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Article ; Online: A Narrative Review of Alternative Symptomatic Treatments for Herpes Simplex Virus.

Chang, Jane Y / Balch, Curt / Puccio, Joseph / Oh, Hyung S

2023 Volume 15, Issue 6

Abstract: Herpes simplex virus-1 (HSV-1) and -2 (HSV-2) are large, spherically shaped, double-stranded DNA viruses that coevolved ... ...

Abstract	Herpes simplex virus-1 (HSV-1) and -2 (HSV-2) are large, spherically shaped, double-stranded DNA viruses that coevolved with
MeSH term(s)	Humans ; Antiviral Agents/therapeutic use ; Acyclovir/therapeutic use ; Herpes Simplex/drug therapy ; Herpesvirus 1, Human ; Herpesvirus 2, Human ; Biological Products/therapeutic use
Chemical Substances	Antiviral Agents ; Acyclovir (X4HES1O11F) ; Biological Products
Language	English
Publishing date	2023-06-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v15061314
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Article: The Epigenomics of Embryonic Pathway Signaling in Colorectal Cancer.

Balch, Curt / Ramapuram, Jayaram B / Tiwari, Amit K

Frontiers in pharmacology

2017 Volume 8, Page(s) 267

Abstract: Colorectal cancer (CRC) is the second-leading cause of cancer death in developed countries. While early detection (e.g., colonoscopy) generally yields excellent outcomes, metastatic and drug-resistant disease is uniformly fatal, and non-compliance for ... ...

Abstract	Colorectal cancer (CRC) is the second-leading cause of cancer death in developed countries. While early detection (e.g., colonoscopy) generally yields excellent outcomes, metastatic and drug-resistant disease is uniformly fatal, and non-compliance for screening remains over 25%. Familial CRCs (10% of total cases) primarily include mutations in the gene
Language	English
Publishing date	2017-05-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2017.00267
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Article: Epigenetic targeting therapies to overcome chemotherapy resistance.

Balch, Curt / Nephew, Kenneth P

Advances in experimental medicine and biology

2013 Volume 754, Page(s) 285–311

Abstract: It is now well established that epigenetic aberrations occur early in malignant transformation, raising the possibility of identifying chemopreventive compounds or reliable diagnostic screening using epigenetic biomarkers. Combinatorial therapies ... ...

Abstract	It is now well established that epigenetic aberrations occur early in malignant transformation, raising the possibility of identifying chemopreventive compounds or reliable diagnostic screening using epigenetic biomarkers. Combinatorial therapies effective for the reexpression of tumor suppressors, facilitating resensitization to conventional chemotherapies, hold great promise for the future therapy of cancer. This approach may also perturb cancer stem cells and thus represent an effective means for managing a number of solid tumors. We believe that in the near future, anticancer drug regimens will routinely include epigenetic therapies, possibly in conjunction with inhibitors of "stemness" signal pathways, to effectively reduce the devastating occurrence of cancer chemotherapy resistance.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; DNA Methylation/drug effects ; Drug Resistance, Neoplasm/genetics ; Epigenesis, Genetic/drug effects ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2013
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-1-4419-9967-2_14
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Article ; Online: Tackling multidrug resistance mediated by efflux transporters in tumor-initiating cells.

McIntosh, Kyle / Balch, Curt / Tiwari, Amit K

Expert opinion on drug metabolism & toxicology

2016 Volume 12, Issue 6, Page(s) 633–644

Abstract: Introduction: Expression of the multifunctional ATP-binding cassette (ABC) efflux transporter gene family is a well-established mechanism for protecting cancer stem cells (CSCs) from damage or death due to toxins. The outcome of such protection makes ... ...

Abstract	Introduction: Expression of the multifunctional ATP-binding cassette (ABC) efflux transporter gene family is a well-established mechanism for protecting cancer stem cells (CSCs) from damage or death due to toxins. The outcome of such protection makes CSCs innately multidrug resistant (MDR) to conventional chemotherapy. Areas covered: While research has focused on gaining better insight into the role of ABC transporters in CSC drug resistance, various strategies to circumvent the function of these transporters have been proposed, including inhibition of transporter function through targeted tyrosine kinase inhibitors, competitive and allosteric modulators, shRNA-mediated inhibition, nanoparticle-mediated delivery of inhibitors, and modulating the regulation of transcriptional and signaling pathways involving ABC transporters. This review highlights the role of MDR mediated by ABC transporters, particularly in CSCs, and the current progress and pitfalls of strategies to circumvent MDR in CSCs. Expert opinion: Cancer stem cells are now a subject of intense research, as it is hypothesized that these progenitors predominantly beget tumorigenesis, chemoresistance, and metastasis. Consequently, the design and synthesis of more effective ABC transporter inhibitors, to increase cytotoxic drug concentrations in CSCs (thus increasing their eradication), is a promising approach for the field of oncology.
MeSH term(s)	ATP-Binding Cassette Transporters/metabolism ; Animals ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/pharmacokinetics ; Antineoplastic Agents/pharmacology ; Drug Delivery Systems ; Drug Resistance, Multiple ; Drug Resistance, Neoplasm ; Humans ; Nanoparticles ; Neoplasms/drug therapy ; Neoplasms/pathology ; Neoplastic Stem Cells/metabolism
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2016-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2214462-6
ISSN	1744-7607 ; 1742-5255
ISSN (online)	1744-7607
ISSN	1742-5255
DOI	10.1080/17425255.2016.1179280
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Zs.A 6264: Show issues

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Article ; Online: Systematic Inspection of the Clinical Relevance of TP53 Missense Mutations in Gastric Cancer.

Moon, SeongRyeol / Balch, Curt / Park, Sungjin / Lee, Jinhyuk / Sung, Jiyong / Nam, Seungyoon

IEEE/ACM transactions on computational biology and bioinformatics

2018 Volume 16, Issue 5, Page(s) 1693–1701

Abstract: The "guardian of the genome," TP53, is one of the most frequently mutated genes of all cancers. Despite the important biological roles of TP53, the clinical relevance of TP53 mutations, in gastric cancer (GC), remains largely unknown. Here, we ... ...

Abstract	The "guardian of the genome," TP53, is one of the most frequently mutated genes of all cancers. Despite the important biological roles of TP53, the clinical relevance of TP53 mutations, in gastric cancer (GC), remains largely unknown. Here, we systematically assessed clinical relevance, in terms of TP53 mutation positions, finding substantial variability. Thus, we hypothesized that the position of the TP53 mutation might affect clinical outcomes in GC. We systematically inspected missense mutations in TP53, from a TCGA (The Cancer Genome Atlas) GC dataset in UCSC Xena repository. Specifically, we examined five aspects of each mutational position: (1) the whole gene body; (2) known hot-spots; (3) the DNA-binding domain; (4) the secondary structure of the domain; and (5) individual mutation positions. We then analyzed the clinical outcomes for each aspect. These results showed that, in terms of secondary structure, patients with mutations in turn regions showed poor prognosis, compared to those with mutations in beta strand regions (log rank ${\text{p}}= {{0.043}}$p=0.043). Also, in terms of individual mutation positions, patients having mutations at R248 showed poorer survival than other patients having mutations at different TP53 positions (log rank ${\text{p}}= {{0.035}}$p=0.035).
MeSH term(s)	Computational Biology ; Databases, Genetic ; Humans ; Kaplan-Meier Estimate ; Mutation, Missense/genetics ; Stomach Neoplasms/genetics ; Stomach Neoplasms/mortality ; Tumor Suppressor Protein p53/genetics
Chemical Substances	TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2018-03-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1557-9964
ISSN (online)	1557-9964
DOI	10.1109/TCBB.2018.2814049
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Article ; Online: Rational design of small molecule RHOA inhibitors for gastric cancer.

Kim, Jin-Hee / Park, Sungjin / Lim, Seung Mook / Eom, Hyo Jin / Balch, Curt / Lee, Jinhyuk / Kim, Gi Jin / Jeong, Jin-Hyun / Nam, Seungyoon / Kim, Yon Hui

The pharmacogenomics journal

2020 Volume 20, Issue 4, Page(s) 601–612

Abstract: Previously, we identified Ras homologous A (RHOA) as a major signaling hub in gastric cancer (GC), the third most common cause of cancer death in the world, prompting us to rationally design an efficacious inhibitor of this oncogenic GTPase. Here, based ... ...

Abstract	Previously, we identified Ras homologous A (RHOA) as a major signaling hub in gastric cancer (GC), the third most common cause of cancer death in the world, prompting us to rationally design an efficacious inhibitor of this oncogenic GTPase. Here, based on that previous work, we extend those computational analyses to further pharmacologically optimize anti-RHOA hydrazide derivatives for greater anti-GC potency. Two of these, JK-136 and JK-139, potently inhibited cell viability and migration/invasion of GC cell lines, and mouse xenografts, diversely expressing RHOA. Moreover, JK-136's binding affinity for RHOA was >140-fold greater than Rhosin, a nonclinical RHOA inhibitor. Network analysis of JK-136/-139 vs. Rhosin treatments indicated downregulation of the sphingosine-1-phosphate, as an emerging cancer metabolic pathway in cell migration and motility. We assert that identifying and targeting oncogenic signaling hubs, such as RHOA, represents an emerging strategy for the design, characterization, and translation of new antineoplastics, against gastric and other cancers.
MeSH term(s)	Animals ; Antineoplastic Agents/chemical synthesis ; Antineoplastic Agents/metabolism ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Cell Line, Tumor ; Drug Design ; Humans ; Mice ; Mice, SCID ; Molecular Docking Simulation/methods ; Protein Structure, Secondary ; Stomach Neoplasms/drug therapy ; Stomach Neoplasms/metabolism ; Stomach Neoplasms/pathology ; Xenograft Model Antitumor Assays/methods ; rhoA GTP-Binding Protein/antagonists & inhibitors ; rhoA GTP-Binding Protein/chemistry ; rhoA GTP-Binding Protein/metabolism
Chemical Substances	Antineoplastic Agents ; RHOA protein, human (124671-05-2) ; rhoA GTP-Binding Protein (EC 3.6.5.2)
Language	English
Publishing date	2020-02-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2106831-8
ISSN	1473-1150 ; 1470-269X
ISSN (online)	1473-1150
ISSN	1470-269X
DOI	10.1038/s41397-020-0153-6
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Zs.A 5806: Show issues

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Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Natural Polyphenols in Cancer Chemoresistance.

Hussain, Saad A / Sulaiman, Amal A / Balch, Curt / Chauhan, Harsh / Alhadidi, Qasim M / Tiwari, Amit K

Nutrition and cancer

2016 Volume 68, Issue 6, Page(s) 879–891

Abstract: Resistance to chemotherapy remains a major impediment to the management of most types of cancer. Both intrinsic and acquired drug resistance are mediated by several cellular and molecular mechanisms, including alternative growth-signaling pathways ... ...

Abstract	Resistance to chemotherapy remains a major impediment to the management of most types of cancer. Both intrinsic and acquired drug resistance are mediated by several cellular and molecular mechanisms, including alternative growth-signaling pathways unaffected by specific therapies, alterations in the tumor microenvironment (e.g., hypoxia and angiogenesis), and active transport of drugs out of the cell. Epidemiological studies have validated an inverse correlation between the consumption of dietary polyphenols and the risk of cancer, which has been attributed to polyphenol antioxidant capacity and their potential to inhibit activation of procarcinogens, cancer cell proliferation, metastasis, and angiogenesis, and inhibition or downregulation of active drug efflux transporters. Moreover, polyphenols can induce apoptosis in cancer cells and modulate immune responses and inflammatory cascades. Augmentation of the efficacy of chemotherapy and prevention of multidrug resistance are other important effects of dietary polyphenols that deserve further research, especially after the discovery of tight "crosstalk" between aberrant growth signaling and metabolic dysfunction in cancer cells. In this review, we cover what is currently known about the role of natural polyphenolic compounds in overcoming cancer drug resistance mediated by diverse primary and secondary resistance mechanisms.
Language	English
Publishing date	2016-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	424433-3
ISSN	1532-7914 ; 0163-5581
ISSN (online)	1532-7914
ISSN	0163-5581
DOI	10.1080/01635581.2016.1192201
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Zs.A 1496: Show issues

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Article ; Online: TET1 promotes 5hmC-dependent stemness, and inhibits a 5hmC-independent epithelial-mesenchymal transition, in cervical precancerous lesions.

Su, Po-Hsuan / Hsu, Yaw-Wen / Huang, Rui-Lan / Chen, Lin-Yu / Chao, Tai-Kuang / Liao, Chi-Chun / Chen, Chien-Wen / Wu, Tzu-I / Mao, Shih-Peng / Balch, Curt / Lai, Hung-Cheng

Cancer letters

2019 Volume 450, Page(s) 53–62

Abstract: DNA hypermethylation is a driving force in carcinogenesis. However, the role of active DNA hypomethylation in cancer remains largely unknown. This process, facilitated by ten-eleven translocation methylcytosine dioxygenase 1 (TET1), which oxidizes 5- ... ...

Abstract	DNA hypermethylation is a driving force in carcinogenesis. However, the role of active DNA hypomethylation in cancer remains largely unknown. This process, facilitated by ten-eleven translocation methylcytosine dioxygenase 1 (TET1), which oxidizes 5-methylcytosine (5 mC) to 5-hydroxymethylcytosine (5hmC), has never been studied in cervical cancer. Here, we found that TET1 and 5hmC correlative increases from normal cervix to Low-grade squamous intraepithelial lesion (LSIL), maximizing in High-grade squamous intraepithelial lesion (HSIL), and decreasing in invasive cancer. Full-length HPV-immortalized HSIL cells demonstrated higher TET1/5hmC levels, and stemness properties, compared to invasive cancer cells. TET1 silencing promoted the epithelial-mesenchymal transition (EMT), to transform precancerous cells in vivo. TET1 increased 5hmC in the ZEB1 and VIM promoters, surprisingly, silencing both genes. TET1 interaction with the histone modifiers, LSD1 and EZH2, on the ZEB1 promoter, resulted in gene silencing, via loss of histone H3K4 trimethylation, and gain of histone H3K27 trimethylation. Taken together, TET1 promotes stemness properties, and inhibits EMT, in HSIL cells, through 5hmC-dependent and -independent mechanisms.
MeSH term(s)	5-Methylcytosine/analogs & derivatives ; 5-Methylcytosine/metabolism ; Animals ; Cell Line, Tumor ; Cervical Intraepithelial Neoplasia/metabolism ; Cervical Intraepithelial Neoplasia/pathology ; Epithelial-Mesenchymal Transition ; Female ; HeLa Cells ; Heterografts ; Humans ; Mice ; Mixed Function Oxygenases/biosynthesis ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Precancerous Conditions/metabolism ; Precancerous Conditions/pathology ; Proto-Oncogene Proteins/biosynthesis ; Squamous Intraepithelial Lesions of the Cervix/metabolism ; Squamous Intraepithelial Lesions of the Cervix/pathology ; Uterine Cervical Neoplasms/metabolism ; Uterine Cervical Neoplasms/pathology ; Vimentin ; Zinc Finger E-box-Binding Homeobox 1
Chemical Substances	Proto-Oncogene Proteins ; VIM protein, human ; Vimentin ; ZEB1 protein, human ; Zinc Finger E-box-Binding Homeobox 1 ; 5-hydroxymethylcytosine (1123-95-1) ; 5-Methylcytosine (6R795CQT4H) ; Mixed Function Oxygenases (EC 1.-) ; TET1 protein, human (EC 1.-)
Language	English
Publishing date	2019-02-13
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2019.01.033
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Zs.A 1177: Show issues

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Article: Methyl group acceptance assay for the determination of global DNA methylation levels.

Nephew, Kenneth P / Balch, Curt / Skalnik, David G

Methods in molecular biology (Clifton, N.J.)

2009 Volume 507, Page(s) 35–41

Abstract: DNA methylation levels are affected by numerous environmental influences, including diet and xenobiotic exposure, and neoplasia has been firmly associated with genomic hypomethylation and localized hypermethylation of tumor suppressor genes. To reverse ... ...

Abstract	DNA methylation levels are affected by numerous environmental influences, including diet and xenobiotic exposure, and neoplasia has been firmly associated with genomic hypomethylation and localized hypermethylation of tumor suppressor genes. To reverse methylation-induced gene repression, DNA hypomethylating agents are currently in clinical trials for various malignancies, with two of these now approved for the therapy of myelodysplastic syndrome, and the efficacy of these drugs can be assessed by the monitoring of global DNA methylation levels. Herein, we outline a simple, well-established method for the evaluation of genomic DNA methylation levels, based on the ability of isolated DNA to "accept" radiolabeled methyl groups from S-[3H-methyl] adenosylmethionine, using the bacterial CpG methyltransferase SssI. As this enzyme methylates all unmethylated CpG dinucleotides in the genome, radiolabeled methyl group acceptance is inversely proportional to the level of preexisting methylation. This assay is applicable to a number of translational and basic research questions.
MeSH term(s)	Animals ; Cell Line, Tumor ; CpG Islands ; DNA/chemistry ; DNA/genetics ; DNA Methylation/genetics ; DNA, Neoplasm/chemistry ; DNA, Neoplasm/genetics ; Genes, Tumor Suppressor ; Myelodysplastic Syndromes/genetics ; Neoplasms/chemistry ; Neoplasms/genetics
Chemical Substances	DNA, Neoplasm ; DNA (9007-49-2)
Language	English
Publishing date	2009
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1064-3745
ISSN	1064-3745
DOI	10.1007/978-1-59745-522-0_3
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Article ; Online: Network Comparison of Inflammation in Colorectal Cancer and Alzheimer's Disease.

Park, Sungjin / Yu, Seok Jong / Cho, Yongseong / Balch, Curt / Lee, Jinhyuk / Kim, Yon Hui / Nam, Seungyoon

BioMed research international

2015 Volume 2015, Page(s) 205247

Abstract: Recently, a large clinical study revealed an inverse correlation of individual risk of cancer versus Alzheimer's disease (AD). However, no explanation exists for this anticorrelation at the molecular level; however, inflammation is crucial to the ... ...

Abstract	Recently, a large clinical study revealed an inverse correlation of individual risk of cancer versus Alzheimer's disease (AD). However, no explanation exists for this anticorrelation at the molecular level; however, inflammation is crucial to the pathogenesis of both diseases, necessitating a need to understand differing signaling usage during inflammatory responses distinct to both diseases. Using a subpathway analysis approach, we identified numerous well-known and previously unknown pathways enriched in datasets from both diseases. Here, we present the quantitative importance of the inflammatory response in the two disease pathologies and summarize signal transduction pathways common to both diseases that are affected by inflammation.
MeSH term(s)	Alzheimer Disease/metabolism ; Colorectal Neoplasms/metabolism ; Computer Simulation ; Cytokines/metabolism ; Gene Expression Profiling/methods ; Humans ; Inflammation/complications ; Inflammation/metabolism ; Models, Biological ; Protein Interaction Mapping/methods ; Signal Transduction
Chemical Substances	Cytokines
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2698540-8
ISSN	2314-6141 ; 2314-6133
ISSN (online)	2314-6141
ISSN	2314-6133
DOI	10.1155/2015/205247
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