About

Mike Arnold is a Professor and the Director of The Gardens at Texas A&M University, affiliated with the Department of Horticultural Sciences within the College of Agriculture & Life Sciences. His educational background includes a B.S. in Business Administration and a B.S. in Agriculture from Ohio State University, as well as an M.S. in Landscape Horticulture from Ohio State University. He earned his Ph.D. in Horticultural Sciences from North Carolina State University. His professional focus is rooted in horticultural sciences, with a particular emphasis on sustainable interior and exterior green space management, floral design, and viticulture and enology. As a faculty member, he contributes to the department's academic and research missions, guiding undergraduate and graduate students, and engaging in extension activities. His leadership role as Director of The Gardens at TAMU underscores his commitment to horticultural education, research, and community engagement.

Research topics

• Biology
• Cancer research
• Pathology
• Genetics
• Medicine
• Gastroenterology
• Internal medicine

Selected publications

• Artificial intelligence in the diagnosis of Hirschsprung disease: A scoping review and rationale for a multicentric approach

  Journal of Pediatric Surgery · 2026-01-19 · 1 citations

  article
  PublisherDOI

• Therapy-related mutational signatures in subsequent neoplasms among survivors of childhood cancer

  Cancer Discovery · 2026-04-19

  articleOpen access

  Childhood cancer survivors have heightened risk of developing subsequent neoplasms (SNs) related to therapy. We analyzed whole-genome, exome and RNA sequencing of 200 breast, meningioma, and thyroid SNs, which developed a median of 26.4 years after childhood cancer, among 160 survivors. Meningioma and thyroid SNs were enriched for driver gene rearrangements compared to de novo tumors, including NF2-disrupting alterations and kinase fusions potentially induced by radiation. Radiation correlated with increased insertion-deletion signature ID5. Nitrogen mustard treatment correlated with elevated "flat" signature SBS5 in breast and meningioma SNs; in vitro, these agents caused an unresolved flat signature associated with multiple flat COSMIC signatures. In meningioma, platinum therapy correlated with NF2 splice-site variants. Analysis of 19 multi-sample survivors revealed intrapatient heterogeneity in meningioma, including clonally independent tumors. These results demonstrate the long-term impact of childhood cancer treatment on the genomes of SNs developing in adulthood, which may guide SN treatment and prevention.

  PublisherDOI

• 1554 ALK-rearranged Epithelioid Mesenchymal Neoplasms in Children and Young Adults Represent an Epigenetically Diverse Group of Tumors

  Laboratory Investigation · 2026-03-01

  articleOpen access
  PublisherOA PDFDOI

• The Abundance of Available Precursor Cells Can Drive Pediatric Cancer Incidence: Insights From an Algebraic Model

  Archives of Pathology & Laboratory Medicine · 2025-11-25

  articleOpen accessSenior author

  Context.—: Cancers in children show incidence distributions by age that cannot be explained by mathematical models designed to understand carcinogenesis in adults. Unlike carcinomas that tend to increase in incidence with age, pediatric cancers demonstrate unique phases of increasing incidence with a peak age of incidence followed by declining incidence. To date, mathematical models of this phenomenon are limited to statistical representations describing the frequency of oncogenic second genetic alterations in genetically susceptible individuals. Objective.—: To develop a mathematical description of pediatric cancer incidence, we created an algebraic model based on the concept that a limited cell population is available to become Ewing sarcoma. Design.—: Our algebraic models for the incidence of Ewing sarcoma express incidence as a function of both the risk of oncogenic genetic events and the number of available cells capable of becoming Ewing sarcoma. Results.—: Our models allow predictions about changes in the abundance of available cells capable of undergoing oncogenesis. This concept can explain the anatomic distribution and incidence of Ewing sarcoma by age. We believe that this concept also explains how the same genetic alterations can be seen in diverse cancer types. Conclusions.—: Verification of our models for Ewing sarcoma with experimental data can predict how the risk of oncogenic events for pediatric cancers changes with age. Our algebraic model is a novel articulation of the biological concepts that drive pediatric oncogenesis and can be applied to the observed age distributions of nearly all pediatric cancer types.

  PublisherOA PDFDOI

• Nonorbital, Nonparameningeal Head and Neck Rhabdomyosarcoma: A Report From the Children's Oncology Group

  Pediatric Blood & Cancer · 2025-03-19 · 1 citations

  articleOpen access

  ABSTRACT Background Rhabdomyosarcoma (RMS) is the most common pediatric head and neck soft‐tissue sarcoma. Intergroup Rhabdomyosarcoma Study I–IV demonstrated that patients with alveolar RMS (ARMS), Group III disease, or clinically involved regional lymph nodes had a worse prognosis. The outcomes and prognostic features of patients with nonorbital, nonparameningeal head and neck (NONPHN) RMS treated in subsequent Children's Oncology Group (COG) trials have not been reported. Procedure Patients enrolled in COG low‐risk (D9602 or ARST0331), intermediate‐risk (D9803 or ARST0531), and high‐risk (D9802, ARST0431, or ARST08P1) trials were included. All patients received chemotherapy. Those with Group I (completely resected) ARMS and those with Group II (microscopic residual) or Group III (macroscopic residual) RMS received 36–50.4 Gy adjuvant radiotherapy (RT). Results One hundred seventy‐two patients with NONPHN RMS were treated across the seven trials. Most patients had cheek primaries (30%), Group II (38%) or Group III (34%) disease, no clinical or radiological evidence of nodal involvement (N 0 , 80%), and received RT (70%). The median follow‐up was 7.7 years. Five‐year event‐free survival and overall survival were 70.8% and 83.7%, respectively. The regional failure rate for patients with N 0 disease was 2%. Conclusions Outcomes for patients with NONPHN RMS were similar to contemporary studies. Despite lower RT target volumes on the ARST‐series versus the D‐series protocols, patients with Group III tumors maintained comparable outcomes. Low regional failure rates suggested that sentinel lymph node sampling in patients with N 0 disease and elective nodal RT in patients with ARMS and N 0 disease are not necessary.

  PublisherOA PDFDOI

• The impact of genetic ancestry on survival outcomes in pediatric rhabdomyosarcoma: A report from the Children’s Oncology Group

  Human Genetics and Genomics Advances · 2025-06-09

  articleOpen access

  Emerging evidence suggests genetic ancestry may influence childhood cancer outcomes, but its impact on pediatric rhabdomyosarcoma (RMS) is unknown. We explored genetic ancestry's impact on survival among children with RMS. This multi-center observational cohort study is a secondary analysis of previously collected biobanking, genomic, and clinical data. The study included 920 individuals with newly diagnosed RMS under 40 years of age enrolled from 2005 to 2017 under the COG soft tissue sarcoma biobanking protocol D9902. The primary endpoints were (1) event-free survival (EFS), defined as the time from study enrollment to tumor recurrence/progression, secondary malignancy, or death from any cause; and (2) overall survival (OS), defined as the time from study enrollment to death from any cause. Genetic ancestry was estimated using Grafpop software, and Cox regression assessed the association between genetic ancestry and EFS and OS, considering RMS overall, by fusion status, and by histological subtype. Covariates included sex, age at diagnosis, tumor stage, and histology, except during stratified analyses. In embryonal RMS and PAX3/7:FOXO1 fusion-negative RMS, individuals with South Asian or Asian-Pacific Islander ancestry showed worse EFS (hazard ratio [HR] 2.06, 95% confidence interval [CI] 1.07-3.97, p = 0.03 and HR 2.01, 95% CI 1.07-3.76, p = 0.03, respectively) and OS (HR 2.30, 95% CI 1.09-4.84, p = 0.03 and HR 2.33, 95% CI 1.15-4.70, p = 0.020, respectively) compared to those with primarily European genetic ancestry. These findings suggest that genetic ancestry influences survival outcomes within RMS subtypes, and further understanding may improve precision-medicine-based efforts.

  PublisherDOI

• Abstract 712: The genomic landscape of subsequent breast, meningioma, and thyroid neoplasms after treatment for childhood cancer: a report from the Childhood Cancer Survivor Study

  Cancer Research · 2025-04-21

  article

  Abstract While >85% of children with cancer will become five-year survivors, they are at substantially increased risk of developing subsequent neoplasms (SNs) in part due to DNA-damaging therapy. However, the effects of primary cancer therapy on the SN genomic landscape are unknown. We utilized biospecimens collected through the Childhood Cancer Survivor Study (CCSS) and employed whole-genome, exome, and RNA sequencing to analyze 199 SNs (median diagnosis age of 37.8 years, range 13.0-54.4) and matched germline tissue from 159 childhood cancer survivors, including 62 breast, 57 meningioma, and 42 thyroid SN patients. Overall, each SN type had similar somatic driver alterations to corresponding de novo cancers though at different frequencies, including increased frequency of kinase fusions and copy number alterations in thyroid SNs compared to de novo thyroid cancers. Meningioma and thyroid SNs had significantly elevated somatic single-nucleotide variant (SNV) and insertion-deletion (indel) burdens compared to de novo tumors from published cohorts such as The Cancer Genome Atlas, while breast SNs and de novo breast cancers had similar SNV and indel burdens. Prior treatment with nitrogen mustards, such as cyclophosphamide, was associated with increased levels of ubiquitous clock-like SNV mutational signature SBS5 in breast and meningioma SNs. We confirmed this association experimentally by treating cultured breast epithelial cells with an active cyclophosphamide metabolite followed by WGS, which revealed an SBS5-like signature induced by the treatment. In addition, we observed platinum-induced signatures SBS31 and SBS35 in 4 of 5 meningioma and thyroid SNs previously treated with platinum therapy, and identified and functionally validated NF2 splice variants which were predicted to be platinum-induced in meningioma based on their occurrence at platinum signature hotspots. Driver alterations occurred evolutionarily early in most breast and thyroid SNs (12 of 14 multi-sample patients) as evidenced by their truncal status (detected in all samples at clonal variant allele fractions), while most meningioma patients (3 of 5) show intrapatient driver divergence, including a lack of shared mutations indicative of genetically independent tumors. Together, these results demonstrate the long-term impact of childhood cancer treatment on the genomes of SNs developing in adulthood, which may guide efforts to treat and prevent SNs. Citation Format: Samuel W. Brady, Michael A. Arnold, Mingjuan Wang, Ramzi Alsallaq, Li Dong, Mohammad A. Khan, Wentao Yang, Kayla L. Stratton, Wei Liu, Yan Chen, Emily Plyler, Jacob Steele, Brent B. Powers, David Rosenfeld, Michael N. Edmonson, Sasi Arunachalam, Heather L. Mulder, Deo Kumar Srivastava, Michael Rusch, Vikki Nolan, Aaron McDonald, Lucie Turcotte, Cindy Im, John Easton, Zhaoming Wang, Wendy Leisenring, Miriam Conces, Joseph P. Neglia, Yutaka Yasui, Smita Bhatia, Jinghui Zhang, Gregory T. Armstrong. The genomic landscape of subsequent breast, meningioma, and thyroid neoplasms after treatment for childhood cancer: a report from the Childhood Cancer Survivor Study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 712.

  PublisherDOI

• Treatment, toxicity, and mortality after subsequent breast cancer in female survivors of childhood cancer

  Nature Communications · 2025-03-31 · 4 citations

  articleOpen access

  Childhood cancer survivors, particularly those who received chest radiotherapy, are at high risk for developing subsequent breast cancer. Minimizing long-term toxicity risks associated with additional radiotherapy and chemotherapy is a priority, but therapeutic tradeoffs have not been comprehensively characterized and their impact on survival is unknown. In this study, 431 female childhood cancer survivors with subsequent breast cancer from a multicenter retrospective cohort study were evaluated. Compared with one-to-one matched females with first primary breast cancer, survivors are as likely to be prescribed guideline-concordant treatment (N = 344 pairs; survivors: 94%, controls: 93%), but more frequently undergo mastectomy (survivors: 81%, controls: 60%) and are less likely to be treated with anthracyclines (survivors: 47%, controls: 66%) or radiotherapy (survivors: 18%, controls: 61%). Despite this, survivors have nearly 3.5-fold (95% CI = 2.17-5.57) greater mortality risk. Here, we show survivors with subsequent breast cancer face excess mortality despite therapeutic tradeoffs and require specialized treatment guidelines.

  PublisherOA PDFDOI

• 1338 Mathematical Models of Ewing Sarcoma Incidence Can Estimate the Frequency of Sarcomagenic EWSR1 Gene Fusion Events

  Laboratory Investigation · 2025-03-01

  articleOpen access1st authorCorresponding
  PublisherOA PDFDOI

• Basal cell carcinoma risk prediction in survivors of childhood cancer

  JNCI Journal of the National Cancer Institute · 2025-08-16 · 2 citations

  article

  BACKGROUND: Survivors of childhood cancer face excess risk of developing basal cell carcinoma. Age-specific basal cell carcinoma risk prediction models for survivors may support targeted screening recommendations. METHODS: We developed models predicting basal cell carcinoma risk by ages 40 and 50 years featuring detailed cancer treatment predictors, utilizing statistical and machine-learning algorithms and data from 23 166 five-year survivors in the Childhood Cancer Survivor Study, a multi-institutional retrospective cohort study. Selected models were externally validated in 5314 survivors in the St Jude Lifetime Cohort. Model discrimination and precision were evaluated using the area under the receiver operating characteristic curve (AUROC) and area under the precision-recall curve (AUPRC) and benchmarked against the current Children's Oncology Group Long-Term Follow-Up Guidelines (COG LTFU, v6.0) for skin cancer screening. RESULTS: By ages 40 and 50 years, basal cell carcinoma cumulative incidence was 5% and 15% in the Childhood Cancer Survivor Study and 7% and 21% in the St Jude Lifetime Cohort, respectively. The XGBoost algorithm-based models with treatment dose-specific predictors performed best, showing good external discrimination (age 40 years: AUROC = 0.75; age 50 years: AUROC = 0.76) and precision (age 40 years: AUPRC = 0.20; age 50 years: AUPRC = 0.52), outperforming COG LTFU Guideline-directed risk stratification (age 40 years: AUROC = 0.65; age 50 years: AUROC = 0.62; age 40 years: AUPRC = 0.09; age 50 years: AUPRC = 0.26; P < .01). These novel models reclassified 37% of survivors with COG-recommended skin cancer screening as low risk by age 40 years and 29% of survivors without COG-recommended screening as moderate or high risk by age 50 years, suggesting these recommendations overestimate risk in younger survivors and miss relevant predictors (eg, attained age, chemotherapy). CONCLUSIONS: In this study, we present validated basal cell carcinoma risk prediction models for childhood cancer survivors that outperform current practice guidelines. The associated online risk calculator can inform risk- and age-based screening recommendations.

  PublisherDOI

Frequent coauthors

• W. Todd Watson

  Texas A&M University

  151 shared

• Miriam Conces

  Nationwide Children's Hospital

  119 shared

• David N. Appel

  Plant (United States)

  119 shared

• Selene C. Koo

  St. Jude Children's Research Hospital

  110 shared

• Christina A. Arnold

  HSD Hochschule Döpfer

  81 shared

• Susana Galli

  Georgetown University

  80 shared

• Mai He

  Washington University in St. Louis

  72 shared

• Louis P. Dehner

  Washington University Medical Center

  72 shared

Education

• B.S., Agriculture

  Ohio State University

• B.S., Business Administration

  Ohio State University

• M.S., Landscape Horticulture

  Ohio State University

• Ph.D., Horticultural Sciences

  North Carolina State University