Giselle Lopez

Overview:

I am a physician scientist with a clinical focus on neuropathology, and a research interest in brain tumors. Originally from Maryland, I completed my undergraduate training at the University of Maryland, completing degrees in Physiology and Neurobiology as well as Spanish Language and Literature. I subsequently came to Duke for my MD and PhD, and discovered a passion for brain tumor research, and quickly realized that this was my life's calling. After completing a residency and fellowship at the University of California, San Francisco, I returned to Duke as an Assistant Professor of Pathology. Clinically, I now specialize in neuropathology, with my research focusing on brain tumors of all types. By better understanding these tumors, I hope to identify new ways to treat these tumors and improve the lives of patients with brain tumors.

Positions:

Assistant Professor in Pathology

Pathology
School of Medicine

Assistant Professor in Neurosurgery

Neurosurgery
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

B.S. 2005

University of Maryland, College Park

B.A. 2005

University of Maryland, College Park

MD./PhD. 2014

Duke University School of Medicine

Certificate, Cell And Molecular Biology

Duke University

Residency, Anatomic Pathology

University of California - San Francisco

Fellowship, Neuropathology

University of California - San Francisco

Publications:

Proinflammatory cytokines and ARDS pulmonary edema fluid induce CD40 on human mesenchymal stromal cells-A potential mechanism for immune modulation.

Human mesenchymal stem/stromal cells (hMSCs) are a promising therapy for acute respiratory distress syndrome (ARDS) and other inflammatory conditions. While considerable research has focused on paracrine effects and mitochondrial transfer that improve lung fluid balance, hMSCs are well known to have immunomodulatory properties as well. Some of these immunomodulatory properties have been related to previously reported paracrine effectors such as indoleamine-2,3-dioxygenase (IDO), but these effects cannot fully account for cell-contact dependent immunomodulation. Here, we report that CD40 is upregulated on hMSCs under the same conditions previously reported to induce IDO. Further, CD40 transcription is also upregulated on hMSCs by ARDS pulmonary edema fluid but not by hydrostatic pulmonary edema fluid. Transcription of CD40, as well as paracrine effectors TSG6 and PTGS2 remained significantly upregulated for at least 12 hours after withdrawal of cytokine stimulation. Finally, induction of this immune phenotype altered the transdifferentiation of hMSCs, one of their hallmark properties. CD40 may play an important role in the immunomodulatory effects of hMSCs in ARDS and inflammation.
Authors
Wilfong, EM; Croze, R; Fang, X; Schwede, M; Niemi, E; López, GY; Lee, J-W; Nakamura, MC; Matthay, MA
MLA Citation
Wilfong, Erin M., et al. “Proinflammatory cytokines and ARDS pulmonary edema fluid induce CD40 on human mesenchymal stromal cells-A potential mechanism for immune modulation.Plos One, vol. 15, no. 10, 2020, p. e0240319. Pubmed, doi:10.1371/journal.pone.0240319.
URI
https://scholars.duke.edu/individual/pub1462082
PMID
33021986
Source
pubmed
Published In
Plos One
Volume
15
Published Date
Start Page
e0240319
DOI
10.1371/journal.pone.0240319

Eosinophilic globules in a classic ependymoma: evidence of a possible secretory role.

A number of neoplasms of the central nervous system can demonstrate diffuse eosinophilic globules, known to be secretory products of the corresponding cell type, but they have not been a salient feature in descriptions of classic ependymoma. Here, we present a case of a posterior fossa ependymoma demonstrating glassy PAS-positive, diastase-resistant, eosinophilic globules with light microscopic and ultrastructural features resembling Reissner fiber, the secretory product of the subcommissural organ. While there has been a single published description of an ependymoma with intra- and extracellular granulofibrillary material suggested to be evidence of secretory differentiation, ours is the first case to demonstrate diffuse eosinophilic globules in an ependymoma. The extent of globules allowed full study by electron microscopy to provide new insight into the secretory material and the surrounding structures. Our findings suggest that neoplastic ependymal cells can recapitulate the secretory capacity of the subcommissural organ.
Authors
MLA Citation
Ahn, Janice S., et al. “Eosinophilic globules in a classic ependymoma: evidence of a possible secretory role.Ultrastruct Pathol, vol. 44, no. 4–6, Nov. 2020, pp. 511–18. Pubmed, doi:10.1080/01913123.2020.1843578.
URI
https://scholars.duke.edu/individual/pub1464178
PMID
33148106
Source
pubmed
Published In
Ultrastruct Pathol
Volume
44
Published Date
Start Page
511
End Page
518
DOI
10.1080/01913123.2020.1843578

EGFR PHOSPHORYLATION OF DCBLD2 RECRUITS TRAF6 AND STIMULATES AKT-PROMOTED TUMORIGENESIS

Authors
Cheng, S; Feng, H; Lopez, GY; Kim, CK; Duncan, CG; Alvarez, A; Nishikawa, R; Nagane, M; Su, A-J; Auron, PE; Hedberg, ML; Wang, L; Grandis, JR; McLendon, RE; Bigner, DD; Nakano, I; Joshi, K; Kim, S; Lin, H-K; Furnari, FB; Cavenee, WK; Hu, B; Yan, H; Cheng, S-Y
MLA Citation
Cheng, S., et al. “EGFR PHOSPHORYLATION OF DCBLD2 RECRUITS TRAF6 AND STIMULATES AKT-PROMOTED TUMORIGENESIS.” Neuro Oncology, vol. 16, no. suppl 3, Oxford University Press (OUP), 2014, pp. iii16–17. Crossref, doi:10.1093/neuonc/nou206.60.
URI
https://scholars.duke.edu/individual/pub1451307
Source
crossref
Published In
Neuro Oncology
Volume
16
Published Date
Start Page
iii16
End Page
iii17
DOI
10.1093/neuonc/nou206.60

Management of glioblastoma: State of the art and future directions.

Glioblastoma is the most common malignant primary brain tumor. Overall, the prognosis for patients with this disease is poor, with a median survival of <2 years. There is a slight predominance in males, and incidence increases with age. The standard approach to therapy in the newly diagnosed setting includes surgery followed by concurrent radiotherapy with temozolomide and further adjuvant temozolomide. Tumor-treating fields, delivering low-intensity alternating electric fields, can also be given concurrently with adjuvant temozolomide. At recurrence, there is no standard of care; however, surgery, radiotherapy, and systemic therapy with chemotherapy or bevacizumab are all potential options, depending on the patient's circumstances. Supportive and palliative care remain important considerations throughout the disease course in the multimodality approach to management. The recently revised classification of glioblastoma based on molecular profiling, notably isocitrate dehydrogenase (IDH) mutation status, is a result of enhanced understanding of the underlying pathogenesis of disease. There is a clear need for better therapeutic options, and there have been substantial efforts exploring immunotherapy and precision oncology approaches. In contrast to other solid tumors, however, biological factors, such as the blood-brain barrier and the unique tumor and immune microenvironment, represent significant challenges in the development of novel therapies. Innovative clinical trial designs with biomarker-enrichment strategies are needed to ultimately improve the outcome of patients with glioblastoma.
Authors
Tan, AC; Ashley, DM; López, GY; Malinzak, M; Friedman, HS; Khasraw, M
MLA Citation
Tan, Aaron C., et al. “Management of glioblastoma: State of the art and future directions.Ca Cancer J Clin, vol. 70, no. 4, July 2020, pp. 299–312. Pubmed, doi:10.3322/caac.21613.
URI
https://scholars.duke.edu/individual/pub1446606
PMID
32478924
Source
pubmed
Published In
Ca: a Cancer Journal for Clinicians
Volume
70
Published Date
Start Page
299
End Page
312
DOI
10.3322/caac.21613

Frequent Mutations of POT1 Distinguish Pulmonary Sarcomatoid Carcinoma From Other Lung Cancer Histologies.

INTRODUCTION: Pulmonary sarcomatoid carcinoma (PSC) is a rare subtype of non-small-cell lung cancer (NSCLC) harboring mutations in many canonical NSCLC-driver genes (eg, TP53, KRAS, MET). Protection of telomeres 1 (POT1) mutations are observed in angiosarcoma and chronic lymphocytic leukemia, but their frequency in other solid tumors, including NSCLC subtypes, has not been rigorously explored. MATERIALS AND METHODS: We analyzed next-generation sequencing data from 62,368 tumors, including 11,134 NSCLCs and 100 PSCs. We performed logistic regression to identify associations between POT1 mutation frequency and tumor histology across 184 tumor categories, adjusting for tumor mutational burden. We further explored co-occurring gene mutations in genes previously reported to underlie PSC tumorigenesis. RESULTS: Across 184 tumor categories, POT1 mutations were most frequent in PSC and were 14 times more common in PSC (28%) than in other tumor types (P = 1.23 × 10-31) and 6.7 times more common in PSC than other NSCLCs (P = 5.1 × 10-17). PSCs harboring KRAS mutations were significantly more likely to harbor POT1 mutations (P = 1.3 × 10-3), whereas those with TP53 mutations were less likely to harbor POT1 mutations (P = .037). One-fourth of POT1-mutated PSCs harbored a second POT1 mutation. Across all PSCs, 83% of POT1 mutations were in the OB1/OB2 (DNA-binding) domain (P = 1.5 × 10-5), an enrichment not observed in other tumor types. CONCLUSION: We report an unanticipated association between POT1 mutation and PSC. Unlike other molecular alterations that are frequent across NSCLC subtypes, POT1 mutations are largely unique to PSC. This finding may help to develop disease-defining molecular subgroups within PSC and presents opportunities for molecularly stratified prognostication and therapy.
Authors
MLA Citation
Shen, Erica, et al. “Frequent Mutations of POT1 Distinguish Pulmonary Sarcomatoid Carcinoma From Other Lung Cancer Histologies.Clin Lung Cancer, vol. 21, no. 6, Nov. 2020, pp. e523–27. Pubmed, doi:10.1016/j.cllc.2020.04.002.
URI
https://scholars.duke.edu/individual/pub1441311
PMID
32414627
Source
pubmed
Published In
Clin Lung Cancer
Volume
21
Published Date
Start Page
e523
End Page
e527
DOI
10.1016/j.cllc.2020.04.002

Research Areas:

Astrocytomas
Cancer
Intracranial tumors
Intracranial tumors in children
Supratentorial brain tumors
Supratentorial brain tumors in children
Tumor Cells, Cultured
Tumor Markers, Biological
Tumor Microenvironment
Tumors
Tumors--Growth