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Article ; Online: Regulation and role of CAMKK2 in prostate cancer.

Pulliam, Thomas L / Goli, Pavithr / Awad, Dominik / Lin, Chenchu / Wilkenfeld, Sandi R / Frigo, Daniel E

2022 Volume 19, Issue 6, Page(s) 367–380

Abstract: In 2011, CAMKK2, the gene encoding calcium/calmodulin-dependent kinase kinase 2 (CAMKK2), was demonstrated to be a direct target of the androgen receptor and a driver of prostate cancer progression. Results from multiple independent studies have ... ...

Abstract	In 2011, CAMKK2, the gene encoding calcium/calmodulin-dependent kinase kinase 2 (CAMKK2), was demonstrated to be a direct target of the androgen receptor and a driver of prostate cancer progression. Results from multiple independent studies have confirmed these findings and demonstrated the potential role of CAMKK2 as a clinical biomarker and therapeutic target in advanced prostate cancer using a variety of preclinical models. Drug development efforts targeting CAMKK2 have begun accordingly. CAMKK2 regulation can vary across disease stages, which might have important implications in the use of CAMKK2 as a biomarker. Moreover, new non-cell-autonomous roles for CAMKK2 that could affect tumorigenesis, metastasis and possible comorbidities linked to disease and treatment have emerged and could present novel treatment opportunities for prostate cancer.
MeSH term(s)	Calcium-Calmodulin-Dependent Protein Kinase Kinase/genetics ; Cell Line, Tumor ; Cell Transformation, Neoplastic ; Humans ; Male ; Prostate/pathology ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; Prostatic Neoplasms/therapy
Chemical Substances	CAMKK2 protein, human (EC 2.7.11.17) ; Calcium-Calmodulin-Dependent Protein Kinase Kinase (EC 2.7.11.17)
Language	English
Publishing date	2022-04-26
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2493737-X
ISSN	1759-4820 ; 1759-4812
ISSN (online)	1759-4820
ISSN	1759-4812
DOI	10.1038/s41585-022-00588-z
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Article: Intersection of Two Checkpoints: Could Inhibiting the DNA Damage Response Checkpoint Rescue Immune Checkpoint-Refractory Cancer?

Goff, Peter H / Bhakuni, Rashmi / Pulliam, Thomas / Lee, Jung Hyun / Hall, Evan T / Nghiem, Paul

Cancers

2021 Volume 13, Issue 14

Abstract: Metastatic cancers resistant to immunotherapy require novel management strategies. DNA damage response (DDR) proteins, including ATR (ataxia telangiectasia and Rad3-related), ATM (ataxia telangiectasia mutated) and DNA-PK (DNA-dependent protein kinase), ... ...

Abstract	Metastatic cancers resistant to immunotherapy require novel management strategies. DNA damage response (DDR) proteins, including ATR (ataxia telangiectasia and Rad3-related), ATM (ataxia telangiectasia mutated) and DNA-PK (DNA-dependent protein kinase), have been promising therapeutic targets for decades. Specific, potent DDR inhibitors (DDRi) recently entered clinical trials. Surprisingly, preclinical studies have now indicated that DDRi may stimulate anti-tumor immunity to augment immunotherapy. The mechanisms governing how DDRi could promote anti-tumor immunity are not well understood; however, early evidence suggests that they can potentiate immunogenic cell death to recruit and activate antigen-presenting cells to prime an adaptive immune response. Merkel cell carcinoma (MCC) is well suited to test these concepts. It is inherently immunogenic as ~50% of patients with advanced MCC persistently benefit from immunotherapy, making MCC one of the most responsive solid tumors. As is typical of neuroendocrine cancers, dysfunction of p53 and Rb with upregulation of Myc leads to the very rapid growth of MCC. This suggests high replication stress and susceptibility to DDRi and DNA-damaging agents. Indeed, MCC tumors are particularly radiosensitive. Given its inherent immunogenicity, cell cycle checkpoint deficiencies and sensitivity to DNA damage, MCC may be ideal for testing whether targeting the intersection of the DDR checkpoint and the immune checkpoint could help patients with immunotherapy-refractory cancers.
Language	English
Publishing date	2021-07-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13143415
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Article ; Online: Merkel cell polyomavirus-specific and CD39

Ryu, Heeju / Bi, Timothy M / Pulliam, Thomas H / Sarkar, Korok / Church, Candice D / Kumar, Nandita / Mayer-Blackwell, Koshlan / Jani, Saumya / Ramchurren, Nirasha / Hansen, Ulla K / Hadrup, Sine R / Fling, Steven P / Koelle, David M / Nghiem, Paul / Newell, Evan W

Cell reports. Medicine

2024 Volume 5, Issue 2, Page(s) 101390

Abstract: Merkel cell carcinoma is a skin cancer often driven by Merkel cell polyomavirus (MCPyV) with high rates of response to anti-PD-1 therapy despite low mutational burden. MCPyV-specific CD8 T cells are implicated in anti-PD-1-associated immune responses and ...

Abstract	Merkel cell carcinoma is a skin cancer often driven by Merkel cell polyomavirus (MCPyV) with high rates of response to anti-PD-1 therapy despite low mutational burden. MCPyV-specific CD8 T cells are implicated in anti-PD-1-associated immune responses and provide a means to directly study tumor-specific T cell responses to treatment. Using mass cytometry and combinatorial tetramer staining, we find that baseline frequencies of blood MCPyV-specific cells correlated with response and survival. Frequencies of these cells decrease markedly during response to therapy. Phenotypes of MCPyV-specific CD8 T cells have distinct expression patterns of CD39, cutaneous lymphocyte-associated antigen (CLA), and CD103. Correspondingly, overall bulk CD39
MeSH term(s)	Humans ; Carcinoma, Merkel Cell/drug therapy ; Carcinoma, Merkel Cell/metabolism ; Carcinoma, Merkel Cell/pathology ; Merkel cell polyomavirus/metabolism ; Programmed Cell Death 1 Receptor/metabolism ; CD8-Positive T-Lymphocytes ; Skin Neoplasms/drug therapy ; Skin Neoplasms/metabolism ; Biomarkers/metabolism ; Sialyl Lewis X Antigen/analogs & derivatives ; Oligosaccharides
Chemical Substances	6-sulfo sialyl Lewis X ; Programmed Cell Death 1 Receptor ; Biomarkers ; Sialyl Lewis X Antigen ; Oligosaccharides
Language	English
Publishing date	2024-02-09
Publishing country	United States
Document type	Journal Article
ISSN	2666-3791
ISSN (online)	2666-3791
DOI	10.1016/j.xcrm.2023.101390
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Article ; Online: Circulating cancer-specific CD8 T cell frequency is associated with response to PD-1 blockade in Merkel cell carcinoma.

Pulliam, Thomas / Jani, Saumya / Jing, Lichen / Ryu, Heeju / Jojic, Ana / Shasha, Carolyn / Zhang, Jiajia / Kulikauskas, Rima / Church, Candice / Garnett-Benson, Charlie / Gooley, Ted / Chapuis, Aude / Paulson, Kelly / Smith, Kellie N / Pardoll, Drew M / Newell, Evan W / Koelle, David M / Topalian, Suzanne L / Nghiem, Paul

Cell reports. Medicine

2024 Volume 5, Issue 2, Page(s) 101412

Abstract: Understanding cancer immunobiology has been hampered by difficulty identifying cancer-specific T cells. Merkel cell polyomavirus (MCPyV) causes most Merkel cell carcinomas (MCCs). All patients with virus-driven MCC express MCPyV oncoproteins, ... ...

Abstract	Understanding cancer immunobiology has been hampered by difficulty identifying cancer-specific T cells. Merkel cell polyomavirus (MCPyV) causes most Merkel cell carcinomas (MCCs). All patients with virus-driven MCC express MCPyV oncoproteins, facilitating identification of virus (cancer)-specific T cells. We studied MCPyV-specific T cells from 27 patients with MCC using MCPyV peptide-HLA-I multimers, 26-color flow cytometry, single-cell transcriptomics, and T cell receptor (TCR) sequencing. In a prospective clinical trial, higher circulating MCPyV-specific CD8 T cell frequency before anti-PD-1 treatment was strongly associated with 2-year recurrence-free survival (75% if detectable, 0% if undetectable, p = 0.0018; ClinicalTrial.gov: NCT02488759). Intratumorally, such T cells were typically present, but their frequency did not significantly associate with response. Circulating MCPyV-specific CD8 T cells had increased stem/memory and decreased exhaustion signatures relative to their intratumoral counterparts. These results suggest that cancer-specific CD8 T cells in the blood may play a role in anti-PD-1 responses. Thus, strategies that augment their number or mobilize them into tumors could improve outcomes.
MeSH term(s)	Humans ; Carcinoma, Merkel Cell/drug therapy ; Carcinoma, Merkel Cell/pathology ; CD8-Positive T-Lymphocytes/pathology ; Programmed Cell Death 1 Receptor ; Prospective Studies ; Skin Neoplasms/drug therapy ; Skin Neoplasms/pathology ; Clinical Trials as Topic
Chemical Substances	Programmed Cell Death 1 Receptor
Language	English
Publishing date	2024-02-10
Publishing country	United States
Document type	Journal Article
ISSN	2666-3791
ISSN (online)	2666-3791
DOI	10.1016/j.xcrm.2024.101412
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Article ; Online: Merkel Cell Carcinoma in the Age of Immunotherapy: Facts and Hopes.

Colunga, Aric / Pulliam, Thomas / Nghiem, Paul

Clinical cancer research : an official journal of the American Association for Cancer Research

2017 Volume 24, Issue 9, Page(s) 2035–2043

Abstract: Merkel cell carcinoma (MCC) is a rare (∼2,000 U.S. cases/year) but aggressive neuroendocrine tumor of the skin. For advanced MCC, cytotoxic chemotherapy only infrequently ( ... 1 year), suggesting a great ... ...

Abstract	Merkel cell carcinoma (MCC) is a rare (∼2,000 U.S. cases/year) but aggressive neuroendocrine tumor of the skin. For advanced MCC, cytotoxic chemotherapy only infrequently (<10% of cases) offers durable clinical responses (>1 year), suggesting a great need for improved therapeutic options. In 2008, the Merkel cell polyomavirus (MCPyV) was discovered and is clonally integrated in approximately 80% of MCC tumors. The remaining 20% of MCC tumors have large numbers of UV-associated mutations. Importantly, both the UV-induced neoantigens in virus-negative tumors and the MCPyV T antigen oncogenes that are required for virus-positive tumor growth are immunogenic. Indeed, antigen-specific T cells detected in patients are frequently dysfunctional/"exhausted," and the inhibitory ligand, PD-L1, is often present in MCC tumors. These findings led to recent clinical trials involving PD-1 pathway blockade in advanced MCC. The combined data from these trials involving three PD-1 pathway blocking agents-avelumab, pembrolizumab, and nivolumab-indicated a high frequency of durable responses in treated patients. Of note, prior treatment with chemotherapy was associated with decreased response rates to PD-1 checkpoint blockade. Over the past year, these striking data led to major changes in advanced MCC therapy, including the first-ever FDA drug approval for this disease. Despite these successes, approximately 50% of patients with MCC do not persistently benefit from PD-1 pathway blockade, underscoring the need for novel strategies to broaden antitumor immune responses in these patients. Here, we highlight recent progress in MCC including the underlying mechanisms of immune evasion and emerging approaches to augment the efficacy of PD-1 pathway blockade.
MeSH term(s)	Animals ; Antibodies, Viral/immunology ; Antibodies, Viral/pharmacology ; Antigens, Viral, Tumor/immunology ; Antineoplastic Combined Chemotherapy Protocols/adverse effects ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Biomarkers, Tumor ; Carcinoma, Merkel Cell/diagnosis ; Carcinoma, Merkel Cell/etiology ; Carcinoma, Merkel Cell/immunology ; Carcinoma, Merkel Cell/therapy ; Combined Modality Therapy ; Humans ; Immunomodulation ; Immunotherapy/methods ; Merkel cell polyomavirus/immunology ; Polyomavirus Infections/complications ; Polyomavirus Infections/immunology ; Polyomavirus Infections/virology ; Programmed Cell Death 1 Receptor/metabolism ; Standard of Care ; Tumor Burden ; Tumor Virus Infections/complications ; Tumor Virus Infections/immunology ; Tumor Virus Infections/virology ; Ultraviolet Rays
Chemical Substances	Antibodies, Viral ; Antigens, Viral, Tumor ; Biomarkers, Tumor ; PDCD1 protein, human ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2017-12-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-17-0439
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Zs.A 4223: Show issues

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Article ; Online: Characterization of Immunosuppressive Myeloid Cells in Merkel Cell Carcinoma: Correlation with Resistance to PD-1 Pathway Blockade.

Tabachnick-Cherny, Shira / Pulliam, Thomas / Rodriguez, Haroldo J / Fan, Xinyi / Hippe, Daniel S / Jones, Daniel C / Moshiri, Ata S / Smythe, Kimberly S / Kulikauskas, Rima M / Zaba, Lisa C / Paulson, Kelly G / Nghiem, Paul

Clinical cancer research : an official journal of the American Association for Cancer Research

2023 Volume 30, Issue 6, Page(s) 1189–1199

Abstract: Purpose: Merkel cell carcinoma (MCC) is a highly immunogenic skin cancer. Although essentially all MCCs are antigenic through viral antigens or high tumor mutation burden, MCC has a response rate of only approximately 50% to PD-(L)1 blockade suggesting ... ...

Abstract	Purpose: Merkel cell carcinoma (MCC) is a highly immunogenic skin cancer. Although essentially all MCCs are antigenic through viral antigens or high tumor mutation burden, MCC has a response rate of only approximately 50% to PD-(L)1 blockade suggesting barriers to T-cell responses. Prior studies of MCC immunobiology have focused on CD8 T-cell infiltration and their exhaustion status, while the role of innate immunity, particularly myeloid cells, in MCC remains underexplored. Experimental design: We utilized single-cell transcriptomics from 9 patients with MCC and multiplex IHC staining of 54 patients' preimmunotherapy tumors, to identify myeloid cells and evaluate association with immunotherapy response. Results: Single-cell transcriptomics identified tumor-associated macrophages (TAM) as the dominant myeloid component within MCC tumors. These TAMs express an immunosuppressive gene signature characteristic of monocytic myeloid-derived suppressor cells and importantly express several targetable immune checkpoint molecules, including PD-L1 and LILRB receptors, that are not present on tumor cells. Analysis of 54 preimmunotherapy tumor samples showed that a subset of TAMs (CD163+, CD14+, S100A8+) selectively infiltrated tumors that had significant CD8 T cells. Indeed, higher TAM prevalence was associated with resistance to PD-1 blockade. While spatial interactions between TAMs and CD8 T cells were not associated with response, myeloid transcriptomic data showed evidence for cytokine signaling and expression of LILRB receptors, suggesting potential immunosuppressive mechanisms. Conclusions: This study further characterizes TAMs in MCC tumors and provides insights into their possible immunosuppressive mechanism. TAMs may reduce the likelihood of treatment response in MCC by counteracting the benefit of CD8 T-cell infiltration. See related commentary by Silk and Davar, p. 1076.
MeSH term(s)	Humans ; Carcinoma, Merkel Cell/drug therapy ; Carcinoma, Merkel Cell/genetics ; Carcinoma, Merkel Cell/metabolism ; Programmed Cell Death 1 Receptor ; Skin Neoplasms/drug therapy ; Skin Neoplasms/genetics ; Skin Neoplasms/metabolism ; CD8-Positive T-Lymphocytes ; Myeloid Cells/metabolism
Chemical Substances	Programmed Cell Death 1 Receptor
Language	English
Publishing date	2023-10-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-23-1957
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Article ; Online: Polyomavirus-driven Merkel cell carcinoma: Prospects for therapeutic vaccine development.

Tabachnick-Cherny, Shira / Pulliam, Thomas / Church, Candice / Koelle, David M / Nghiem, Paul

Molecular carcinogenesis

2020 Volume 59, Issue 7, Page(s) 807–821

Abstract: Great strides have been made in cancer immunotherapy including the breakthrough successes of anti-PD-(L)1 checkpoint inhibitors. In Merkel cell carcinoma (MCC), a rare and aggressive skin cancer, PD-(L)1 blockade is highly effective. Yet, ~50% of ... ...

Abstract	Great strides have been made in cancer immunotherapy including the breakthrough successes of anti-PD-(L)1 checkpoint inhibitors. In Merkel cell carcinoma (MCC), a rare and aggressive skin cancer, PD-(L)1 blockade is highly effective. Yet, ~50% of patients either do not respond to therapy or develop PD-(L)1 refractory disease and, thus, do not experience long-term benefit. For these patients, additional or combination therapies are needed to augment immune responses that target and eliminate cancer cells. Therapeutic vaccines targeting tumor-associated antigens, mutated self-antigens, or immunogenic viral oncoproteins are currently being developed to augment T-cell responses. Approximately 80% of MCC cases in the United States are driven by the ongoing expression of viral T-antigen (T-Ag) oncoproteins from genomically integrated Merkel cell polyomavirus (MCPyV). Since T-Ag elicits specific B- and T-cell immune responses in most persons with virus-positive MCC (VP-MCC), and ongoing T-Ag expression is required to drive VP-MCC cell proliferation, therapeutic vaccination with T-Ag is a rational potential component of immunotherapy. Failure of the endogenous T-cell response to clear VP-MCC (allowing clinically evident tumors to arise) implies that therapeutic vaccination will need to be potent anśd synergize with other mechanisms to enhance T-cell activity against tumor cells. Here, we review the relevant underlying biology of VP-MCC, potentially applicable therapeutic vaccine platforms, and antigen delivery formats. We also describe early successes in the field of therapeutic cancer vaccines and address several clinical scenarios in which VP-MCC patients could potentially benefit from a therapeutic vaccine.
MeSH term(s)	Animals ; Antigens, Viral, Tumor/immunology ; Carcinoma, Merkel Cell/immunology ; Carcinoma, Merkel Cell/therapy ; Carcinoma, Merkel Cell/virology ; Humans ; Immunotherapy/methods ; Merkel cell polyomavirus/immunology ; Skin Neoplasms/immunology ; Skin Neoplasms/therapy ; Skin Neoplasms/virology ; T-Lymphocytes/immunology ; Vaccines/immunology
Chemical Substances	Antigens, Viral, Tumor ; Vaccines
Language	English
Publishing date	2020-03-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1004029-8
ISSN	1098-2744 ; 0899-1987
ISSN (online)	1098-2744
ISSN	0899-1987
DOI	10.1002/mc.23190
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Zs.A 2664: Show issues

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Article ; Online: Extended duration of treatment using reduced-frequency dosing of anti-PD-1 therapy in patients with advanced melanoma and Merkel cell carcinoma.

Tachiki, Lisa May Ling / Hippe, Daniel S / Williams Silva, Karly / Hall, Evan Thomas / McCamy, William / Fritzsche, Dane / Perdue, Andrea / Majovski, Julia / Pulliam, Thomas / Goldstein, Daniel A / Veatch, Joshua / Ho, Joel / Nghiem, Paul T / Thompson, John A / Bhatia, Shailender

Cancer immunology, immunotherapy : CII

2023 Volume 72, Issue 11, Page(s) 3839–3850

Abstract: Background: Optimal duration of treatment (DoT) with immune checkpoint inhibitors (ICI) in metastatic cancers remains unclear. Many patients, especially those without radiologic complete remission, develop progressive disease after ICI discontinuation. ... ...

Abstract	Background: Optimal duration of treatment (DoT) with immune checkpoint inhibitors (ICI) in metastatic cancers remains unclear. Many patients, especially those without radiologic complete remission, develop progressive disease after ICI discontinuation. Extending DoT with ICI may potentially improve efficacy outcomes but presents major logistical and cost challenges with standard frequency dosing (SFD). Receptor occupancy data supports reduced frequency dosing (RFD) of anti-PD-1 antibodies, which may represent a more practical and economically viable option to extend DoT. Methods: We conducted a retrospective study of patients with metastatic melanoma and Merkel cell carcinoma (MCC), who received ICI at RFD administered every 3 months, after initial disease control at SFD. We evaluated efficacy, safety, and cost-savings of the RFD approach in this cohort. Results: Between 2014 and 2021, 23 patients with advanced melanoma (N = 18) or MCC (N = 5) received anti-PD-1 therapy at RFD. Median DoT was 1.1 years at SFD and 1.2 years at RFD. The 3 year PFS after start of RFD was 73% in melanoma and 100% in MCC patients, which compare favorably to historical control rates. In the subset of 15 patients who received at least 2 years of therapy, total savings amounted to $1.1 million in drug costs and 384 h saved despite the extended DoT (median 3.4 years), as compared to the calculated cost of 2 years at SFD. Conclusions: ICI administration at RFD can allow extension of treatment duration, while preserving efficacy and reducing logistical and financial burden. RFD approach deserves further exploration in prospective clinical trials.
MeSH term(s)	Humans ; Carcinoma, Merkel Cell/drug therapy ; Duration of Therapy ; Melanoma/drug therapy ; Prospective Studies ; Retrospective Studies ; Skin Neoplasms/drug therapy ; Immune Checkpoint Inhibitors/therapeutic use
Chemical Substances	Immune Checkpoint Inhibitors
Language	English
Publishing date	2023-09-21
Publishing country	Germany
Document type	Journal Article
ZDB-ID	195342-4
ISSN	1432-0851 ; 0340-7004
ISSN (online)	1432-0851
ISSN	0340-7004
DOI	10.1007/s00262-023-03539-8
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Article ; Online: Correction to: Extended duration of treatment using reduced‑frequency dosing of anti‑PD‑1 therapy in patients with advanced melanoma and Merkel cell carcinoma.

Tachiki, Lisa May Ling / Hippe, Daniel S / Silva, Karly Williams / Hall, Evan Thomas / McCamy, William / Fritzsche, Dane / Perdue, Andrea / Majovski, Julia / Pulliam, Thomas / Goldstein, Daniel A / Veatch, Joshua / Ho, Joel / Nghiem, Paul T / Thompson, John A / Bhatia, Shailender

Cancer immunology, immunotherapy : CII

2023 Volume 72, Issue 12, Page(s) 4471

Language	English
Publishing date	2023-11-18
Publishing country	Germany
Document type	Published Erratum
ZDB-ID	195342-4
ISSN	1432-0851 ; 0340-7004
ISSN (online)	1432-0851
ISSN	0340-7004
DOI	10.1007/s00262-023-03575-4
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Article ; Online: Systemic Ablation of

Pulliam, Thomas L / Awad, Dominik / Han, Jenny J / Murray, Mollianne M / Ackroyd, Jeffrey J / Goli, Pavithr / Oakhill, Jonathan S / Scott, John W / Ittmann, Michael M / Frigo, Daniel E

Cells

2022 Volume 11, Issue 12

Abstract: Despite early studies linking calcium-calmodulin protein kinase kinase 2 (CAMKK2) to prostate cancer cell migration and invasion, the role of CAMKK2 in metastasis in vivo remains unclear. Moreover, while CAMKK2 is known to regulate systemic metabolism, ... ...

Abstract	Despite early studies linking calcium-calmodulin protein kinase kinase 2 (CAMKK2) to prostate cancer cell migration and invasion, the role of CAMKK2 in metastasis in vivo remains unclear. Moreover, while CAMKK2 is known to regulate systemic metabolism, whether CAMKK2's effects on whole-body metabolism would impact prostate cancer progression and/or related comorbidities is not known. Here, we demonstrate that germline ablation of
MeSH term(s)	Adenocarcinoma/pathology ; Animals ; Calcium-Calmodulin-Dependent Protein Kinase Kinase/genetics ; Calcium-Calmodulin-Dependent Protein Kinase Kinase/metabolism ; Carcinogenesis/pathology ; Cell Transformation, Neoplastic ; Disease Models, Animal ; Humans ; Insulin Resistance ; Lung Neoplasms ; Male ; Mice ; Mice, Transgenic ; Prostatic Neoplasms/pathology ; Protein Kinases
Chemical Substances	Protein Kinases (EC 2.7.-) ; CAMKK2 protein, human (EC 2.7.11.17) ; Calcium-Calmodulin-Dependent Protein Kinase Kinase (EC 2.7.11.17) ; Camkk2 protein, mouse (EC 2.7.11.17)
Language	English
Publishing date	2022-06-10
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11121890
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