Candace Reveles
- Assistant Professor, Pathology - (Clinical Scholar Track)
- (520) 626-6830
- Arizona Health Sciences Center, Rm. 5205
- Tucson, AZ 85724
- candacer@arizona.edu
Biography
I am a home-grown, native Tucsonan. I completed my bachelors of science in Molecular & Cellular Biology at the University of Arizona, where I also went on to complete medical school and residency training. I completed a hematopathology fellowship at Stanford. I am boared-certified in Clinical and Anatomic Pathology, as well as Hematopathology. Currently, I am an assistant professor at Banner University Medical Center, where I practive Hematopathology. I am also training as an HLA fellow where I will be able to sign out HLA cases in addition to my hematopathology role.
Degrees
- M.D.
- University of Arizona, Tucson, Arizona, United States
- B.S. Molecular and Cellular Biology
- University of Arizona, Tucson, Arizona, United States
Licensure & Certification
- Anatomic and Clinical Pathology, The American Board of Pathology (2019)
- Hematopathology, The American Board of Pathology (2020)
Interests
Research
I am interested in myeloid malignancies, including acute myeloid leukemias as well as myeloproliferative neoplasms.
Teaching
I have a keen interest in the edification of residents. I hope that by the end of residency, all residents graduating from our program will be able to recognize and diagnose basic hematopathology diagnostic entities and perceive which cases should be sent out for expert opinion in the private practice setting.
Courses
2024-25 Courses
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Mechanisms of Human Disease
CBIO 515 (Spring 2025) -
Mechanisms of Human Disease
CMM 415 (Spring 2025) -
Mechanisms of Human Disease
CMM 515 (Spring 2025) -
Mechanisms of Human Disease
PATH 415 (Spring 2025) -
Mechanisms of Human Disease
PATH 515 (Spring 2025) -
Mechanisms of Human Disease
PCOL 515 (Spring 2025)
2023-24 Courses
-
Mechanisms of Human Disease
CBIO 515 (Spring 2024) -
Mechanisms of Human Disease
CMM 415 (Spring 2024) -
Mechanisms of Human Disease
PATH 415 (Spring 2024) -
Mechanisms of Human Disease
PATH 515 (Spring 2024)
2022-23 Courses
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Clinical Pathology
PATH 850B (Spring 2023) -
Clinical Pathology
PATH 850B (Fall 2022)
2021-22 Courses
-
Clinical Pathology
PATH 850B (Fall 2021)
2020-21 Courses
-
Clinical Pathology
PATH 850B (Spring 2021)
Scholarly Contributions
Journals/Publications
- Shponka, V., Rimsza, L. M., Reveles, C. Y., Maguire, A., Kendrick, S., Jaramillo, M. C., & Alam, S. (2020). Frequent expression of activation-induced cytidine deaminase in diffuse large B-cell lymphoma tissues from persons living with HIV.. AIDS (London, England), 34(14), 2025-2035. doi:10.1097/qad.0000000000002653More infoThe increased risk for persons living with HIV to develop diffuse large B-cell lymphoma (DLBCL) even in the post-antiretroviral therapy eras suggests a role beyond immunosuppression in lymphoma development. However, the mechanisms leading to lymphoma in the HIV setting are not fully understood. HIV is known to induce activation-induced cytidine deaminase (AID) levels in nonneoplastic B cells in vitro and chronic AID expression may play an important role in lymphomagenesis. Although AID expression is observed in B-cell lymphoma, studies in HIV-associated DLBCL are limited..In this study, we conducted a retrospective review of DLBCL tissues from patients with and without HIV infection to compare expression of AID and B-cell receptors potentially involved in HIV and B-cell interaction..We evaluated DLBCL formalin-fixed paraffin-embedded tissues from 72 HIV-seropositive and 58 HIV-seronegative patients for AID, DC-SIGN, and CD40 protein expression. BCL2 and MYC, two well established prognostically significant oncoproteins in DLBCL, were also assessed at the protein and mRNA levels. Subset analysis was performed according to DLBCL subtype and EBV status..Of note, AID expression was more frequent in HIV-associated DLBCL compared with non-HIV-associated DLBCL regardless of cell-of-origin subtype, and also displayed significantly less BCL2 expression. Despite no direct correlation with AID expression, the HIV-DLBCL tissues also exhibited high levels of the DC-SIGN receptor..Collectively, these findings support a potential role for AID in the pathogenesis of HIV-associated lymphomas and suggest the need of further investigations into the involvement of the DC-SIGN receptor-signaling pathway.
- Anwer, F., Reveles, C. Y., Katsanis, E., Okolo, O. N., & Yun, S. (2017). Allogeneic Transplant in ELANE and MEFV Mutation Positive Severe Cyclic Neutropenia: Review of Prognostic Factors for Secondary Severe Events. Case Reports in Hematology, 2017, 1-7. doi:10.1155/2017/5375793