculous mycobacteria (NTM) are environmentally ubiquitous organisms that predominately cause NTM pulmonary disease (NTMPD) in individuals over the age of 65. The incidence of NTMPD has increased in the U.S., exceeding that of Mycobacterium tuberculosis . However, the mechanisms leading to higher susceptibility and severity of NTMPD with aging are poorly defined in part due to the lack of animal models that accurately recapitulate human disease. Here, we compared bacterial load, microbial communities, and host responses longitudinally between three young (two female and one male) and two aged (two female) rhesus macaques inoculated with Mycobacterium avium subsp. hominissuis (MAH) in the right caudal lobe. Unilateral infection resulted in a low bacterial load in both young and aged animals confined to the infected side. Although a robust inflammatory response was only observed in the inoculated lung, immune cell infiltration and antigen-specific T cells were detected in both lungs. Computed tomography, gross pathology, and histopathology revealed increased disease severity and persistence of bacterial DNA in aged animals. Additional analyses showed the translocation of gut and oral-pharyngeal bacterial DNA into the lower respiratory microbiome. Finally, single-cell RNA sequencing revealed a heightened inflammatory response to MAH infection by alveolar macrophages in aged animals. These data are consistent with the model that increased disease severity in the aged is mediated by a dysregulated macrophage response that may be sustained through persistent antigen presence., Importance: Nontuberculous mycobacteria (NTM) are emerging as pathogens of high consequence, as cases of NTM pulmonary disease (NTMPD) have exceeded those of Mycobacterium tuberculosis . NTMPD can be debilitating, particularly in patients over 65 years of age, as it causes chronic cough and fatigue requiring prolonged treatments with antibiotics. The underlying mechanisms of this increased disease severity with age are poorly understood, hampering the development of therapeutics and vaccines. Here, we use a rhesus macaque model to investigate the impact of age on host-NTM interactions. This work shows that aging is associated with increased disease severity and bacterial persistence in aged rhesus macaques, thus providing a preclinical model to develop and test novel therapeutics and interventions., Competing Interests: The authors declare no conflict of interest.

Published
2024
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40. Single-cell analysis characterizes PLK1 as a catalyst of an immunosuppressive tumor microenvironment in LUAD.

Author

Kong Y, Li C, Liu J, Zhang M, Allison DB, Hassan F, He D, Wang X, Mao F, Zhang Q, Zhang Y, Li Z, Wu S, Wang C, and Liu X

Abstract

PLK1 (Polo-like kinase 1) plays a critical role in the progression of lung adenocarcinoma (LUAD). Recent studies have unveiled that targeting PLK1 improves the efficacy of immunotherapy, highlighting its important role in the regulation of tumor immunity. Nevertheless, our understanding of the intricate interplay between PLK1 and the tumor microenvironment (TME) remains incomplete. Here, using genetically engineered mouse model and single-cell RNA-seq analysis, we report that PLK1 promotes an immunosuppressive TME in LUAD, characterized with enhanced M2 polarization of tumor associated macrophages (TAM) and dampened antigen presentation process. Mechanistically, elevated PLK1 coincides with increased secretion of CXCL2 cytokine, which promotes M2 polarization of TAM and diminishes expression of class II major histocompatibility complex (MHC-II) in professional antigen-presenting cells. Furthermore, PLK1 negatively regulates MHC-II expression in cancer cells, which has been shown to be associated with compromised tumor immunity and unfavorable patient outcomes. Taken together, our results reveal PLK1 as a novel modulator of TME in LUAD and provide possible therapeutic interventions.

Published
2023
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