Jadee Neff

Overview:

As a diagnostic hematopathologist and molecular genetic pathologist, my clinical interests are focused on the histologic examination of tissue and bone marrow biopsies to diagnose hematologic malignancies (leukemia, lymphoma, myeloma, etc.) as well as testing DNA from tumors or from blood to detect inherited or acquired mutations that can guide therapeutic management and predict clinical outcome.  My research interests involve 1) understanding the biology of T-cell and NK-cell neoplasms; 2) defining the immunomodulatory response to neoplastic disease; 3) developing methods to monitor immune response and thereby refine tumor immunotherapy; and 4) exploring novel applications of tumor genetics in the diagnosis, prognosis, and management of cancer.

Positions:

Assistant Professor of Pathology

Pathology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

Ph.D. 2007

Mayo Clinic, Alix School of Medicine

M.D. 2011

Mayo Clinic, Alix School of Medicine

Postdoctoral Research Fellowship, Department Of Immunology

Mayo Clinic

Anatomic and Clinical Pathology Residency, Laboratory Medicine And Pathology

Mayo Clinic

Hematopathology Residency, Laboratory Medicine And Pathology

Mayo Clinic

Molecular Genetic Pathology Fellowship, Laboratory Medicine And Pathology

Mayo Clinic

Publications:

Plasma cells are essentially absent in the luminal gastrointestinal tract of patients with "complete" 22q11.2 deletion syndrome (DiGeorge syndrome).

Gastrointestinal symptoms are commonly reported in patients with 22q11.2 deletion syndrome or DiGeorge syndrome (DGS) in addition to the dominant cardiac manifestations and immunodeficiency. But literature providing specific morphologic details of the gastrointestinal tract pathology is very limited. Here, we provide the first comprehensive morphologic description of the luminal gastrointestinal tract changes in patients with DGS. Cytogenetically confirmed DGS patients were identified, clinical and laboratory data were reviewed to determine the severity of immunodeficiency, and patients were stratified into mildly immunocompromised, that is, partial DiGeorge anomaly or severely immunosuppressed, that is, complete DiGeorge anomaly groups. Gastrointestinal tract biopsies from these patients were retrospectively reviewed and compared with those from controls without the history of DGS. Patients with immunosuppressed DGS showed a near complete absence of plasma cells in the stomach, duodenum, and colon lamina propria by hematoxylin and eosin evaluation. Immunohistochemistry for CD138 used to highlight plasma cells confirmed this finding. The notable absence of plasma cells adds to the existing knowledge of the pathophysiology underlying DGS and expands the differential diagnostic considerations for this finding, which has been previously described in common variable immunodeficiency. It also provides a useful morphologic marker observable by the readily accessible light microscopy. Second, patients with DGS showed a mild increase in epithelial cell apoptosis in their colon. This finding is significant because of its overlap with morphologic features of gastrointestinal graft versus host disease as thymus transplantation is being used as a treatment option for patients with complete DGS.
Authors
Pendse, AA; Maule, JG; Neff, JL; McCall, S
MLA Citation
Pendse, Avani A., et al. “Plasma cells are essentially absent in the luminal gastrointestinal tract of patients with "complete" 22q11.2 deletion syndrome (DiGeorge syndrome).Hum Pathol, vol. 117, Nov. 2021, pp. 1–8. Pubmed, doi:10.1016/j.humpath.2021.08.002.
URI
https://scholars.duke.edu/individual/pub1494123
PMID
34391747
Source
pubmed
Published In
Hum Pathol
Volume
117
Published Date
Start Page
1
End Page
8
DOI
10.1016/j.humpath.2021.08.002

A Cautionary Tale: Florid Splenic γδ T-cell Proliferation and False-Positive T-cell Clonality by PCR Leads to a Grave Misdiagnosis.

The discrimination of benign from malignant lymphoproliferative disorders is sometimes difficult because there can be overlap in their histological and immunophenotypic features. In such situations, molecularly based clonality testing is often used to discriminate benign (polyclonal) from malignant (monoclonal) processes. Clonality testing by polymerase chain reaction (PCR) has a number of pitfalls that may result in spurious results. Here we report the case of a woman diagnosed by 2 major academic institutions with hepatosplenic T-cell lymphoma based on a dense infiltration of the spleen by a γδ T-cell population with mild cytologic atypia, resulting in expansion of the splenic red pulp, and a positive T-cell receptor clonality test by PCR. There was likewise mild involvement of the liver and bone marrow by the "atypical" T-cell population. Close attention to her uncharacteristically well clinical appearance led to repeat T-cell receptor clonality testing using next-generation sequencing. Definitive demonstration of polyclonality by this test showed that she in fact did not have hepatosplenic T-cell lymphoma but rather a reactive condition, and allogeneic stem cell transplantation could be safely avoided. As molecular clonality testing is widely used in the practice of hematology, this case brings attention to the pitfalls of clonality testing by PCR that practitioners may encounter. It is therefore a cautionary tale highlighting the need for critical interpretation of test results in full clinical context.
Authors
MLA Citation
Hwang, Joyce K., et al. “A Cautionary Tale: Florid Splenic γδ T-cell Proliferation and False-Positive T-cell Clonality by PCR Leads to a Grave Misdiagnosis.Clinical Lymphoma, Myeloma & Leukemia, vol. 21, no. 10, Oct. 2021, pp. e748–51. Epmc, doi:10.1016/j.clml.2021.05.010.
URI
https://scholars.duke.edu/individual/pub1485901
PMID
34158266
Source
epmc
Published In
Clinical Lymphoma, Myeloma & Leukemia
Volume
21
Published Date
Start Page
e748
End Page
e751
DOI
10.1016/j.clml.2021.05.010

Sequential Development of JAK2V617F Mutation and BCR-ABL1 Fusion in Individual Patients With Myeloproliferative Neoplasms: A Linear Clonal Evolution or Parallel Clonal Competition?

CONTEXT.—: Concomitant BCR-ABL1 and JAK2V617F in myeloproliferative neoplasms (MPNs) is rare, and its pathogenesis and clinical significance are unclear. OBJECTIVE.—: To investigate the clonal relationship between the 2 genomic alterations, as well as the clinicopathologic impact. DESIGN.—: Retrospective analysis of MPNs with sequential development of BCR-ABL1 and JAK2V617F. RESULTS.—: Of 6 cases, 5 had JAK2V617F-positive MPN diagnosed before acquiring BCR-ABL1 years later, and 1 had BCR-ABL1+ chronic myeloid leukemia before JAK2V617F-positive myelofibrosis completely replaced the BCR-ABL1+ clone 1 year after tyrosine kinase inhibitor therapy. Among the former group, treatment for the initial MPN involved hydroxyurea, ruxolitinib, and/or supportive care, and the latency to the development of JAK2V617F ranged from 4 to 13 years (median of 9 years). Four cases showed retention of JAK2V617F, whereas BCR-ABL1 emerged as the major clone, including 2 that exhibited parallel increases in JAK2V617F and BCR-ABL1 burdens, with both genomic markers exceeding 50%. Three patients received stem cell transplants and demonstrated sustained engraftment, with the genomic markers below detectable levels. CONCLUSIONS.—: Most MPNs with concomitant JAK2V617F and BCR-ABL1 are actually composite MPNs with a "second hit" residing on a different clone. Rare cases demonstrate a subclone harboring a "double-hit" in a background of a JAK2V617F-positive stem line clone. The probability of a "double-hit" with a BCR-ABL1+ stem line clone is probably reduced by effective tyrosine kinase inhibitor treatment. The treatment often involves combined kinase inhibitors and/or hydroxyurea, but the outcome is unpredictable; hematopoietic stem cell transplantation may be the ultimate therapeutic option for this complicated disease.
Authors
Zhao, Y; Reddi, D; McCracken, J; Iranzad, N; Rehder, C; Neff, J; Wang, E
URI
https://scholars.duke.edu/individual/pub1496234
PMID
34506622
Source
pubmed
Published In
Arch Pathol Lab Med
Published Date
DOI
10.5858/arpa.2021-0096-OA

Morphologic leukemia-free state in acute myeloid leukemia is sufficient for successful allogeneic hematopoietic stem cell transplant.

Authors
Pabon, CM; Li, Z; Hennig, T; de Castro, C; Neff, JL; Horwitz, ME; LeBlanc, TW; Long, GD; Lopez, RD; Sung, AD; Chao, N; Gasparetto, C; Sarantopoulos, S; Adams, DB; Erba, H; Rizzieri, DA
MLA Citation
Pabon, Cindy M., et al. “Morphologic leukemia-free state in acute myeloid leukemia is sufficient for successful allogeneic hematopoietic stem cell transplant.Blood Cancer J, vol. 11, no. 5, May 2021, p. 92. Pubmed, doi:10.1038/s41408-021-00481-9.
URI
https://scholars.duke.edu/individual/pub1482850
PMID
33994546
Source
pubmed
Published In
Blood Cancer Journal
Volume
11
Published Date
Start Page
92
DOI
10.1038/s41408-021-00481-9

Deep Optical Blood Analysis: COVID-19 Detection as a Case Study in Next Generation Blood Screening

Authors
Cooke, C; Kim, K; Xu, S; Yao, X; Yang, X; Glass, C; Neff, J; Pittman, P; McCall, C; Jiang, X; Horstmeyer, R
MLA Citation
Cooke, Colin, et al. “Deep Optical Blood Analysis: COVID-19 Detection as a Case Study in Next Generation Blood Screening.” Modern Pathology, vol. 34, no. SUPPL 2, 2021, pp. 814–16.
URI
https://scholars.duke.edu/individual/pub1478529
Source
wos-lite
Published In
Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc
Volume
34
Published Date
Start Page
814
End Page
816