About

Vikki Noonan is a Clinical Professor of Oral and Maxillofacial Pathology and a Clinical Professor of Oral and Maxillofacial Surgery at the Boston University Henry M. Goldman School of Dental Medicine. She serves as the Director of the Division of Oral and Maxillofacial Pathology and is involved in the clinical oral pathology practice within the Department of Oral and Maxillofacial Surgery. Dr. Noonan completed her dental training at Tufts University School of Dental Medicine and earned her Doctorate of Medical Sciences in Oral Biology, along with Certification in Oral and Maxillofacial Pathology, from Harvard University School of Dental Medicine. She is a Fellow in the American Academy of Oral and Maxillofacial Pathology and a Diplomate of the American Board of Oral and Maxillofacial Pathology. Her primary interests include clinical and surgical oral and maxillofacial pathology, dental education at both pre-doctoral and post-doctoral levels, and research related to the biological basis of oral cancer.

Research topics

• Pathology
• Medicine
• Dentistry
• Surgery
• Internal medicine
• Dermatology
• Pediatrics
• Immunology
• Gastroenterology
• Radiology
• Anatomy
• Orthodontics
• Oncology
• Biology

Selected publications

• Pemphigus foliaceus transforming to pemphigus vulgaris: a case report

  Frontiers in Medicine · 2026-01-02

  articleOpen access

  Pemphigus represents a family of acantholytic autoimmune vesiculobullous diseases. It is classified into multiple subtypes, the two most common of which are pemphigus vulgaris and pemphigus foliaceus. The transition between these two subtypes is uncommon. In this report, we discuss a unique case of biopsy-proven pemphigus foliaceus transitioning to pemphigus vulgaris.

  PublisherOA PDFDOI

• Clinicopathologic correlation case 2: multifocal, symptomatic oral mucosal lesions

  Oral Surgery Oral Medicine Oral Pathology and Oral Radiology · 2025-04-24

  articleSenior author
  PublisherDOI

• Oral Hairy Leukoplakia

  New England Journal of Medicine · 2025-06-04

  letter1st authorCorresponding
  PublisherDOI

• Segmental odontomaxillary dysplasia: a case report

  Oral Surgery Oral Medicine Oral Pathology and Oral Radiology · 2025-07-21

  articleSenior author
  PublisherDOI

• IgG/IgA pemphigus - a rare subtype of pemphigus: a case report

  Oral Surgery Oral Medicine Oral Pathology and Oral Radiology · 2025-07-21

  articleSenior author
  PublisherDOI

• Data from A YAP/TAZ-Regulated Molecular Signature Is Associated with Oral Squamous Cell Carcinoma

  2023-04-03

  preprintOpen access

  <div>Abstract<p>Oral squamous cell carcinoma (OSCC) is a prevalent form of cancer that develops from the epithelium of the oral cavity. OSCC is on the rise worldwide, and death rates associated with the disease are particularly high. Despite progress in understanding the mutational and expression landscape associated with OSCC, advances in deciphering these alterations for the development of therapeutic strategies have been limited. Further insight into the molecular cues that contribute to OSCC is therefore required. Here, we show that the transcriptional regulators YAP (<i>YAP1</i>) and TAZ (<i>WWTR1</i>), which are key effectors of the Hippo pathway, drive protumorigenic signals in OSCC. Regions of premalignant oral tissues exhibit aberrant nuclear YAP accumulation, suggesting that dysregulated YAP activity contributes to the onset of OSCC. Supporting this premise, we determined that nuclear YAP and TAZ activity drives OSCC cell proliferation, survival, and migration <i>in vitro</i>, and is required for OSCC tumor growth and metastasis <i>in vivo</i>. Global gene expression profiles associated with YAP and TAZ knockdown revealed changes in the control of gene expression implicated in protumorigenic signaling, including those required for cell cycle progression and survival. Notably, the transcriptional signature regulated by YAP and TAZ significantly correlates with gene expression changes occurring in human OSCCs identified by The Cancer Genome Atlas (TCGA), emphasizing a central role for YAP and TAZ in OSCC biology.</p><p><b>Implications:</b> This study defines a YAP/TAZ-regulated transcriptional program in OSCC and reveals novel roles for nuclear YAP/TAZ activity in the onset and progression of this cancer. <i>Mol Cancer Res; 13(6); 957–68. ©2015 AACR</i>.</p></div>

  PublisherDOI

• Supplementary Table 6 from A YAP/TAZ-Regulated Molecular Signature Is Associated with Oral Squamous Cell Carcinoma

  2023-04-03

  supplementary-materialsOpen access

  <p>Supplementary Table 6. Hyper-enrichment analysis of YAP/TAZ-regulated molecular signature.</p>

  PublisherDOI

• Supplementary Table 5 from A YAP/TAZ-Regulated Molecular Signature Is Associated with Oral Squamous Cell Carcinoma

  2023-04-03

  supplementary-materialsOpen access

  <p>Supplementary Table 5. Gene list from the cluster analysis in Fig 5B.</p>

  PublisherDOI

• Supplementary Figure S4 from A YAP/TAZ-Regulated Molecular Signature Is Associated with Oral Squamous Cell Carcinoma

  2023-04-03

  preprintOpen access

  <p>Supplementary Figure S4. Correlation of YAP/TAZ activity with respect to tumor grade and stage using ASSIGN.</p>

  PublisherDOI

• Data from A YAP/TAZ-Regulated Molecular Signature Is Associated with Oral Squamous Cell Carcinoma

  2023-04-03

  preprintOpen access

  <div>Abstract<p>Oral squamous cell carcinoma (OSCC) is a prevalent form of cancer that develops from the epithelium of the oral cavity. OSCC is on the rise worldwide, and death rates associated with the disease are particularly high. Despite progress in understanding the mutational and expression landscape associated with OSCC, advances in deciphering these alterations for the development of therapeutic strategies have been limited. Further insight into the molecular cues that contribute to OSCC is therefore required. Here, we show that the transcriptional regulators YAP (<i>YAP1</i>) and TAZ (<i>WWTR1</i>), which are key effectors of the Hippo pathway, drive protumorigenic signals in OSCC. Regions of premalignant oral tissues exhibit aberrant nuclear YAP accumulation, suggesting that dysregulated YAP activity contributes to the onset of OSCC. Supporting this premise, we determined that nuclear YAP and TAZ activity drives OSCC cell proliferation, survival, and migration <i>in vitro</i>, and is required for OSCC tumor growth and metastasis <i>in vivo</i>. Global gene expression profiles associated with YAP and TAZ knockdown revealed changes in the control of gene expression implicated in protumorigenic signaling, including those required for cell cycle progression and survival. Notably, the transcriptional signature regulated by YAP and TAZ significantly correlates with gene expression changes occurring in human OSCCs identified by The Cancer Genome Atlas (TCGA), emphasizing a central role for YAP and TAZ in OSCC biology.</p><p><b>Implications:</b> This study defines a YAP/TAZ-regulated transcriptional program in OSCC and reveals novel roles for nuclear YAP/TAZ activity in the onset and progression of this cancer. <i>Mol Cancer Res; 13(6); 957–68. ©2015 AACR</i>.</p></div>

  PublisherDOI

Frequent coauthors

• Sadru Kabani

  56 shared

• Maria A. Kukuruzinska

  Boston University

  35 shared

• George Gallagher

  30 shared

• Stefano Monti

  24 shared

• Xaralabos Varelas

  Boston University

  23 shared

• Manish V. Bais

  Boston University

  23 shared

• Vinay K. Kartha

  VIR Biotechnology (United States)

  14 shared

• Liye Zhang

  13 shared

Labs

• Division of Oral and Maxillofacial Pathology, Boston University Henry M. Goldman School of Dental MedicinePI

Education

• Other, Dental Medicine

  Tufts University

• Other, Oral Biology

  Harvard University

• Other, Oral and Maxillofacial Pathology

  Harvard University

Awards & honors

• Fellow, American Academy of Oral and Maxillofacial Pathology
• Diplomate, American Board of Oral and Maxillofacial Patholog…