- Cardiothoracic Surgery
- Cardiovascular Critical Care Medicine
- Nurse Practitioner
Clinical Fellowship, Stanford Health Care, Cardiothoracic Surgery (2024)
Board Certification, American Academy of Nurse Practitioners (2023)
Doctorate, Samuel Merritt University (2022)
Additional Clinical Info
Acquired Secondary RAS Mutation in BRAFV600E-Mutated Thyroid Cancer Patients Treated with BRAF Inhibitors.
Thyroid : official journal of the American Thyroid Association
2020; 30 (9): 1288-1296
Background: The BRAFV600E mutation is the most common driver mutation in papillary thyroid cancer (PTC) and anaplastic thyroid cancer (ATC). This mutation is considered actionable and, for BRAFV600E-mutated ATC, a BRAF inhibitor (dabrafenib) in combination with an MEK inhibitor (trametinib) is FDA approved. BRAF inhibitors have also shown efficacy in BRAFV600E-mutated PTC. However, as with all targeted therapies, resistance to these drugs eventually develops. It is essential that we understand the mechanisms of resistance to the BRAF inhibitors in thyroid cancer to develop future strategies to effectively treat these patients and improve survival. Patients: Herein, we describe four patients with thyroid cancer treated with selective BRAF inhibitors, who developed a RAS mutation in addition to the BRAFV600E mutation at progression. Results: Patients 1 and 3 acquired a KRASG12V mutation in the progressive tumor, patient 2 acquired a NRASQ61K mutation in a progressive lymph node, and patient 4 acquired NRASG13D mutation on liquid biopsy performed at the time of radiographic disease progression. Conclusion: Similar to the melanoma experience, the emergence of RAS mutations appears to act as a mechanism of resistance to BRAF inhibitors in thyroid cancers.
View details for DOI 10.1089/thy.2019.0514
View details for PubMedID 32216548
View details for PubMedCentralID PMC7869871
Genetic profiling as a clinical tool in advanced parathyroid carcinoma.
Journal of cancer research and clinical oncology
2019; 145 (8): 1977-1986
Parathyroid carcinoma (PC) is a rare endocrine malignancy with no approved systemic therapies for unresectable locally invasive or distant metastatic disease. Understanding the molecular changes in advanced PC can provide better understanding of this disease and potentially help directing targeted therapy.To evaluate tumor-specific genetic changes using next-generation sequencing (NGS) panels.All patients with advanced PC were tested for hot-spot panels using NGS panels including a 50-gene panel, a 409-gene panel if the standard 50-gene panel (Ion Torrent, Life Technology) was negative or a FoundationOne panel.The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.11 patients with advanced PC were selected to undergo molecular testing.Genetic profiles of advanced PC.Among the 11 patients, 4 patients had the 50-gene panel only, 6 had 409-gene panel after a negative 50-gene panel and 1 had FoundationOne. One patient who had 50-gene panel only also had his metastatic site (esophagus) of his tumor tested with FoundationOne. The most common mutations identified were in the PI3 K (PIK3CA, TSC1 and ATM) (4/11 patients) and TP53 (3/11) pathways. Genes not previously reported to be mutated in PC included: SDHA, TERT promoter and DICER1. Actionable mutations were found in 54% (6/11) of the patients.Mutational profiling using NGS panels in advanced PC has yielded important potentially targetable genetic alterations. Larger studies are needed to identify commonly mutated genes in advanced PC patients. Development of novel therapies targeting these cellular pathways should be considered.
View details for DOI 10.1007/s00432-019-02945-9
View details for PubMedID 31309300
- Medical Treatment of Metastatic Thyroid Cancer Surgical and Medical Management of Diseases of the Thyroid and Parathyroid Plural Publishing. 2019: 533