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Article ; Online: Too much of a good thing? Teamwork in medical education.

Bordonaro, Michael

2024 , Page(s) 1–2

Abstract: Teams and the promotion of teamwork for both faculty and for students can be key components of integrated curriculum and 'flipped classroom' active learning approaches for medical education. The benefits of teams and teamwork are presented to faculty and ...

Abstract	Teams and the promotion of teamwork for both faculty and for students can be key components of integrated curriculum and 'flipped classroom' active learning approaches for medical education. The benefits of teams and teamwork are presented to faculty and students, sometimes
Language	English
Publishing date	2024-03-31
Publishing country	England
Document type	Journal Article
ZDB-ID	424426-6
ISSN	1466-187X ; 0142-159X
ISSN (online)	1466-187X
ISSN	0142-159X
DOI	10.1080/0142159X.2024.2331050
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Article ; Online: Perspective on faulty faculty development.

Bordonaro, Michael

Medical teacher

2023 , Page(s) 1–2

Language	English
Publishing date	2023-12-12
Publishing country	England
Document type	Journal Article
ZDB-ID	424426-6
ISSN	1466-187X ; 0142-159X
ISSN (online)	1466-187X
ISSN	0142-159X
DOI	10.1080/0142159X.2023.2291996
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Article ; Online: Evaluating the medical curriculum: Bias, problems, solutions.

Bordonaro, Michael

Medical teacher

2023 , Page(s) 1–2

Abstract: Medical school curriculums have increasingly shifted to an integrated curriculum and have been replacing lecture with 'flipped classroom' approaches. Analyses of the benefits of the integrated curriculum and flipped classroom model typically report ... ...

Abstract	Medical school curriculums have increasingly shifted to an integrated curriculum and have been replacing lecture with 'flipped classroom' approaches. Analyses of the benefits of the integrated curriculum and flipped classroom model typically report enhanced student performance. However, the question is whether institutional self-evaluation of curricular success is biased to demonstrate success that may not objectively exist and/or whether such biased data are presented during Liaison Committee on Medical Education (LCME) site visits. An objective determination of curricular effectiveness requires an absence of bias and of efforts to put an institutional 'thumb on the scale' to obtain desired results. In addition, bias may exist in the rationale for implementing these curricular changes in the first place; these can include, for example, with respect to career advancement as well as ideological motivation. Thus, in this paper I examine potential problems with institutional bias with evaluation of curriculum and how to overcome these.
Language	English
Publishing date	2023-11-28
Publishing country	England
Document type	Journal Article
ZDB-ID	424426-6
ISSN	1466-187X ; 0142-159X
ISSN (online)	1466-187X
ISSN	0142-159X
DOI	10.1080/0142159X.2023.2287395
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Article ; Online: Hypothesis: functional age and onset of autosomal dominant genetic prion disease.

Bordonaro, Michael

Theory in biosciences = Theorie in den Biowissenschaften

2023 Volume 142, Issue 2, Page(s) 143–150

Abstract: Autosomal dominant diseases typically have an age-related onset. Here, I focus on genetic prion disease (gPrD), caused by various mutations in the PRNP gene. While gPrD typically occurs at or after middle age, there can be considerable variability in the ...

Abstract	Autosomal dominant diseases typically have an age-related onset. Here, I focus on genetic prion disease (gPrD), caused by various mutations in the PRNP gene. While gPrD typically occurs at or after middle age, there can be considerable variability in the specific age of onset. This variability can occur among patients with the same PRNP mutation; in some cases, these differences occur not only between families but even within the same family. It is not known why gPrD onset is typically delayed for decades when the causative mutation is present from birth. Mouse models of gPrD manifest disease; however, unlike human gPrD, which typically takes decades to manifest, mouse models exhibit disease within months. Therefore, the time to onset of prion disease is proportional to species lifespan; however, it is not known why this is the case. I hypothesize that the initiation of gPrD is strongly influenced by the process of aging; therefore, disease onset is related to proportional functional age (e.g., mice vs. humans). I propose approaches to test this hypothesis and discuss its significance with respect to delaying prion disease through suppression of aging.
MeSH term(s)	Middle Aged ; Humans ; Animals ; Mice ; Prions/genetics ; Prion Proteins/genetics ; Prion Diseases/genetics ; Mutation
Chemical Substances	Prions ; Prion Proteins
Language	English
Publishing date	2023-04-05
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1376847-5
ISSN	1611-7530 ; 1431-7613
ISSN (online)	1611-7530
ISSN	1431-7613
DOI	10.1007/s12064-023-00389-x
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Article: Oncogenic and Receptor-Mediated Wnt Signaling Influence the Sensitivity of Colonic Cells to Butyrate.

Bordonaro, Michael

Journal of Cancer

2023 Volume 14, Issue 3, Page(s) 446–453

Abstract: Deregulated Wnt signaling is responsible for most cases of colorectal cancer (CRC). Dietary fiber is protective against CRC and this activity is likely mediated by butyrate, a breakdown product of dietary fiber that hyperactivates Wnt signaling, ... ...

Abstract	Deregulated Wnt signaling is responsible for most cases of colorectal cancer (CRC). Dietary fiber is protective against CRC and this activity is likely mediated by butyrate, a breakdown product of dietary fiber that hyperactivates Wnt signaling, repressing CRC proliferation and inducing apoptosis. Receptor-mediated Wnt signaling and oncogenic Wnt signaling, which is typically initiated by mutation in more downstream elements of the pathway, activate non-overlapping patterns of gene expression. Receptor-mediated signaling is associated with a poor prognosis for CRC while oncogenic signaling is associated with a relatively good prognosis. We have compared the expression of genes differentially expressed in receptor-mediated vs. oncogenic Wnt signaling to microarray data generated in our laboratory. Most importantly we evaluated these gene expression patterns comparing the early stage colon microadenoma line LT97 with the metastatic CRC cell line SW620. LT97 cells exhibit a gene expression pattern more strongly associated with that observed with oncogenic Wnt signaling, while SW620 cells exhibit a gene expression pattern moderately associated with that observed with receptor-mediated Wnt signaling. Given that SW620 cells are more advanced and malignant compared to LT97 cells, these findings are generally consistent with the better prognosis observed with tumors exhibiting a more oncogenic Wnt gene expression pattern. Importantly, LT97 cells are more sensitive to the effects of butyrate on proliferation and apoptosis that are CRC cells. We further examine these gene expression patterns in butyrate-resistant vs. butyrate-sensitive CRC cells. Based upon all of these observations, we hypothesize that colonic neoplastic cells exhibiting a more oncogenic as compared to receptor-mediated Wnt signaling gene expression pattern would be more sensitive to the effects of butyrate, and, hence, fiber, than are those cells exhibiting a more receptor-mediated Wnt signaling pattern of expression. Diet-derived butyrate may affect the differential patient outcomes resulting from the two types of Wnt signaling. We further posit that development of butyrate resistance and concomitant changes in Wnt signaling patterns, including associations with CBP and p300, disrupts the association between the two major types of Wnt signaling (receptor-mediated and oncogenic) and neoplastic progression/prognosis. Ideas about testing the hypothesis and therapeutic implications are briefly considered.
Language	English
Publishing date	2023-02-05
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2573318-7
ISSN	1837-9664
ISSN	1837-9664
DOI	10.7150/jca.82393
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Article: Hypothesis: Cancer Hormesis and Its Potential for Cancer Therapeutics.

Bordonaro, Michael / Lazarova, Darina

Life (Basel, Switzerland)

2024 Volume 14, Issue 3

Abstract: Primary tumors can inhibit the growth of secondary lesions, particularly metastases, in a phenomenon termed "concomitant resistance". Several mechanisms have been proposed for this effect, each supported by experimental data. In this paper, we ... ...

Abstract	Primary tumors can inhibit the growth of secondary lesions, particularly metastases, in a phenomenon termed "concomitant resistance". Several mechanisms have been proposed for this effect, each supported by experimental data. In this paper, we hypothesize that concomitant resistance is a form of hormesis, a biphasic dose response in which a stimulus has a positive and/or stimulatory effect at low dosages and a negative, inhibitory, and/or toxic effect at higher dosages. When this paradigm applies to tumorigenesis, it is referred to as "cancer hormesis". Thus, low numbers of benign neoplastic cells or less tumorigenic malignant cells may result in resistance to the development of malignant neoplasms, including metastases. A host containing a number of (less tumorigenic) neoplastic cells may exhibit greater protection against more tumorigenic malignant neoplasms than a host who lacks neoplastic cells, or who has too few neoplastic cells to stimulate a protective response. As a theoretical endeavor, this paper also proposes that cancer hormesis can be leveraged for therapeutic purposes, by the implantation of safely controlled, benign artificial tumors in high-risk patients. These tumors would prevent the development of endogenous malignant neoplasms by creating an inhibitory environment for such growth. Strategies for testing the hypothesis are proposed.
Language	English
Publishing date	2024-03-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662250-6
ISSN	2075-1729
ISSN	2075-1729
DOI	10.3390/life14030401
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Article: Hypothesis: Sam68 and Pygo2 mediate cell type-specific effects of the modulation of CBP-Wnt and p300-Wnt activities in Colorectal Cancer Cells.

Bordonaro, Michael

Journal of Cancer

2021 Volume 12, Issue 16, Page(s) 5046–5052

Abstract: The preventive activity of dietary fiber against colorectal cancer (CRC) may be in part mediated by the fermentation product of fiber, butyrate, a histone deacetylase inhibitor (HDACi) that induces CRC cell growth arrest and apoptosis. This action of ... ...

Abstract	The preventive activity of dietary fiber against colorectal cancer (CRC) may be in part mediated by the fermentation product of fiber, butyrate, a histone deacetylase inhibitor (HDACi) that induces CRC cell growth arrest and apoptosis. This action of butyrate, and other HDACis, is in part due to the hyperactivation of the deregulated Wnt activity found in the relevant CRC cell lines. The histone acetylases CBP and p300 interact with beta-catenin; and the relative levels of CBP-Wnt vs. p300-Wnt activity influences CRC cell physiology. It has previously been observed that there are cell type-specific differences in how cotreatment with butyrate and ICG-001, an agent that blocks CBP-Wnt activity allowing for p300-Wnt activity, affects CRC cell physiology. These differences may have clinical significance in dealing with treatment of CRC patients with ICG-001-like agents. Sam68 is a factor differentially expressed in cancer cells, with higher expression in cancer cell lines that have cancer stem cell (CSC)-like properties. Sam68 expression sensitizes cancer cells to ICG-001 treatment, as ICG-001 enhances nuclear localization of Sam68, where binding between Sam68 and CBP diminishes CBP-beta-catenin binding and thus CBP-Wnt activity. Pygo2 is a chromatin effector involved with Wnt signaling that is differentially acetylated by CBP and p300; thus CBP-mediated acetylation localized Pygo2 to the nucleus where it functions in transcriptional activation, while p300-mediated acetylation localizes Pygo2 to the cytoplasm. This paper proposes the hypothesis that Sam68 and Pygo2 are responsible for cell type-specific response of CRC cell lines cotreated with ICG-001 and butyrate as well as other HDACis. Further, experiments are proposed to evaluate this hypothesis and consider possible expected results that could be obtained from such studies.
Language	English
Publishing date	2021-06-16
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2573318-7
ISSN	1837-9664
ISSN	1837-9664
DOI	10.7150/jca.59726
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Article: Hypothesis: Retinoblastoma protein inactivation mediates effects of histone deacetylase inhibitor-induced Wnt hyperactivation in colorectal cancer cells.

Bordonaro, Michael

Journal of Cancer

2020 Volume 11, Issue 3, Page(s) 668–677

Abstract: Butyrate, a product of dietary fiber and a histone deacetylase inhibitor, induces apoptosis of colorectal cancer cells; this effect of butyrate is in part mediated by its ability to hyperactivate Wnt signaling, and may in part explain the preventive ... ...

Abstract	Butyrate, a product of dietary fiber and a histone deacetylase inhibitor, induces apoptosis of colorectal cancer cells; this effect of butyrate is in part mediated by its ability to hyperactivate Wnt signaling, and may in part explain the preventive action of dietary fiber against colorectal cancer. However, the mechanisms by which Wnt hyperactivation promotes apoptosis are unknown. Inactivation of the retinoblastoma tumor suppressor occurs in some cancers and can lead to context-dependent cell proliferation or cell death/apoptosis. The function of retinoblastoma protein (Rb) in normal cells is modulation of cell cycle; inactivation of Rb allows for cell cycle progression and, hence, cell proliferation. Wnt signaling is upregulated in a variety of cancers, and deregulated Wnt signaling is a key initiating event in most cases of sporadic colorectal cancer. It has been shown that Wnt signaling activated by APC inactivation can synergize with the inactivation of Rb to induce apoptosis in a manner mediated by increased TORC1 activity, leading to induced metabolic and energy stress. Rb is typically not inactivated in colorectal cancer; however, Rb is phosphorylated and deactivated during cell cycle G1/S transition. This manuscript posits that it is during this time that butyrate/histone deacetylase inhibitor-induced Wnt hyperactivation induces apoptosis in colorectal cancer cells. Thus, the inactivation of Rb in cell cycle progression may synergize with Wnt hyperactivation to induce apoptosis in response to histone deacetylase inhibitors. The hypothesis is that hyperactivation of Wnt signaling enhances colorectal cancer cell apoptosis via the interaction between upregulated Wnt signaling and inactivated Rb during cell cycle progression. This paper discusses this hypothesis and offers initial experimental approaches for testing the hypothesis. A better understanding of how histone deacetylase inhibitors induce colorectal cancer cell apoptosis through hyperactivation of Wnt signaling, and of cross-talk between repression of cell cycle and induction of apoptosis that occurs with treatment with histone deacetylase inhibitors, can assist in the development of novel therapies for colorectal cancer.
Language	English
Publishing date	2020-01-01
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2573318-7
ISSN	1837-9664
ISSN	1837-9664
DOI	10.7150/jca.37864
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Article: Further analysis of p300 in mediating effects of Butyrate in Colorectal Cancer Cells.

Bordonaro, Michael

Journal of Cancer

2020 Volume 11, Issue 20, Page(s) 5861–5866

Abstract: Butyrate, a product of dietary fiber, hyperactivates Wnt signaling in colorectal cancer (CRC) cells; this activity of butyrate is causally associated with the induction of apoptosis, and the repression of proliferation, in these cells. However, CRC can ... ...

Abstract	Butyrate, a product of dietary fiber, hyperactivates Wnt signaling in colorectal cancer (CRC) cells; this activity of butyrate is causally associated with the induction of apoptosis, and the repression of proliferation, in these cells. However, CRC can develop despite a high fiber diet; hence, butyrate resistance likely occurs during colonic neoplasia. To evaluate the mechanisms of butyrate resistance, HCT-116 CRC cells were previously made resistant to butyrate (HCT-R cell line); I observed that butyrate resistance in HCT-R cells is accompanied by repressed Wnt hyperactivation. CBP and p300 competitively bind to the Wnt signaling factor beta-catenin; CBP-Wnt activity is associated with proliferation, while p300-Wnt activity is associated with differentiation and apoptosis. While butyrate sensitive HCT-116 cells express p300, butyrate resistant HCT-R cells do not. Further, HCT-116 p300 knockout cells exhibit butyrate resistance, and restoration of p300 expression in these cells enhances butyrate sensitivity. Thus, p300 activity is a mediator of butyrate sensitivity in HCT-116-derived cell lines. In the present study, YH249, a pharmacological inhibitor of the p300-beta-catenin association, was utilized to more specifically evaluate the role of p300-Wnt signaling in butyrate responsiveness. Unexpectedly, YH249 potentiates butyrate-induced effects on apoptosis and cell proliferation in HCT-116 cells; in addition, potential off-target, p300-independent, effects of YH249 on butyrate-induced Wnt hyperactivation were observed. SW620 metastatic CRC cells express p300, but do not exhibit association of p300 with beta-catenin. Thus, I hypothesized that SW620 cells can be made butyrate resistant without loss of p300 expression, while butyrate resistance would still be associated with repressed Wnt hyperactivation; this hypothesis was confirmed. Thus, the data
Language	English
Publishing date	2020-08-08
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2573318-7
ISSN	1837-9664
ISSN	1837-9664
DOI	10.7150/jca.47160
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Article ; Online: Quantum biology and human carcinogenesis.

Bordonaro, Michael

Bio Systems

2019 Volume 178, Page(s) 16–24

Abstract: Quantum-mediated effects have been observed in biological systems. We have previously discussed basis-dependent quantum selection as a mechanism for directed adaptive mutation, a process in which selective pressure specifically induces mutation in those ... ...

Abstract	Quantum-mediated effects have been observed in biological systems. We have previously discussed basis-dependent quantum selection as a mechanism for directed adaptive mutation, a process in which selective pressure specifically induces mutation in those genes involved in the adaptive response. Tumor progression in cancer easily lends itself to the adaptive evolutionary perspective, as the Darwinian combination of heritable variations together with selection of the better proliferating variants are believed to play a major role in multistep carcinogenesis. Adaptive mutation may play a role in carcinogenesis; accordingly, we propose that the principles of quantum biology are involved in directed adaptive mutation processes that promote tumor formation. In this paper, we discuss the intersection between quantum mechanics, biology, adaptive evolution, and cancer, and present general models by which adaptive mutation may influence neoplastic initiation and progression. As a potential theoretical and experimental model, we use colorectal cancer. Our model of "quantum cancer" suggests experiments to evaluate directed adaptive mutation in tumorigenesis, and may have important implications for cancer therapeutics.
MeSH term(s)	Adaptation, Physiological/genetics ; Carcinogenesis/genetics ; Colorectal Neoplasms/genetics ; DNA/genetics ; DNA/metabolism ; Humans ; Isomerism ; Mechanics ; Mutation ; Neoplasms/genetics ; Quantum Theory ; RNA/genetics ; RNA/metabolism
Chemical Substances	RNA (63231-63-0) ; DNA (9007-49-2)
Language	English
Publishing date	2019-01-26
Publishing country	Ireland
Document type	Journal Article ; Review
ZDB-ID	186234-0
ISSN	1872-8324 ; 0303-2647
ISSN (online)	1872-8324
ISSN	0303-2647
DOI	10.1016/j.biosystems.2019.01.010
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