Aden V. Chudziak
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Aden V. Chudziak has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Abubakar Tauseef
School of Medicine, Creighton University, Omaha, NE 68178, USA
1 shared publication - Akaash Surendra
School of Life Sciences, Arizona State University, Tempe, AZ 85281, USA
1 shared publication - Beau Hsia
School of Medicine, Creighton University, Phoenix, AZ 85012, USA
1 shared publication - David Maliy
College of Natural Sciences, Grand Canyon University, Phoenix, AZ 85017, USA
1 shared publication - Grace S. Saglimbeni
Department of Hematology and Oncology, Creighton University School of Medicine, Phoenix, AZ 85012, USA
1 shared publication - Huijun Li
Division of Hematology and Oncology, Department of Internal Medicine, Creighton University Medical Center, Omaha, NE 68124, USA
1 shared publication
Latest Publications
- Open Access
- 16 January 2026
- Published by MDPI AG in Current Issues in Molecular Biology
- Vol. 48 (1) , 90
Genomic Landscape of Thymic Carcinoma: A Large-Scale Analysis of Somatic Mutations, Demographic Disparities, and Metastatic Drivers from the AACR Project GENIE® Cohort
Thymic carcinoma (TC) is a rare and aggressive malignancy with poor prognosis, and its genomic landscape remains incompletely defined. Identifying the somatic alterations that shape TC biology is essential for improving diagnostic precision, developing targeted therapies, and informing early detection strategies. We performed a retrospective genomic analysis of 141 TC tumor specimens from 134 patients using de-identified data from the American Association for Cancer Research (AACR) Project GENIE® database. Somatic mutations and copy number alterations (CNAs) were characterized, and statistical analyses were conducted to evaluate associations with patient demographics (sex, race) and tumor site (primary vs. metastatic). The cohort was predominantly male (56.7%) and White (56.7%). The most frequently altered genes were TP53 (27.7%), CYLD (17.6%), and CDKN2A (12.1%). Recurrent homozygous deletions at chromosome 9p21.3 involving CDKN2A and CDKN2B were common. Sex-stratified analysis revealed several significant male-specific alterations. Although the Pacific Islander subgroup was small (n = 2), preliminary analysis suggested enrichment of alterations in key cancer-associated genes, including TP53, BRCA1, and STAT5B, underscoring the need for diverse representation in TC genomics. Notably, MTOR mutations were significantly enriched in a subset of local recurrences and lymph node metastases (n = 3; q = 0.013), suggesting a potential role in disease progression. This large-scale genomic analysis reinforces the central involvement of TP53, cell-cycle control, and chromatin-modifying pathways in TC. The identification of sex-associated and race-associated mutational patterns, together with the enrichment of MTOR alterations in recurrent and metastatic disease, highlights biologically plausible mechanisms of progression and potential therapeutic vulnerabilities. These findings support the value of comprehensive genomic profiling in TC and emphasize the need for prospective, multi-omic studies to validate these observations and guide the development of more personalized treatment strategies.
- 16 January 2026
- Published by MDPI AG in Current Issues in Molecular Biology
- Vol. 48 (1) , 90
Open AccessGenomic Landscape of Thymic Carcinoma: A Large-Scale Analysis of Somatic Mutations, Demographic Disparities, and Metastatic Drivers from the AACR Project GENIE® Cohort
Thymic carcinoma (TC) is a rare and aggressive malignancy with poor prognosis, and its genomic landscape remains incompletely defined. Identifying the somatic alterations that shape TC biology is essential for improving diagnostic precision, developing targeted therapies, and informing early detection strategies. We performed a retrospective genomic analysis of 141 TC tumor specimens from 134 patients using de-identified data from the American Association for Cancer Research (AACR) Project GENIE® database. Somatic mutations and copy number alterations (CNAs) were characterized, and statistical analyses were conducted to evaluate associations with patient demographics (sex, race) and tumor site (primary vs. metastatic). The cohort was predominantly male (56.7%) and White (56.7%). The most frequently altered genes were TP53 (27.7%), CYLD (17.6%), and CDKN2A (12.1%). Recurrent homozygous deletions at chromosome 9p21.3 involving CDKN2A and CDKN2B were common. Sex-stratified analysis revealed several significant male-specific alterations. Although the Pacific Islander subgroup was small (n = 2), preliminary analysis suggested enrichment of alterations in key cancer-associated genes, including TP53, BRCA1, and STAT5B, underscoring the need for diverse representation in TC genomics. Notably, MTOR mutations were significantly enriched in a subset of local recurrences and lymph node metastases (n = 3; q = 0.013), suggesting a potential role in disease progression. This large-scale genomic analysis reinforces the central involvement of TP53, cell-cycle control, and chromatin-modifying pathways in TC. The identification of sex-associated and race-associated mutational patterns, together with the enrichment of MTOR alterations in recurrent and metastatic disease, highlights biologically plausible mechanisms of progression and potential therapeutic vulnerabilities. These findings support the value of comprehensive genomic profiling in TC and emphasize the need for prospective, multi-omic studies to validate these observations and guide the development of more personalized treatment strategies.