About

Dr. Mi-Hyeon Jang is an Associate Professor in the Department of Neurosurgery at Rutgers University. Her research focuses on regenerative medicine, specifically understanding the neurobiological mechanisms that promote regenerative processes such as adult neurogenesis, oligodendrogenesis, and myelination. Her laboratory aims to discover novel regenerative strategies to improve learning and memory functions in brain aging, as well as in neurological and neurodegenerative disorders. Building on her earlier work in brain aging, Dr. Jang's research has recently expanded to include chemotherapy-induced cognitive impairment, known as chemobrain, which resembles the brain aging process. Her team seeks to uncover molecular contributors to chemobrain to develop rational, synergistic disease-modifying therapeutic strategies that can ameliorate this condition and ultimately enhance the quality of life for cancer survivors. Dr. Jang is a core member of the Rutgers Brain Health Institute and an active full member of the Cancer Pharmacology Program at the Cancer Institute of New Jersey.

Research topics

• Neuroscience
• Biology
• Cell biology
• Genetics
• Pharmacology
• Medicine
• Biochemistry
• Internal medicine
• Cancer research

Selected publications

• Supplementary Table S1 from Reproducibility of Plasma Metabolome over 1 Year in a Population-Based Cohort of Black Breast Cancer Survivors

  2025-06-03

  supplementary-materialsOpen access

  <p>Supplementary Table S1 presents the within-person reproducibility of all metabolites in the study population, calculated as the ICC</p>

  PublisherDOI

• Supplementary Table S3 from Reproducibility of Plasma Metabolome over 1 Year in a Population-Based Cohort of Black Breast Cancer Survivors

  2025-06-03

  supplementary-materialsOpen access

  <p>Supplementary Table S3 shows that differences in within-person reproducibility across participant characteristics and pre-analytical factors varied by metabolite class and subclass</p>

  PublisherDOI

• Abstract B130: Adiposity-related metabolomic signatures and mortality in a population-based cohort of Black breast cancer survivors

  Cancer Epidemiology Biomarkers & Prevention · 2025-09-18

  article

  Abstract Background: Black women in the U.S. experience higher mortality following a breast cancer (BC) diagnosis than other racial and ethnic groups, partly due to a greater prevalence of obesity. However, the metabolic pathways linking adiposity to mortality after BC diagnosis remain unclear, and distinct metabolic signatures associated with specific adiposity measures, such as central adiposity, warrant further investigation. We aimed to identify adiposity-related metabolites associated with all-cause mortality in a large population-based cohort of Black BC survivors. Methods: In the Women's Circle of Health Follow-up Study, untargeted metabolomic profiling was performed on plasma samples from Black BC survivors (n = 603), collected ∼2 years post-diagnosis. Each log-transformed metabolite was scaled to standard deviation units. Partial Pearson correlations were used to identify metabolites associated with any of the five adiposity measures assessed at the time of blood collection: BMI, waist circumference (WC), waist-to-hip ratio (WHR), fat mass index (FMI), and lean mass index. Metabolites meeting both the Bonferroni-corrected p-value threshold (p < 0.00001) and a correlation coefficient (|r| > 0.15) were subsequently evaluated for associations with all-cause mortality (82 deaths) using multivariable-adjusted Cox proportional hazards models, with statistical significance defined as a false discovery rate < 0.05. Results: Among 805 named metabolites, 109 were associated with adiposity measures, and 11 of these were also significantly associated with all-cause mortality. Higher levels of metabolites indicative of greater adiposity, including those involved in carbohydrate metabolism [glucose (more strongly associated with WC and WHR than with BMI), mannose, and N-acetylglucosamine/N-acetylgalactosamine], lipid metabolism [glycerol, 1-stearoyl-2-docosahexaenoyl-GPE (18:0/22:6)], and secondary bile acid metabolism [glycoursodeoxycholic acid sulfate (1)], as well as N6-carbamoylthreonyladenosine and C-glycosyltryptophan, were positively associated with mortality, with HRs ranging from 1.31 to 1.60. Additionally, three metabolites that were inversely correlated with adiposity measures—asparagine (more strongly with WC, WHR, and FMI than with BMI), 1-linoleoyl-2-arachidonoyl-GPC (18:2/20:4n6), and the xenobiotic 4-hydroxychlorothalonil, a metabolite that may interact with gut microbiome—were inversely associated with mortality, with HRs ranging from 0.66 to 0.71. Conclusions: Our study identifies specific adiposity-related metabolomic signatures associated with mortality risk, including those linked to central adiposity, among Black BC survivors. These metabolites provide insights into underlying metabolic mechanisms and may inform future research and interventions to improve survival in this high-risk population. Citation Format: Bo Qin, Shromona Sarkar, Sneha Manikandan, Tengteng Wang, Nur Zeinomar, Mi-Hyeon Jang, Coral Omene, Steven C. Moore, Chi-Chen Hong, Elisa V. Bandera. Adiposity-related metabolomic signatures and mortality in a population-based cohort of Black breast cancer survivors [abstract]. In: Proceedings of the 18th AACR Conference on the Science of Cancer Health Disparities; 2025 Sep 18-21; Baltimore, MD. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2025;34(9 Suppl):Abstract nr B130.

  PublisherDOI

• Supplementary Table S4 from Reproducibility of Plasma Metabolome over 1 Year in a Population-Based Cohort of Black Breast Cancer Survivors

  2025-06-03

  supplementary-materialsOpen access

  <p>Supplementary Table S4 highlights the specific metabolites that shifted from poor to excellent within-person reproducibility and vice versa across participant characteristics and pre-analytical factors</p>

  PublisherDOI

• Data from Reproducibility of Plasma Metabolome over 1 Year in a Population-Based Cohort of Black Breast Cancer Survivors

  2025-06-03

  preprintOpen access

  <div>AbstractBackground:<p>The metabolomics approach using blood samples from epidemiologic studies has the potential to elucidate pathways or uncover biomarkers for breast cancer outcomes. Therefore, understanding the within-person reproducibility of the blood metabolome and the factors that influence metabolite levels over time in breast cancer survivors are crucial, but these remain largely unknown.</p>Methods:<p>We estimated the within-person reproducibility of plasma metabolites in 61 Black breast cancer survivors from the Women’s Circle of Health Follow-Up Study. Samples were collected from each participant at two time points, approximately 2 and 3 years after diagnosis. Untargeted metabolomic profiles were analyzed by Metabolon using ultrahigh-performance LC/MS-MS. We calculated the intraclass correlation coefficients (ICC) for each metabolite by dividing the between-person variance by the total variance. ICCs were compared across preanalytic factors (e.g., fasting) and participant characteristics using the Wilcoxon test.</p>Results:<p>Among 857 named metabolites, the median ICC was 0.58 (IQR: 0.44–0.70). Of the metabolites, 16.6% showed high within-person reproducibility (ICC ≥ 0.75), spanning all metabolite classes, whereas 65.6% had an ICC within 0.4 to 0.75, and 17.9% had an ICC < 0.4. Reasonable ICCs were also observed for nonfasting samples (median 0.53, IQR: 0.39–0.67), although lower than those for fasting samples (median 0.63, IQR: 0.45–0.77). ICCs were slightly lower in younger, nonobese participants and in women with estrogen receptor–positive breast cancer.</p>Conclusions:<p>The within-person reproducibility of plasma metabolites over 1 year among breast cancer survivors was generally acceptable.</p>Impact:<p>A single-timepoint measurement could be useful in evaluating associations between metabolites and breast cancer outcomes.</p></div>

  PublisherDOI

• Reproducibility of Plasma Metabolome over 1 Year in a Population-Based Cohort of Black Breast Cancer Survivors

  Cancer Epidemiology Biomarkers & Prevention · 2025-04-03 · 1 citations

  articleOpen access

  BACKGROUND: The metabolomics approach using blood samples from epidemiologic studies has the potential to elucidate pathways or uncover biomarkers for breast cancer outcomes. Therefore, understanding the within-person reproducibility of the blood metabolome and the factors that influence metabolite levels over time in breast cancer survivors are crucial, but these remain largely unknown. METHODS: We estimated the within-person reproducibility of plasma metabolites in 61 Black breast cancer survivors from the Women's Circle of Health Follow-Up Study. Samples were collected from each participant at two time points, approximately 2 and 3 years after diagnosis. Untargeted metabolomic profiles were analyzed by Metabolon using ultrahigh-performance LC/MS-MS. We calculated the intraclass correlation coefficients (ICC) for each metabolite by dividing the between-person variance by the total variance. ICCs were compared across preanalytic factors (e.g., fasting) and participant characteristics using the Wilcoxon test. RESULTS: Among 857 named metabolites, the median ICC was 0.58 (IQR: 0.44-0.70). Of the metabolites, 16.6% showed high within-person reproducibility (ICC ≥ 0.75), spanning all metabolite classes, whereas 65.6% had an ICC within 0.4 to 0.75, and 17.9% had an ICC < 0.4. Reasonable ICCs were also observed for nonfasting samples (median 0.53, IQR: 0.39-0.67), although lower than those for fasting samples (median 0.63, IQR: 0.45-0.77). ICCs were slightly lower in younger, nonobese participants and in women with estrogen receptor-positive breast cancer. CONCLUSIONS: The within-person reproducibility of plasma metabolites over 1 year among breast cancer survivors was generally acceptable. IMPACT: A single-timepoint measurement could be useful in evaluating associations between metabolites and breast cancer outcomes.

  PublisherDOI

• Supplementary Table S2 from Reproducibility of Plasma Metabolome over 1 Year in a Population-Based Cohort of Black Breast Cancer Survivors

  2025-06-03

  supplementary-materialsOpen access

  &lt;p&gt;Supplementary Table S2 identifies the metabolites with the lowest within-person reproducibility, defined as an ICC &lt;0.4&lt;/p&gt;

  PublisherDOI

• Recurrent and Novel Pathogenic Variants in Genes Involved with Hearing Loss in the Pakistani Population

  Molecular Diagnosis & Therapy · 2025-05-16 · 1 citations

  articleOpen access

  BACKGROUND: Molecular diagnostic rates for hereditary hearing loss vary by genetic ancestry, highlighting the importance of population-specific studies. In Pakistan, where consanguineous marriages are prevalent, genetic research has identified many autosomal recessive genes, advancing understanding of rare and novel hearing loss mechanisms. This study aimed to identify pathogenic genetic variants in 31 families from Azad Kashmir, Pakistan, presenting non-syndromic hearing loss. METHODS: We conducted exome sequencing and bioinformatics analysis, and targeted gene sequencing on 31 Pakistani families with hearing loss. RESULTS: We identified ten pathogenic, three likely pathogenic variants, and one variant of uncertain significance, comprising six nonsense, four missense, three frameshift, and one deep intronic variant, across ten hearing loss-associated genes (MYO15A, GJB2, SLC26A4, TMC1, HGF, TMIE, SLC19A2, KCNE1, ILDR, PCDH15 and MYO6) in 25 families. The overall diagnostic rate, including families with pathogenic and likely pathogenic variants, was 77.4%. GJB2 was the most frequently affected gene, identified in seven families. Thirteen out of 14 identified variants were homozygous. Notably, we identified two novel variants: MYO15A (NM_016239.4, DFNB3) c.870C>G, p.(Tyr290*) and MYO6 (NM_016239.4, DFNB37) c.3465del, p.(Pro1156Leufs*9). Additionally, we identified c.10475dupA, p.(Leu3493Alafs*25) in MYO15A (NM_016239.4, DFNB3) and c.617T>A, p.(Leu206*) in SLC26A4 (NM_000441.2, DFNB4), previously documented in ClinVar but unpublished. We also propose SLC19A2 as a candidate gene presenting as non-syndromic hearing loss, despite its association with thiamine-responsive megaloblastic anemia syndrome. CONCLUSION: Our work expands the genotypic and phenotypic spectrum of hearing loss by emphasizing the importance of investigating under-represented groups to identify unique genetic variants and clinical characteristics. Such efforts deepen understanding of genetic diversity in under-represented populations to improve diagnosis and treatment strategies.

  PublisherOA PDFDOI

• Supplementary Materials and Methods from Differential Distribution of the DNA-PKcs Inhibitor Peposertib Selectively Radiosensitizes Patient-derived Melanoma Brain Metastasis Xenografts

  2024-09-25

  preprintOpen access

  &lt;p&gt;Supplementary Materials and Data show the cell culture and western blot data&lt;/p&gt;

  PublisherDOI

• Supplementary Figure 2 from Differential Distribution of the DNA-PKcs Inhibitor Peposertib Selectively Radiosensitizes Patient-derived Melanoma Brain Metastasis Xenografts

  2024-05-02

  preprintOpen access

  &lt;p&gt;Supplemental Figure 2 shows bar graph of quantification of cells that have &gt;25 gH2Ax foci per cell in M27 cell line, after treatment with peposertib and radiation&lt;/p&gt;

  PublisherDOI

Recent grants

• NIH Grant R00MH090115

  NIH · $737k · 2015

• NIH Grant K99MH090115

  NIH · $170k · 2012

• [Jang R01AG058560 transfer] Role of BubR1 as a juvenile protective factor in hippocampal aging

  NIH · $2.3M · 2021–2024

• PQ#12; Targeting Nampt-mediated NAD+ metabolism in chemobrain

  NIH · $2.8M · 2019–2025

Frequent coauthors

• Alfredo Oliveros

  61 shared

• Mohammad Abdur Rashid

  53 shared

• Hongjun Song

  52 shared

• Guo‐li Ming

  52 shared

• Junjie U. Guo

  Affiliated Hospital of Qingdao University

  41 shared

• Yasuji Kitabatake

  Osaka University

  34 shared

• Heechul Jun

  University of California, Irvine

  30 shared

• K. Dengke

  University of California, San Francisco

  29 shared

Labs

• Mi-Hyeon Jang LaboratoryPI