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Candace Reveles

  • Clinical Assistant I
  • Assistant Professor, Pathology - (Clinical Scholar Track)
Contact
  • candacer@arizona.edu
  • Bio
  • Interests
  • Courses
  • Scholarly Contributions

Biography

I am a native Tucsonan who completed my Bachelor of Science in Molecular and Cellular Biology at the University of Arizona, followed by medical school and anatomic and clinical pathology residency training at the University of Arizona College of Medicine. I then completed a hematopathology fellowship at Stanford University. I am board-certified in Anatomic and Clinical Pathology, as well as Hematopathology.

I am currently an Assistant Professor of Pathology at Banner University Medical Center–Tucson, where I practice hematopathology and serve as the Hematopathology Fellowship Director. I greatly enjoy teaching and working with residents and fellows and am actively involved in trainee education, mentorship, and curriculum development.

My academic interests include diagnostic hematopathology, medical education, and translational collaboration with clinical colleagues. I have submitted my application for promotion to Associate Professor and remain committed to continued growth as a clinician-educator, mentor, and academic pathologist.

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

  • Hematopathology, The American Board of Pathology (2020)
  • Anatomic and Clinical Pathology, The American Board of Pathology (2019)

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Interests

Research

My scholarly activities are primarily focused on collaborative, case-based scholarship in diagnostic hematopathology. I work closely with residents, fellows, and clinical colleagues to identify interesting, rare, or diagnostically challenging cases and develop them into case reports, case series, and conference abstracts for submission to peer-reviewed journals and national meetings such as the Society for Hematopathology, USCAP, and ASCP. Through these collaborations, I emphasize clinicopathologic correlation, thoughtful use of ancillary studies, and diagnostic findings and their clinical implications.In addition, I have an interest in educational scholarship related to hematopathology training, curriculum development, and innovative teaching models. My long-term scholarly goal is to continue building a portfolio of clinically relevant scholarship that advances diagnostic practice while fostering mentorship and academic development of trainees.

Teaching

My primary teaching interests center on diagnostic hematopathology education across the continuum of training, including medical students, residents, and fellows. I am particularly interested in developing structured, case-based and learner-centered curriculum that integrate morphologic evaluation, immunophenotyping, molecular diagnostics, and clinical correlation. I enjoy mentoring trainees in developing diagnostic reasoning, confidence in independent sign-out, and effective communication of complex pathologic findings in clinically meaningful reports. Additional interests include curriculum development for hematopathology fellowship training, innovative educational models such as resident-led conferences and call read-out sessions. I am committed to fostering a supportive learning environment that promotes professional growth, curiosity, and excellence in patient-centered pathology practice.

Courses

2025-26 Courses

  • Clinical Pathology
    PATH 850B (Spring 2026)
  • Mechanisms of Human Disease
    CBIO 515 (Spring 2026)
  • Mechanisms of Human Disease
    CMM 415 (Spring 2026)
  • Mechanisms of Human Disease
    PATH 415 (Spring 2026)
  • Mechanisms of Human Disease
    PATH 515 (Spring 2026)
  • Mechanisms of Human Disease
    PCOL 515 (Spring 2026)
  • Mechanisms of Human Disease
    CMM 415 (Fall 2025)
  • Mechanisms of Human Disease
    PATH 415 (Fall 2025)

2024-25 Courses

  • Clinical Pathology
    PATH 850B (Spring 2025)
  • 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)
  • Clinical Pathology
    PATH 850B (Fall 2024)

2023-24 Courses

  • Clinical Pathology
    PATH 850B (Spring 2024)
  • 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)
  • Clinical Pathology
    PATH 850B (Fall 2023)

2022-23 Courses

  • 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)

Related Links

UA Course Catalog

Scholarly Contributions

Journals/Publications

  • Menghani, S. V., Diaz-Hanson, J. P., Heimbigner, A., Wakefield, C., Fuchs, D., Reveles, C. Y., Spier, C. M., Amaraneni, A., & Kumar, A. (2023). Peripheral T-Cell Lymphoma in a Patient Previously Diagnosed With Sarcoidosis. Journal of Hematology, 272-276. doi:10.14740/jh1173
    More info
    Sarcoidosis is a multisystem disorder characterized by granulomatous inflammation on histopathological evaluation. Diagnosis of sarcoidosis requires thorough elimination of malignancy and alternative causes of noncaseating granulomatous inflammation. Sarcoidosis and several subtypes of lymphoma have similar clinical presentations and can potentially have similar histopathological findings. Patients with a histopathology-confirmed diagnosis of sarcoidosis are at higher risk of developing malignancies. In this report, we present a case of a 64-year-old male diagnosed with sarcoidosis 2 years before presenting to the emergency department with a 4-month history of generalized weakness, cough, and very high fever. After a thorough workup involving cervical lymph node biopsy and bone marrow biopsy, he was diagnosed with peripheral T-cell lymphoma, not otherwise specified (PTCL, NOS). Due to the patient's current lymphoma diagnosis and features noted on pathology, a retrospective review of the prior biopsy specimen was performed, finding similar hematopathological features on both initial lymph node biopsy diagnosing sarcoidosis and current biopsies diagnosing lymphoma. Given these findings, our patient likely had early manifestation of PTCL misdiagnosed as sarcoidosis. In summary, lymphoma should be considered in all patients with suspected sarcoidosis, especially those who do not respond to treatment or who present with persistent hematological abnormalities.
  • 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.0000000000002653
    More info
    The 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

Presentations

  • Reveles, C., Perry, C. S., Fuchs, D., Heimbigner, A., & Hansen Smith, M. (2023, November). From Sarcoidosis to Lymphoma: A Diagnostic Journey to Peripheral T Cell Lymphoma, NOS

    Presentation by Mary Hansen Smith, MD
    . Progress in T- and NK-Cell Lymphomas/LeukemiasSociety for Hematopathology.

Profiles With Related Publications

  • Lisa M Rimsza
  • Emmanuel Katsanis
  • Deborah Fuchs
  • Holly E Pariury
  • Catherine S Perry
  • Maria A Proytcheva

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