Kyle Strickland

Overview:

Dr. Strickland specializes in cytopathology and women's and perinatal surgical pathology.  His areas of interest include epithelial and mesenchymal gynecologic neoplasia and fine needle aspiration cytology.

Positions:

Assistant Professor of Pathology

Pathology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

B.S. 2005

College of Charleston

B.A. 2005

College of Charleston

MD./PhD. 2013

Medical University of South Carolina, School of Medicine

Resident, Anatomic Pathology, Harvard Medical School

Brigham and Women's Hospital

Fellow, Cytopathology, Harvard Medical School

Brigham and Women's Hospital

Fellow, Women's and Perinatal Pathology, Harvard Medical School

Brigham and Women's Hospital

Grants:

Population Health Research Support - Study of Pregnancy and Neonatal Health (SPAN) Task A

Administered By
Obstetrics and Gynecology, Maternal Fetal Medicine
Awarded By
National Institutes of Health
Role
Faculty Member
Start Date
End Date

Point-of-care cellular and molecular pathology of breast tumors on a cell phone

Administered By
Biomedical Engineering
Awarded By
National Institutes of Health
Role
Co Investigator
Start Date
End Date

Are ESR1 mutations associated with shorter progression free survival in copy number-low endometrial adenocarcinomas?

Administered By
Pathology
Awarded By
Foundation for Women's Cancer
Role
Principal Investigator
Start Date
End Date

TIME Aim of the Study of Pregnancy and Neonatal Health (SPAN) Task Order A

Administered By
Obstetrics and Gynecology, Maternal Fetal Medicine
Awarded By
National Institutes of Health
Role
Faculty Member
Start Date
End Date

Molecular classification of endometrial advanced stage cancers and association with survival outcomes: Ancillary analysis of GOG-0258

Administered By
Obstetrics and Gynecology, Gynecologic Oncology
Awarded By
American Association of Obstetricians and Gynecologists Foundation
Role
Co Investigator
Start Date
End Date

Publications:

Author Correction: Cellphone enabled point-of-care assessment of breast tumor cytology and molecular HER2 expression from fine-needle aspirates.

Authors
Joh, DY; Heggestad, JT; Zhang, S; Anderson, GR; Bhattacharyya, J; Wardell, SE; Wall, SA; Cheng, AB; Albarghouthi, F; Liu, J; Oshima, S; Hucknall, AM; Hyslop, T; Hall, AHS; Wood, KC; Shelley Hwang, E; Strickland, KC; Wei, Q; Chilkoti, A
MLA Citation
Joh, Daniel Y., et al. “Author Correction: Cellphone enabled point-of-care assessment of breast tumor cytology and molecular HER2 expression from fine-needle aspirates.Npj Breast Cancer, vol. 7, no. 1, Sept. 2021, p. 126. Pubmed, doi:10.1038/s41523-021-00335-4.
URI
https://scholars.duke.edu/individual/pub1497086
PMID
34535683
Source
pubmed
Published In
Npj Breast Cancer
Volume
7
Published Date
Start Page
126
DOI
10.1038/s41523-021-00335-4

Placental uterine artery embolization followed by delayed hysterectomy for placenta percreta: A case series.

We describe outcomes of patients with suspected placenta percreta treated with placental uterine artery embolization (P-UAE) followed by delayed hysterectomy. This is a prospective case series of subjects from 2005 to 2018 with suspected placenta percreta who underwent P-UAE at the time of cesarean delivery followed by delayed hysterectomy. Both scheduled and unscheduled surgical cases were included. Maternal characteristics, surgical approaches, intra- and postoperative outcomes were abstracted from medical records. In total, twenty-two subjects were included. Median (interquartile range, IQR) delivery gestational age was 34.6 (31.9, 35.7) weeks, occurring as scheduled in 17 (77.3%) subjects and unscheduled in 5 (22.7%). Delayed hysterectomy was performed as scheduled in 17 (77.3%) subjects at a median (IQR) 40.5 (38.0, 44.0) days after delivery, and 5 (22.7%) subjects had a hysterectomy prior to scheduled date, median (IQR) 27.0 (17.0, 35.0) days after delivery. Indications for the 5 unscheduled hysterectomies included bleeding (n = 3) and suspected endometritis (n = 2). Three subjects (13.6%) received a blood transfusion (1, 3, 3 units) during delivery, and 7 (31.8%) were transfused during delayed hysterectomy (median [IQR] 2 [1,3] units). Three (13.6%) subjects had bladder resection at the time of hysterectomy; 1 (4.5%) had an unintentional cystotomy and 1 (4.5%) had a ureteral injury. P-UAE followed by delayed hysterectomy appears to be a safe and feasible, although appropriate patient selection and close surveillance are imperative, as 22.7% of patients underwent unscheduled hysterectomy.
Authors
Gatta, LA; Lee, PS; Gilner, JB; Weber, JM; Adkins, L; Salinaro, JR; Habib, AS; Pabon-Ramos, W; Strickland, KC; Ronald, J; Erkanli, A; Mehdiratta, JE; Grotegut, CA; Secord, AA
MLA Citation
Gatta, Luke A., et al. “Placental uterine artery embolization followed by delayed hysterectomy for placenta percreta: A case series.Gynecol Oncol Rep, vol. 37, Aug. 2021, p. 100833. Pubmed, doi:10.1016/j.gore.2021.100833.
URI
https://scholars.duke.edu/individual/pub1493074
PMID
34368412
Source
pubmed
Published In
Gynecologic Oncology Reports
Volume
37
Published Date
Start Page
100833
DOI
10.1016/j.gore.2021.100833

Cellphone enabled point-of-care assessment of breast tumor cytology and molecular HER2 expression from fine-needle aspirates.

Management of breast cancer in limited-resource settings is hindered by a lack of low-cost, logistically sustainable approaches toward molecular and cellular diagnostic pathology services that are needed to guide therapy. To address these limitations, we have developed a multimodal cellphone-based platform-the EpiView-D4-that can evaluate both cellular morphology and molecular expression of clinically relevant biomarkers directly from fine-needle aspiration (FNA) of breast tissue specimens within 1 h. The EpiView-D4 is comprised of two components: (1) an immunodiagnostic chip built upon a "non-fouling" polymer brush-coating (the "D4") which quantifies expression of protein biomarkers directly from crude cell lysates, and (2) a custom cellphone-based optical microscope ("EpiView") designed for imaging cytology preparations and D4 assay readout. As a proof-of-concept, we used the EpiView-D4 for assessment of human epidermal growth factor receptor-2 (HER2) expression and validated the performance using cancer cell lines, animal models, and human tissue specimens. We found that FNA cytology specimens (prepared in less than 5 min with rapid staining kits) imaged by the EpiView-D4 were adequate for assessment of lesional cellularity and tumor content. We also found our device could reliably distinguish between HER2 expression levels across multiple different cell lines and animal xenografts. In a pilot study with human tissue (n = 19), we were able to accurately categorize HER2-negative and HER2-positve tumors from FNA specimens. Taken together, the EpiView-D4 offers a promising alternative to invasive-and often unavailable-pathology services and may enable the democratization of effective breast cancer management in limited-resource settings.
Authors
Joh, DY; Heggestad, JT; Zhang, S; Anderson, GR; Bhattacharyya, J; Wardell, SE; Wall, SA; Cheng, AB; Albarghouthi, F; Liu, J; Oshima, S; Hucknall, AM; Hyslop, T; Hall, AHS; Wood, KC; Shelley Hwang, E; Strickland, KC; Wei, Q; Chilkoti, A
MLA Citation
Joh, Daniel Y., et al. “Cellphone enabled point-of-care assessment of breast tumor cytology and molecular HER2 expression from fine-needle aspirates.Npj Breast Cancer, vol. 7, no. 1, July 2021, p. 85. Pubmed, doi:10.1038/s41523-021-00290-0.
URI
https://scholars.duke.edu/individual/pub1487266
PMID
34215753
Source
pubmed
Published In
Npj Breast Cancer
Volume
7
Published Date
Start Page
85
DOI
10.1038/s41523-021-00290-0

Knockout of Putative Tumor Suppressor Aldh1l1 in Mice Reprograms Metabolism to Accelerate Growth of Tumors in a Diethylnitrosamine (DEN) Model of Liver Carcinogenesis.

Cytosolic 10-formyltetrahydrofolate dehydrogenase (ALDH1L1) is commonly downregulated in human cancers through promoter methylation. We proposed that ALDH1L1 loss promotes malignant tumor growth. Here, we investigated the effect of the <i>Aldh1l1</i> mouse knockout (<i>Aldh1l1<sup>-/-</sup></i>) on hepatocellular carcinoma using a chemical carcinogenesis model. Fifteen-day-old male <i>Aldh1l1</i> knockout mice and their wild-type littermate controls (<i>Aldh1l1<sup>+/+</sup></i>) were injected intraperitoneally with 20 μg/g body weight of DEN (diethylnitrosamine). Mice were sacrificed 10, 20, 28, and 36 weeks post-DEN injection, and livers were examined for tumor multiplicity and size. We observed that while tumor multiplicity did not differ between <i>Aldh1l1<sup>-/-</sup></i> and <i>Aldh1l1<sup>+/+</sup></i> animals, larger tumors grew in <i>Aldh1l1<sup>-/-</sup></i> compared to <i>Aldh1l1<sup>+/+</sup></i> mice at 28 and 36 weeks. Profound differences between <i>Aldh1l1<sup>-/-</sup></i> and <i>Aldh1l1<sup>+/+</sup></i> mice in the expression of inflammation-related genes were seen at 10 and 20 weeks. Of note, large tumors from wild-type mice showed a strong decrease of ALDH1L1 protein at 36 weeks. Metabolomic analysis of liver tissues at 20 weeks showed stronger differences in <i>Aldh1l1<sup>+/+</sup></i> versus <i>Aldh1l1<sup>-/-</sup></i> metabotypes than at 10 weeks, which underscores metabolic pathways that respond to DEN in an ALDH1L1-dependent manner. Our study indicates that <i>Aldh1l1</i> knockout promoted liver tumor growth without affecting tumor initiation or multiplicity.
Authors
Krupenko, NI; Sharma, J; Fogle, HM; Pediaditakis, P; Strickland, KC; Du, X; Helke, KL; Sumner, S; Krupenko, SA
MLA Citation
URI
https://scholars.duke.edu/individual/pub1487875
PMID
34203215
Source
epmc
Published In
Cancers
Volume
13
Published Date
DOI
10.3390/cancers13133219

Molecular Classification to Prognosticate Response in Medically Managed Endometrial Cancers and Endometrial Intraepithelial Neoplasia.

BACKGROUND: The aim of this study was to evaluate whether molecular classification prognosticates treatment response in women with endometrial cancers and endometrial intraepithelial neoplasia (EIN) treated with levonorgestrel intrauterine system (LNG-IUS). METHODS: Patients treated with LNG-IUS for endometrial cancer or EIN from 2013 to 2018 were evaluated. Using immunohistochemistry and single gene sequencing of POLE, patients were classified into four groups as per the Proactive Molecular Risk Classifier for Endometrial cancer (ProMisE): POLE-mutated, mismatch repair-deficient (MMRd), p53 wild type (p53wt), and p53-abnormal (p53abn). Groups were assessed relative to the primary outcome of progression or receipt of definitive treatment. RESULTS: Fifty-eight subjects with endometrioid endometrial cancer or EIN treated with LNG-IUS were included. Of these, 22 subjects (37.9%) had endometrial cancer and 36 subjects (62.1%) had EIN. Per the ProMisE algorithm, 44 patients (75.9%) were classified as p53wt, 6 (10.3%) as MMRd, 4 (6.9%) as p53abn, and 4 (6.9%) as POLE-mutated. Of the 58 patients, 11 (19.0%) progressed or opted for definitive therapy. Median time to progression or definitive therapy was 7.5 months, with p53abn tumors having the shortest time to progression or definitive therapy. CONCLUSIONS: Molecular classification of endometrial cancer and EIN prior to management with LNG-IUS is feasible and may predict patients at risk of progression.
Authors
Puechl, AM; Spinosa, D; Berchuck, A; Secord, AA; Drury, KE; Broadwater, G; Wong, J; Whitaker, R; Devos, N; Corcoran, DL; Strickland, KC; Previs, RA
MLA Citation
Puechl, Allison M., et al. “Molecular Classification to Prognosticate Response in Medically Managed Endometrial Cancers and Endometrial Intraepithelial Neoplasia.Cancers (Basel), vol. 13, no. 11, June 2021. Pubmed, doi:10.3390/cancers13112847.
URI
https://scholars.duke.edu/individual/pub1484762
PMID
34200374
Source
pubmed
Published In
Cancers
Volume
13
Published Date
DOI
10.3390/cancers13112847