About
Francis Barany is a researcher whose work spans various aspects of molecular biology, cancer diagnostics, and therapeutic strategies. His research includes the development of innovative molecular assays such as multiplex PCR/LDR platforms for the detection and identification of infectious pathogens, blood-based biomarkers for cancer detection, and the study of gene dysregulation driven by somatic copy number aberrations in colon tumors. His contributions also involve the design of self-assembling inhibitors targeting human β-tryptase, and the application of microfluidic systems for high-throughput molecular profiling and circulating tumor cell analysis. Barany's work emphasizes the integration of molecular techniques with clinical applications, aiming to improve diagnostic accuracy and therapeutic approaches in cancer and infectious diseases.
Research topics
- Chemistry
- Biochemistry
- Nanotechnology
- Combinatorial chemistry
- Genetics
- Stereochemistry
- Cell biology
- Biology
- Biophysics
- Organic chemistry
Selected publications
Future Medicinal Chemistry · 2026-02-19
articleSenior authorCorrespondingJournal of Personalized Medicine · 2026-05-18
articleOpen accessBackground/Objectives: Bisulfite-based cell-free DNA (cfDNA) methylation assays enable the detection of clinically valuable epigenetic biomarkers but often cause DNA degradation and inconsistent conversion efficiency, limiting performance in low-input liquid biopsy samples. We aimed to develop and evaluate a fully enzymatic cfDNA methylation workflow that preserves DNA integrity and supports quantitative clinical detection. Methods: The assay integrates TET2-mediated oxidation and APOBEC3A deamination with RNase H2-guided primer design, uracil-DNA glycosylase error suppression, and dual-probe detection compatible with quantitative PCR (qPCR) and digital PCR (dPCR). Performance was assessed using serial dilutions of methylated HT29 DNA, unmethylated controls, and plasma cfDNA from colorectal cancer (CRC) patients and healthy donors. Analytical sensitivity, linearity, and concordance between platforms were evaluated. Results: The 40-marker panel demonstrated higher cumulative methylation scores and more frequent methylation-positive signals in CRC cfDNA compared to controls. dPCR confirmed single-molecule resolution and clear discrimination between methylated and unmethylated templates, with occasional double-positive partitions consistent with mixed allelic methylation. Signal intensity across the dilution series followed a four-parameter logistic model, achieving detection sensitivity below 0.2% methylated DNA. qPCR and dPCR results showed strong correlation across the HT29 dilution series (R2 = 0.80) and high concordance in classifying CRC and healthy samples. Conclusions: This TET2–APOBEC-based enzymatic cfDNA assay enables sensitive, quantitative, sequencing-free methylation detection under gentle conditions, supporting its application in early colorectal cancer screening and routine clinical liquid biopsy workflows.
Journal of Medicinal Chemistry · 2024-03-30 · 10 citations
articleSenior authorCorrespondingProteolysis-Targeting Chimeras (PROTACs) are bifunctional molecules that bring a target protein and an E3 ubiquitin ligase into proximity to append ubiquitin, thus directing target degradation. Although numerous PROTACs have entered clinical trials, their development remains challenging, and their large size can produce poor drug-like properties. To overcome these limitations, we have modified our Coferon platform to generate Combinatorial Ubiquitination REal-time PROteolysis (CURE-PROs). CURE-PROs are small molecule degraders designed to self-assemble through reversible bio-orthogonal linkers to form covalent heterodimers. By modifying known ligands for Cereblon, MDM2, VHL, and BRD with complementary phenylboronic acid and diol/catechol linkers, we have successfully created CURE-PROs that direct degradation of BRD4 both in vitro and in vivo. The combinatorial nature of our platform significantly reduces synthesis time and effort to identify the optimal linker length and E3 ligase partner to each target and is readily amenable to screening for new targets.
2023-03-31
preprintOpen accessSenior authorCCR Translation on this Article from CpG Island Methylator Phenotype Associates with Low-Degree Chromosomal Abnormalities in Colorectal Cancer
2023-03-31
preprintOpen accessSenior author<div>Abstract<p><b>Purpose:</b> Aberrant promoter methylation and genomic instability occur frequently during colorectal cancer development. CpG island methylator phenotype (CIMP) has been shown to associate with microsatellite instability, and <i>BRAF</i> mutation and is often found in the right-side colon. Nevertheless, the relative importance of CIMP and chromosomal instability (CIN) for tumorigenesis has yet to be thoroughly investigated in sporadic colorectal cancers.</p><p><b>Experimental Design:</b> We determined CIMP in 161 primary colorectal cancers and 66 matched normal mucosae using a quantitative bisulfite/PCR/ligase detection reaction (LDR)/Universal Array assay. The validity of CIMP was confirmed in a subset of 60 primary tumors using MethyLight assay and five independent markers. In parallel, CIN was analyzed in the same study cohort using Affymetrix 50K Human Mapping arrays.</p><p><b>Results:</b> The identified CIMP-positive cancers correlate with microsatellite instability (<i>P</i> = 0.075) and the <i>BRAF</i> mutation V600E (<i>P</i> = 0.00005). The array-based high-resolution analysis of chromosomal aberrations indicated that the degree of aneuploidy is spread over a wide spectrum among analyzed colorectal cancers. Whether CIN was defined by copy number variations in selected microsatellite loci (criterion 1) or considered as a continuous variable (criterion 2), CIMP-positive samples showed a strong correlation with low-degree chromosomal aberrations (<i>P</i> = 0.075 and <i>P</i> = 0.012, respectively). Similar correlations were observed when CIMP was determined by MethyLight assay (<i>P</i> = 0.001 and <i>P</i> = 0.013, respectively).</p><p><b>Conclusion:</b> CIMP-positive tumors generally possess lower chromosomal aberrations, which may only be revealed using a genome-wide approach. The significant difference in the degree of chromosomal aberrations between CIMP-positive and the remainder of samples suggests that epigenetic (CIMP) and genetic (CIN) abnormalities may arise from independent molecular mechanisms of tumor progression.</p></div>
2023-03-31
preprintOpen accessSupplementary Figure A from GROα Is Highly Expressed in Adenocarcinoma of the Colon and Down-Regulates Fibulin-1
2023-03-30
preprintOpen accessSupplementary Figure S2 from Relationship of Gene Expression and Chromosomal Abnormalities in Colorectal Cancer
Reversible Assembly of Proteolysis Targeting Chimeras
ACS Chemical Biology · 2023 · 27 citations
- Cell biology
- Chemistry
- Biology
PROteolysis TArgeting Chimeras (PROTACs) are of significant current interest for the development of probe molecules and drug leads. However, they suffer from certain limitations. PROTACs are rule-breaking molecules with sub-optimal cellular permeability, solubility, and other drug-like properties. In particular, they exhibit an unusual dose-response curve where high concentrations of the bivalent molecule inhibit degradation activity, a phenomenon known as the hook effect. This will likely complicate their use in vivo. In this study, we explore a novel approach to create PROTACs that do not exhibit a hook effect. This is achieved by equipping the target protein and E3 ubiquitin ligase ligands with functionalities that undergo rapid and reversible covalent assembly in cellulo. We report the development of Self-Assembled Proteolysis Targeting Chimeras that mediate the degradation of the Von Hippel-Lindau E3 ubiquitin ligase and do not evince a hook effect.
Supplementary Information from The Signatures of Autozygosity among Patients with Colorectal Cancer
2023-03-30
preprintOpen accessSenior authorSupplementary Information from The Signatures of Autozygosity among Patients with Colorectal Cancer
Data from GROα Is Highly Expressed in Adenocarcinoma of the Colon and Down-Regulates Fibulin-1
2023-03-31
preprintOpen access<div>Abstract<p><b>Purpose:</b> The growth-related oncogene α (GROα) is a secreted interleukin-like molecule that interacts with the CXCR2 G-protein–coupled receptor. We found that the mRNA and protein products of <i>GROα</i> are more highly expressed in neoplastic than normal colon epithelium, and we studied potential mechanisms by which GROα may contribute to tumor initiation or growth.</p><p><b>Experimental Design:</b> Cell lines that constitutively overexpress GROα were tested for growth rate, focus formation, and tumor formation in a xenograft model. GROα expression was determined by Affymetrix GeneChip (241 microdissected colon samples), real-time PCR (<i>n</i> = 32), and immunohistochemistry. Primary colon cancer samples were also employed to determine copy number changes and loss of heterozygosity related to the <i>GROα</i> and <i>fibulin-1</i> genes.</p><p><b>Results:</b> In cell cultures, GROα transfection transformed NIH 3T3 cells, whereas inhibition of GROα by inhibitory RNA was associated with apoptosis, decreased growth rate, and marked up-regulation of the matrix protein fibulin-1. Forced expression of GROα was associated with decreased expression of fibulin-1. Expression of GROα mRNA was higher in primary adenocarcinomas (<i>n</i> = 132), adenomas (<i>n</i> = 32), and metastases (<i>n</i> = 52) than in normal colon epithelium (<i>P</i> < 0.001). These results were confirmed by real-time PCR and by immunohistochemistry. Samples of primary and metastatic colon cancer showed underexpression of fibulin-1 when compared with normal samples. There were no consistent changes in gene copy number of <i>GROα</i> or <i>fibulin-1</i>, implying a transcriptional basis for these findings.</p><p><b>Conclusion:</b> Elevated expression of GROα is frequent in adenocarcinoma of the colon and is associated with down-regulation of the matrix protein fibulin-1 in experimental models and in clinical samples. GROα overexpression abrogates contact inhibition in cell culture models, whereas inhibition of GROα expression is associated with apoptosis. Importantly, coexpression of fibulin-1 with GROα abrogates key aspects of the transformed phenotype, including tumor formation in a murine xenograft model. Targeting GRO proteins may provide new opportunities for treatment of colon cancer.</p></div>
Recent grants
NIH · $4.4M · 2009
NIH · $1.9M · 1998
NIH · $25.2M · 2015–2027
NIH · $1.6M · 2002
NIH · $18.7M · 2007
Frequent coauthors
- 84 shared
Manny D. Bacolod
Cornell University
- 65 shared
Sarah F. Giardina
Cornell University
- 58 shared
Philip B. Paty
- 45 shared
Reyna Favis
- 45 shared
Daniel A. Notterman
Princeton University
- 39 shared
Weiguo Cao
Clemson University
- 37 shared
Jianmin Huang
Fujian Provincial Hospital
- 37 shared
Steven A. Soper
University of Kansas
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