Wen Foo

Positions:

Associate Professor of Pathology

Pathology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

M.D. 2008

Duke University School of Medicine

Anatomic and Clinical Pathology, Pathology

Duke University School of Medicine

Cytopathology Fellowship, Pathology

Harvard Medical School

Grants:

Publications:

Discordant and heterogeneous clinically relevant genomic alterations in circulating tumor cells vs plasma DNA from men with metastatic castration resistant prostate cancer.

Circulating tumor cell (CTC) and cell-free (cf) DNA-based genomic alterations are increasingly being used for clinical decision-making in oncology. However, the concordance and discordance between paired CTC and cfDNA genomic profiles remain largely unknown. We performed comparative genomic hybridization (CGH) on CTCs and cfDNA, and low-pass whole genome sequencing (lpWGS) on cfDNA to characterize genomic alterations (CNA) and tumor content in two independent prospective studies of 93 men with mCRPC treated with enzalutamide/abiraterone, or radium-223. Comprehensive analysis of 69 patient CTCs and 72 cfDNA samples from 93 men with mCRPC, including 64 paired samples, identified common concordant gains in FOXA1, AR, and MYC, and losses in BRCA1, PTEN, and RB1 between CTCs and cfDNA. Concordant PTEN loss and discordant BRCA2 gain were associated with significantly worse outcomes in Epic AR-V7 negative men with mCRPC treated with abiraterone/enzalutamide. We identified and externally validated CTC-specific genomic alternations that were discordant in paired cfDNA, even in samples with high tumor content. These CTC/cfDNA-discordant regions included key genomic regulators of lineage plasticity, osteomimicry, and cellular differentiation, including MYCN gain in CTCs (31%) that was rarely detected in cfDNA. CTC MYCN gain was associated with poor clinical outcomes in AR-V7 negative men and small cell transformation. In conclusion, we demonstrated concordance of multiple genomic alterations across CTC and cfDNA platforms; however, some genomic alterations displayed substantial discordance between CTC DNA and cfDNA despite the use of identical copy number analysis methods, suggesting tumor heterogeneity and divergent evolution associated with poor clinical outcomes.
Authors
Gupta, S; Hovelson, DH; Kemeny, G; Halabi, S; Foo, W-C; Anand, M; Somarelli, JA; Tomlins, SA; Antonarakis, ES; Luo, J; Dittamore, RV; George, DJ; Rothwell, C; Nanus, DM; Armstrong, AJ; Gregory, SG
URI
https://scholars.duke.edu/individual/pub1421556
PMID
31705765
Source
pubmed
Published In
Genes Chromosomes Cancer
Published Date
DOI
10.1002/gcc.22824

Diabetic bladder dysfunction is associated with bladder inflammation triggered through hyperglycemia, not polyuria.

Purpose: Diabetes is a grave and progressive condition characterized by debilitating complications. Diabetic bladder dysfunction (DBD) is a very common complication with no specific treatments currently available. Unlike other tissues affected by this disease, the bladder is subjected to two independent insults; 1) polyuria, created by the osmotic effects of glucose in the urine, and 2) hyperglycemia itself. Based on our understanding of inflammation as a major contributor to the underlying organ damage in several other diabetic complications, its presence in the bladder during DBD and the contribution of polyuria and hyperglycemia to its development were assessed. Methods: Awake, restrained cystometry was performed on wild type C57BL/6 mice and diabetic (Akita) mice on a C57BL/6 background at 15 weeks of age. A subgroup of the Akita mice were treated with phlorizin, an inhibitor of sodium-glucose linked transporter types 1 and 2 that prevents glucose reabsorption in the kidney. All groups were assessed for serum glucose, 4-hour voiding totals, and inflammation in the bladder (Evans blue assay). Results: Akita mice develop cystometrically-defined DBD by 15 weeks of age, as evidenced by an increase in urinary frequency, a decrease in voiding volume, and an increase in post-voiding residual volume. Phlorizin effectively normalized serum glucose in these animals while increasing the urine output. Inflammation in the bladder was present in the diabetic animals at this time point, but not detectable in animals receiving phlorizin. Conclusion: Inflammation in the bladder of diabetic mice correlates with the development of DBD and is triggered by hyperglycemia, not polyuria.
Authors
Inouye, BM; Hughes, FM; Jin, H; Lütolf, R; Potnis, KC; Routh, JC; Rouse, DC; Foo, W-C; Purves, JT
MLA Citation
Inouye, Brian M., et al. “Diabetic bladder dysfunction is associated with bladder inflammation triggered through hyperglycemia, not polyuria..” Res Rep Urol, vol. 10, 2018, pp. 219–25. Pubmed, doi:10.2147/RRU.S177633.
URI
https://scholars.duke.edu/individual/pub1358817
PMID
30533402
Source
pubmed
Published In
Research and Reports in Urology
Volume
10
Published Date
Start Page
219
End Page
225
DOI
10.2147/RRU.S177633

Primary intracerebral Hodgkin lymphoma with recurrence.

OBJECTIVE: To report a case of primary intracerebral Hodgkin lymphoma with disease recurrence. METHODS: Case report and review of the literature. RESULTS: A 58-year-old immunocompetent male presented with aphasia. Neuroimaging revealed a left temporal lobe lesion. A craniotomy and resection were performed, and the diagnosis of classical Hodgkin lymphoma was made. Systemic work-up for lymphoma was negative. Postoperatively, the patient was treated with whole brain irradiation. 14 months later, the patient developed an enhancing lesion in his pons and received combination chemotherapy and radiation therapy. Repeat imaging demonstrated leptomeningeal enhancement and multiple lesions throughout the cerebral hemispheres, cerebellum and brainstem. COMMENT: We report what appears to be the first case of a patient with aggressive primary intracerebral Hodgkin lymphoma with disease recurrence.
MLA Citation
Foo, W. .. C., et al. “Primary intracerebral Hodgkin lymphoma with recurrence..” Clin Neuropathol, vol. 30, no. 2, Mar. 2011, pp. 75–79. Pubmed, doi:10.5414/npp30075.
URI
https://scholars.duke.edu/individual/pub767238
PMID
21329616
Source
pubmed
Published In
Clinical Neuropathology
Volume
30
Published Date
Start Page
75
End Page
79
DOI
10.5414/npp30075

Immunocytochemistry for SOX-11 and TFE3 as diagnostic markers for solid pseudopapillary neoplasms of the pancreas in FNA biopsies.

BACKGROUND: Solid pseudopapillary neoplasms (SPNs) of the pancreas are rare malignant tumors that can be sampled via endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA). Although diagnosing SPNs can be straightforward in cases with a classic morphology and a typical immunoprofile, challenges can occur with morphologic variants or limited specimens. Recently, 2 immunohistochemical stains, SRY-related high-mobility group box 11 (SOX-11) and transcription factor E3 (TFE3), have been demonstrated to be highly sensitive and specific for SPNs in pancreatic resection specimens. The current study evaluates the diagnostic utility of these stains with EUS-FNA. METHODS: Thirteen EUS-FNA specimens from SPNs with sufficient material for immunocytochemistry were identified from 2000 to 2016. These cases were compared with 13 EUS-FNA specimens of non-SPN pancreatic neoplasms. Immunocytochemistry for SOX-11, TFE3, and β-catenin was performed on all cell blocks and then was scored independently by 2 pathologists in a masked manner. RESULTS: Nuclear reactivity for SOX-11 was detected in 13 of 13 SPNs and in 0 of 13 non-SPNs; this resulted in sensitivity and specificity values of 100%, a positive predictive value (PPV) of 1, and a negative predictive value (NPV) of 1. Nuclear reactivity for TFE3 was detected in 9 of 13 SPNs and in 0 of 13 non-SPNs; this resulted in a sensitivity of 69.2%, a specificity of 100%, a PPV of 1, and an NPV of 0.765. Nuclear reactivity for β-catenin was detected in 13 of 13 SPNs and in 1 of 13 non-SPNs; this resulted in a sensitivity of 100%, a specificity of 92.3%, a PPV of 0.929, and an NPV of 1. CONCLUSIONS: SOX-11 is a sensitive and specific immunocytochemical stain for SPNs in EUS-FNA specimens, and it may be useful as a diagnostic marker for distinguishing SPNs from its cytologic mimics. Cancer Cytopathol 2017;125:831-7. © 2017 American Cancer Society.
Authors
MLA Citation
Foo, Wen-Chi, et al. “Immunocytochemistry for SOX-11 and TFE3 as diagnostic markers for solid pseudopapillary neoplasms of the pancreas in FNA biopsies..” Cancer Cytopathol, vol. 125, no. 11, Nov. 2017, pp. 831–37. Pubmed, doi:10.1002/cncy.21931.
URI
https://scholars.duke.edu/individual/pub1279750
PMID
29045075
Source
pubmed
Published In
Cancer Cytopathol
Volume
125
Published Date
Start Page
831
End Page
837
DOI
10.1002/cncy.21931

Concurrent classical Hodgkin lymphoma and plasmablastic lymphoma in a patient with chronic lymphocytic leukemia/small lymphocytic lymphoma treated with fludarabine: a dimorphic presentation of iatrogenic immunodeficiency-associated lymphoproliferative dis

A small fraction of patients with chronic lymphocytic leukemia/small lymphocytic lymphoma develop Epstein-Barr virus-positive B-cell lymphoproliferative disorders. These Epstein-Barr virus-B-cell lymphoproliferative disorders are thought to be related to immune suppression induced by fludarabine/other chemotherapeutic regimens. As in other immunodeficiency-associated lymphoproliferative disorders, these disorders demonstrate a heterogeneous histological spectrum that ranges from polymorphic to monomorphic to classical Hodgkin lymphoma-like lesions. We report a case of concurrent classical Hodgkin lymphoma and plasmablastic lymphoma in a patient with chronic lymphocytic leukemia/small lymphocytic lymphoma treated with fludarabine. Both classical Hodgkin lymphoma and plasmablastic lymphoma were positive for Epstein-Barr virus-encoded RNA, whereas classical Hodgkin lymphoma was also positive for Epstein-Barr virus- latent membrane protein 1, suggesting a different viral latency. Immunoglobulin gene rearrangement studies demonstrated distinct clones in the plasmablastic lymphoma and chronic lymphocytic leukemia/small lymphocytic lymphoma. These findings suggest biclonal secondary lymphomas associated with iatrogenic immunodeficiency. Epstein-Barr virus-B-cell lymphoproliferative disorders in the setting of chronic lymphocytic leukemia/small lymphocytic lymphoma, in particular those arising after chemotherapy, should be separated from true Richter's transformation, and be categorized as (iatrogenic) immunodeficiency-associated lymphoproliferative disorder.
Authors
Foo, W-C; Huang, Q; Sebastian, S; Hutchinson, CB; Burchette, J; Wang, E
URI
https://scholars.duke.edu/individual/pub797495
PMID
20869749
Source
pubmed
Published In
Hum Pathol
Volume
41
Published Date
Start Page
1802
End Page
1808
DOI
10.1016/j.humpath.2010.04.019