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Article: TERT expression increases with tumor grade in a cohort of

Jalasutram, Anvesh / Caniglia, John L / Velpula, Kiran K / Guda, Maheedhara R / Bach, Sarah E / Tsung, Andrew J

American journal of translational research

2022 Volume 14, Issue 1, Page(s) 295–303

Abstract: The molecular mechanisms underlying progression from astrocytoma to secondary glioblastoma are poorly understood. Telomerase reverse transcriptase (TERT), a gene encoding for the catalytic subunit of telomerase, is upregulated in various cancers. ... ...

Abstract	The molecular mechanisms underlying progression from astrocytoma to secondary glioblastoma are poorly understood. Telomerase reverse transcriptase (TERT), a gene encoding for the catalytic subunit of telomerase, is upregulated in various cancers. Upregulation of TERT is a likely mechanism by which malignant cells delay senescence and evade cell death. TERT activity is also the primary mechanism by which malignant cells replenish telomeres, with the other means of telomere replacement being the alternative lengthening of the telomeres (ALT) system. The ALT system is known to be upregulated in tumors harboring loss of function mutations in ATRX. This study analyzed aggregate data on TERT and ATRX expression in astrocytoma, anaplastic astrocytoma, and secondary glioblastoma and then supplemented the data with our findings. In data obtained from Oncomine, significantly higher TERT expression is seen in astrocytomas and secondary glioblastomas compared to normal brain tissue. Additionally, The Cancer Genome Atlas data shows that TERT expression is a significant predictor of overall survival in low-grade gliomas. However, studies comparing the expression of TERT across all grades of astrocytomas had not been performed to date. Using immunohistochemical staining, we showed that controlling for ATRX and IDH mutational status, TERT expression increased with tumor grade in a cohort of patient-derived astrocytoma, anaplastic astrocytoma, and secondary glioblastoma samples. These findings indicate that TERT expression increases as astrocytomas become more aggressive tumors, and probably plays a role in their progression.
Language	English
Publishing date	2022-01-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2471058-1
ISSN	1943-8141
ISSN	1943-8141
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: A potential role for Galectin-3 inhibitors in the treatment of COVID-19.

Caniglia, John L / Guda, Maheedhara R / Asuthkar, Swapna / Tsung, Andrew J / Velpula, Kiran K

PeerJ

2020 Volume 8, Page(s) e9392

Abstract: The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), the causative agent of coronavirus disease 2019 (COVID-19), has been declared a global pandemic by the World Health Organization. With no standard of care for the treatment of ... ...

Abstract	The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), the causative agent of coronavirus disease 2019 (COVID-19), has been declared a global pandemic by the World Health Organization. With no standard of care for the treatment of COVID-19, there is an urgent need to identify therapies that may be effective in treatment. Recent evidence has implicated the development of cytokine release syndrome as the major cause of fatality in COVID-19 patients, with elevated levels of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) observed in patients. Galectin-3 (Gal-3) is an animal lectin that has been implicated in the disease process of a variety of inflammatory conditions. Inhibitors of the small molecule Gal-3 have been shown to reduce the levels of both IL-6 and TNF-α in vitro and have shown anti-inflammatory effects in vivo. Additionally, a key domain in the spike protein of β-coronaviridae, a genus which includes SARS-CoV2, is nearly identical in morphology to human Gal-3. These spike proteins are critical for the virus' entry into host cells. Here we provide a systematic review of the available literature and an impetus for further research on the use of Gal-3 inhibitors in the treatment of COVID-19. Further, we propose a dual mechanism by which Gal-3 inhibition may be beneficial in the treatment of COVID-19, both suppressing the host inflammatory response and impeding viral attachment to host cells.
Keywords	covid19
Language	English
Publishing date	2020-06-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2703241-3
ISSN	2167-8359
ISSN	2167-8359
DOI	10.7717/peerj.9392
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Immunopathology of galectin-3: an increasingly promising target in COVID-19.

Caniglia, John L / Asuthkar, Swapna / Tsung, Andrew J / Guda, Maheedhara R / Velpula, Kiran K

F1000Research

2020 Volume 9, Page(s) 1078

Abstract: The pandemic brought on by the outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) has become a global health crisis, with over 22 million confirmed cases and 777,000 fatalities due to coronavirus disease 2019 (COVID-19) reported ... ...

Abstract	The pandemic brought on by the outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) has become a global health crisis, with over 22 million confirmed cases and 777,000 fatalities due to coronavirus disease 2019 (COVID-19) reported worldwide. The major cause of fatality in infected patients, now referred to as the "Cytokine Storm Syndrome" (CSS), is a direct result of aberrant immune activation following SARS-CoV2 infection and results in excess release of inflammatory cytokines, such as interleukin (IL)-1, tumor necrosis factor α (TNF-α), and IL-6, by macrophages, monocytes, and dendritic cells. Single cell analysis has also shown significantly elevated levels of galectin 3 (Gal-3) in macrophages, monocytes, and dendritic cells in patients with severe COVID-19 as compared to mild disease. Inhibition of Gal-3 reduces the release of IL-1, IL-6, and TNF-α from macrophages
MeSH term(s)	Humans ; Betacoronavirus ; Coronavirus Infections/pathology ; COVID-19 ; Cytokine Release Syndrome/virology ; Galectin 3/immunology ; N-Acetylneuraminic Acid ; Pandemics ; Pneumonia, Viral/pathology ; SARS-CoV-2
Chemical Substances	Galectin 3 ; N-Acetylneuraminic Acid (GZP2782OP0)
Keywords	covid19
Language	English
Publishing date	2020-09-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2699932-8
ISSN	2046-1402 ; 2046-1402
ISSN (online)	2046-1402
ISSN	2046-1402
DOI	10.12688/f1000research.25979.2
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Beyond glucose: alternative sources of energy in glioblastoma.

Caniglia, John L / Jalasutram, Anvesh / Asuthkar, Swapna / Sahagun, Joseph / Park, Simon / Ravindra, Aditya / Tsung, Andrew J / Guda, Maheedhara R / Velpula, Kiran K

Theranostics

2021 Volume 11, Issue 5, Page(s) 2048–2057

Abstract: Glioblastoma multiforme (GBM) is the most common malignant brain tumor in adults. With a designation of WHO Grade IV, it is also the most lethal primary brain tumor with a median survival of just 15 months. This is often despite aggressive treatment that ...

Abstract	Glioblastoma multiforme (GBM) is the most common malignant brain tumor in adults. With a designation of WHO Grade IV, it is also the most lethal primary brain tumor with a median survival of just 15 months. This is often despite aggressive treatment that includes surgical resection, radiation therapy, and chemotherapy. Based on the poor outcomes and prevalence of the tumor, the demand for innovative therapies continues to represent a pressing issue for clinicians and researchers. In terms of therapies targeting metabolism, the prevalence of the Warburg effect has led to a focus on targeting glucose metabolism to halt tumor progression. While glucose is the dominant source of growth substrate in GBM, a number of unique metabolic pathways are exploited in GBM to meet the increased demand for replication and progression. In this review we aim to explore how metabolites from fatty acid oxidation, the urea cycle, the glutamate-glutamine cycle, and one-carbon metabolism are shunted toward energy producing pathways to meet the high energy demand in GBM. We will also explore how the process of autophagy provides a reservoir of nutrients to support viable tumor cells. By so doing, we aim to establish a foundation of implicated metabolic mechanisms supporting growth and tumorigenesis of GBM within the literature. With the sparse number of therapeutic interventions specifically targeting metabolic pathways in GBM, we hope that this review expands further insight into the development of novel treatment modalities.
MeSH term(s)	Animals ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Energy Metabolism ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Glucose/metabolism ; Humans
Chemical Substances	Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-01-01
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.53506
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Immunopathology of galectin-3

John L. Caniglia / Swapna Asuthkar / Andrew J. Tsung / Maheedhara R. Guda / Kiran K. Velpula

F1000Research, Vol

an increasingly promising target in COVID-19 [version 2; peer review: 2 approved]

2020 Volume 9

Abstract	The pandemic brought on by the outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) has become a global health crisis, with over 22 million confirmed cases and 777,000 fatalities due to coronavirus disease 2019 (COVID-19) reported worldwide. The major cause of fatality in infected patients, now referred to as the “Cytokine Storm Syndrome” (CSS), is a direct result of aberrant immune activation following SARS-CoV2 infection and results in excess release of inflammatory cytokines, such as interleukin (IL)-1, tumor necrosis factor α (TNF-α), and IL-6, by macrophages, monocytes, and dendritic cells. Single cell analysis has also shown significantly elevated levels of galectin 3 (Gal-3) in macrophages, monocytes, and dendritic cells in patients with severe COVID-19 as compared to mild disease. Inhibition of Gal-3 reduces the release of IL-1, IL-6, and TNF-α from macrophages in vitro, and as such may hold promise in reducing the incidence of CSS. In addition, Gal-3 inhibition shows promise in reducing transforming growth factor ß (TGF-ß) mediated pulmonary fibrosis, likely to be a major consequence in survivors of severe COVID-19. Finally, a key domain in the spike protein of SARS-CoV2 has been shown to bind N-acetylneuraminic acid (Neu5Ac), a process that may be essential to cell entry by the virus. This Neu5Ac-binding domain shares striking morphological, sequence, and functional similarities with human Gal-3. Here we provide an updated review of the literature linking Gal-3 to COVID-19 pathogenesis. Dually targeting galectins and the Neu5Ac-binding domain of SARS-CoV2 shows tentative promise in several stages of the disease: preventing viral entry, modulating the host immune response, and reducing the post-infectious incidence of pulmonary fibrosis.
Keywords	Medicine ; R ; Science ; Q ; covid19
Subject code	610
Language	English
Publishing date	2020-09-01T00:00:00Z
Publisher	F1000 Research Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A potential role for Galectin-3 inhibitors in the treatment of COVID-19

John L. Caniglia / Maheedhara R. Guda / Swapna Asuthkar / Andrew J. Tsung / Kiran K. Velpula

PeerJ, Vol 8, p e

2020 Volume 9392

Abstract	The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), the causative agent of coronavirus disease 2019 (COVID-19), has been declared a global pandemic by the World Health Organization. With no standard of care for the treatment of COVID-19, there is an urgent need to identify therapies that may be effective in treatment. Recent evidence has implicated the development of cytokine release syndrome as the major cause of fatality in COVID-19 patients, with elevated levels of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) observed in patients. Galectin-3 (Gal-3) is an animal lectin that has been implicated in the disease process of a variety of inflammatory conditions. Inhibitors of the small molecule Gal-3 have been shown to reduce the levels of both IL-6 and TNF-α in vitro and have shown anti-inflammatory effects in vivo. Additionally, a key domain in the spike protein of β-coronaviridae, a genus which includes SARS-CoV2, is nearly identical in morphology to human Gal-3. These spike proteins are critical for the virus’ entry into host cells. Here we provide a systematic review of the available literature and an impetus for further research on the use of Gal-3 inhibitors in the treatment of COVID-19. Further, we propose a dual mechanism by which Gal-3 inhibition may be beneficial in the treatment of COVID-19, both suppressing the host inflammatory response and impeding viral attachment to host cells.
Keywords	Galectin-3 ; Cytokines ; COVID-19 ; Medicine ; R ; Biology (General) ; QH301-705.5 ; covid19
Subject code	610
Language	English
Publishing date	2020-06-01T00:00:00Z
Publisher	PeerJ Inc.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A potential role for Galectin-3 inhibitors in the treatment of COVID-19

Caniglia, John L. / Guda, Maheedhara R. / Asuthkar, Swapna / Tsung, Andrew J. / Velpula, Kiran K.

PeerJ

2020 Volume 8, Page(s) e9392

Abstract	The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), the causative agent of coronavirus disease 2019 (COVID-19), has been declared a global pandemic by the World Health Organization. With no standard of care for the treatment of COVID-19, there is an urgent need to identify therapies that may be effective in treatment. Recent evidence has implicated the development of cytokine release syndrome as the major cause of fatality in COVID-19 patients, with elevated levels of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) observed in patients. Galectin-3 (Gal-3) is an animal lectin that has been implicated in the disease process of a variety of inflammatory conditions. Inhibitors of the small molecule Gal-3 have been shown to reduce the levels of both IL-6 and TNF-α in vitro and have shown anti-inflammatory effects in vivo. Additionally, a key domain in the spike protein of β-coronaviridae, a genus which includes SARS-CoV2, is nearly identical in morphology to human Gal-3. These spike proteins are critical for the virus’ entry into host cells. Here we provide a systematic review of the available literature and an impetus for further research on the use of Gal-3 inhibitors in the treatment of COVID-19. Further, we propose a dual mechanism by which Gal-3 inhibition may be beneficial in the treatment of COVID-19, both suppressing the host inflammatory response and impeding viral attachment to host cells.
Keywords	General Biochemistry, Genetics and Molecular Biology ; General Neuroscience ; General Agricultural and Biological Sciences ; General Medicine ; covid19
Language	English
Publisher	PeerJ
Publishing country	us
Document type	Article ; Online
ZDB-ID	2703241-3
ISSN	2167-8359
ISSN	2167-8359
DOI	10.7717/peerj.9392
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: A potential role for Galectin-3 inhibitors in the treatment of COVID-19

Caniglia, John L. / Guda, Maheedhara R. / Asuthkar, Swapna / Tsung, Andrew J. / Velpula, Kiran K.

PeerJ

Abstract: The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), the causative agent of coronavirus disease 2019 (COVID-19), has been declared a global pandemic by the World Health Organization With no standard of care for the treatment of ... ...

Abstract	The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), the causative agent of coronavirus disease 2019 (COVID-19), has been declared a global pandemic by the World Health Organization With no standard of care for the treatment of COVID-19, there is an urgent need to identify therapies that may be effective in treatment Recent evidence has implicated the development of cytokine release syndrome as the major cause of fatality in COVID-19 patients, with elevated levels of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) observed in patients Galectin-3 (Gal-3) is an animal lectin that has been implicated in the disease process of a variety of inflammatory conditions Inhibitors of the small molecule Gal-3 have been shown to reduce the levels of both IL-6 and TNF-α in vitro and have shown anti-inflammatory effects in vivo Additionally, a key domain in the spike protein of β-coronaviridae, a genus which includes SARS-CoV2, is nearly identical in morphology to human Gal-3 These spike proteins are critical for the virus’ entry into host cells Here we provide a systematic review of the available literature and an impetus for further research on the use of Gal-3 inhibitors in the treatment of COVID-19 Further, we propose a dual mechanism by which Gal-3 inhibition may be beneficial in the treatment of COVID-19, both suppressing the host inflammatory response and impeding viral attachment to host cells
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #602799
Database	COVID19

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Article ; Online: Assessing knowledge, attitudes, and practices towards causal directed acyclic graphs: a qualitative research project.

Barnard-Mayers, Ruby / Childs, Ellen / Corlin, Laura / Caniglia, Ellen C / Fox, Matthew P / Donnelly, John P / Murray, Eleanor J

European journal of epidemiology

2021 Volume 36, Issue 7, Page(s) 659–667

Abstract: Causal graphs provide a key tool for optimizing the validity of causal effect estimates. Although a large literature exists on the mathematical theory underlying the use of causal graphs, less literature exists to aid applied researchers in understanding ...

Abstract	Causal graphs provide a key tool for optimizing the validity of causal effect estimates. Although a large literature exists on the mathematical theory underlying the use of causal graphs, less literature exists to aid applied researchers in understanding how best to develop and use causal graphs in their research projects. We sought to understand why researchers do or do not regularly use DAGs by surveying practicing epidemiologists and medical researchers on their knowledge, level of interest, attitudes, and practices towards the use of causal graphs in applied epidemiology and health research. We used Twitter and the Society for Epidemiologic Research to disseminate the survey. Overall, a majority of participants reported being comfortable with using causal graphs and reported using them 'sometimes', 'often', or 'always' in their research. Having received training appeared to improve comprehension of the assumptions displayed in causal graphs. Many of the respondents who did not use causal graphs reported lack of knowledge as a barrier to using DAGs in their research. Causal graphs are of interest to epidemiologists and medical researchers, but there are several barriers to their uptake. Additional training and clearer guidance are needed. In addition, methodological developments regarding visualization of effect measure modification and interaction on causal graphs is needed.
MeSH term(s)	Attitude of Health Personnel ; Causality ; Computer Graphics ; Data Interpretation, Statistical ; Epidemiologic Research Design ; Epidemiologists ; Female ; Humans ; Male ; Qualitative Research ; Research Personnel ; Surveys and Questionnaires
Language	English
Publishing date	2021-06-10
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	632614-6
ISSN	1573-7284 ; 0393-2990
ISSN (online)	1573-7284
ISSN	0393-2990
DOI	10.1007/s10654-021-00771-3
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Pleiotropic role of macrophage migration inhibitory factor in cancer.

Guda, Maheedhara R / Rashid, Matthew A / Asuthkar, Swapna / Jalasutram, Anvesh / Caniglia, John L / Tsung, Andrew J / Velpula, Kiran K

American journal of cancer research

2019 Volume 9, Issue 12, Page(s) 2760–2773

Abstract: Macrophage migration inhibitory factor (MIF) is an inflammatory cytokine that serves many roles in inflammation and immunity; however, it is also involved in carcinogenesis. This is a review of the clinical and experimental data published on MIF and its ... ...

Abstract	Macrophage migration inhibitory factor (MIF) is an inflammatory cytokine that serves many roles in inflammation and immunity; however, it is also involved in carcinogenesis. This is a review of the clinical and experimental data published on MIF and its role in various types of cancers such as glioblastomas, lung cancer, breast cancer, gastric cancer, melanoma, bladder cancer, and head and neck cancers. The goal of this review is to show MIFs role in various types of cancers. Data show that MIF is overexpressed in these malignancies in humans, and contributes to the deregulation of the cell cycle, angiogenesis, and metastasis. Clinical studies show that MIF overexpression in these types of tumors significantly decreases survival rate, and increases tumor aggression. There are multiple anti-MIF molecules that are currently being explored and investigations should be continued.
Language	English
Publishing date	2019-12-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2589522-9
ISSN	2156-6976
ISSN	2156-6976
Database	MEDical Literature Analysis and Retrieval System OnLINE

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