Paul Mayor

Dr. Paul Mayor


Research Focus & Metrics

Academic Career Length

11Years (2016-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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7 March 2019 in JCI Insight
Verified
Journal Article
Closed access
PDF file
KSKelly L. Singel
Kelly L. Singel
TETiffany R. Emmons
Tiffany R. Emmons
AKAnm Nazmul H. Khan
Anm Nazmul H. Khan
PMPaul Mayor
Paul Mayor
SSShichen Shen
Shichen Shen
BSBrahm H. Segal
Brahm H. Segal
Epithelial ovarian cancer (EOC) often presents with metastases and ascites. Granulocytic myeloid–derived suppressor cells are an immature population that impairs antitumor immunity. Since suppressive granulocytes in the ascites of patients with newly diagnosed EOC were morphologically mature, we hypothesized that PMN were rendered suppressive in the tumor microenvironment (TME). Circulating PMN from patients were not suppressive but acquired a suppressor phenotype (defined as ≥1 log 10 reduction of anti-CD3/CD28–stimulated T cell proliferation) after ascites supernatant exposure. Ascites supernatants (20 of 31 supernatants) recapitulated the suppressor phenotype in PMN from healthy donors. T cell proliferation was restored with ascites removal and restimulation. PMN suppressors also inhibited T cell activation and cytokine production. PMN suppressors completely suppressed proliferation in naive, central memory, and effector memory T cells and in engineered tumor antigen–specific cytotoxic T lymphocytes, while antigen-specific cell lysis was unaffected. Inhibition of complement C3 activation and PMN effector functions, including CR3 signaling, protein synthesis, and vesicular trafficking, abrogated the PMN suppressor phenotype. Moreover, malignant effusions from patients with various metastatic cancers also induced the C3-dependent PMN suppressor phenotype. These results point to PMN impairing T cell expansion and activation in the TME and the potential for complement inhibition to abrogate this barrier to antitumor immunity.

1 August 2018 in Gynecologic Oncology
Verified
Journal Article
Closed access
PMPaul Mayor
Paul Mayor
KSKristen Starbuck
Kristen Starbuck
EZEmese Zsiros
Emese Zsiros

1 August 2017 in Gynecologic Oncology Reports
Verified
Journal Article
Open access
PMPaul Mayor
Paul Mayor
LGLaurie M. Gay
Laurie M. Gay
SLShashikant Lele
Shashikant Lele
JEJulia A. Elvin
Julia A. Elvin
•Secondary, reversion mutations in BRCA genes can restore protein function.•Reversion mutations can underlie resistance to therapies such as PARP inhibitors.•Reversion mutations arise during the course of treatment.

23 September 2016 in Cancers
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Journal Article
Open access
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PMPaul Mayor
Paul Mayor
SLShashikant Lele
Shashikant Lele
Photodynamic therapy (PDT) is a treatment modality used in the management of solid tumor malignancies that employs the use of a photosensitizing agent, a light source and oxygen in order to illicit a direct cytotoxic effect. Its use in gynecologic malignancies is somewhat novel and has been used for palliative and curative intent. At the Roswell Park Cancer Institute, the use of PDT in the management of gynecologic cancers began in the mid 1980s and since that time 35 patients have received PDT as a treatment for recurrent or metastatic cutaneous and vulvar, vaginal, anal, and cervical recurrences. In our experience, 85% patients with metastatic cutaneous lesions had a complete response. Twenty-seven percent of patients with metastatic vaginal, cervical or anal recurrences had a complete response to therapy with a median response time of 28 months. Side effects from the treatment included moderate to severe burning sensation, pain and edema at the treatment site requiring narcotic pain medication for symptom management in patients who underwent treatment to cutaneous lesions as well as lower genital tract recurrences. PDT should be considered an option in patients who are too frail to undergo the standard of care or decline the standard of care in lieu of a less invasive treatment modality.

31 August 2017 in Cancer Epidemiology, Biomarkers & Prevention
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Journal Article
Open access
PDF file
AMAlbina N. Minlikeeva
Albina N. Minlikeeva
JFJo Freudenheim
Jo Freudenheim
KEKevin H. Eng
Kevin H. Eng
RCRikki A. Cannioto
Rikki A. Cannioto
GFGrace Friel
Grace Friel
KMKirsten B. Moysich
Kirsten B. Moysich
Background: Comorbidities can affect survival of ovarian cancer patients by influencing treatment efficacy. However, little evidence exists on the association between individual concurrent comorbidities and prognosis in ovarian cancer patients. Methods: Among patients diagnosed with invasive ovarian carcinoma who participated in 23 studies included in the Ovarian Cancer Association Consortium, we explored associations between histories of endometriosis; asthma; depression; osteoporosis; and autoimmune, gallbladder, kidney, liver, and neurological diseases and overall and progression-free survival. Using Cox proportional hazards regression models adjusted for age at diagnosis, stage of disease, histology, and study site, we estimated pooled HRs and 95% confidence intervals to assess associations between each comorbidity and ovarian cancer outcomes. Results: None of the comorbidities were associated with ovarian cancer outcome in the overall sample nor in strata defined by histologic subtype, weight status, age at diagnosis, or stage of disease (local/regional vs. advanced). Conclusions: Histories of endometriosis; asthma; depression; osteoporosis; and autoimmune, gallbladder, kidney, liver, or neurologic diseases were not associated with ovarian cancer overall or progression-free survival. Impact: These previously diagnosed chronic diseases do not appear to affect ovarian cancer prognosis. Cancer Epidemiol Biomarkers Prev; 26(9); 1470–3. ©2017 AACR.

20 May 2017 in Journal of Clinical Oncology
Verified
Journal Article
Closed access
PMPaul Mayor
Paul Mayor
JEJohn Etter
John Etter
JSJames Brian Szender
James Brian Szender
EZEmese Zsiros
Emese Zsiros
PFPeter Jonathan Frederick
Peter Jonathan Frederick
SLShashikant B. Lele
Shashikant B. Lele
E18093 Background: The purpose of this study is to determine and compare the overall rates of surgical site infections (SSI) in patients undergoing breast surgery, hysterectomy and combined breast surgery and hysterectomy. Methods: We inspected the National Surgical Quality Improvement Program (NSQIP) Participant Use Files from 2005-2014 for subjects undergoing breast surgery (CPT codes 19300-19307, 19340, 19342, 19350, 19357, 19361, 19364, 19366-19369, 19380, 19396), Gynecologic surgery ( CPT Codes 58150, 58152, 58180, 58200, 58210, 58240, 58260, 58262, 58263, 58267, 58270, 58275, 58280, 58285, 58290-58294, 58541-58544, 58548, 58550, 58552-58554, 58570-58573), or a combined surgery (the NSQIP databased was queried for encounters that contained both a breast surgery code and hysterectomy procedure code). We then queried the database for SSI rates within 30 days of surgery. SSI rates were compared using a χ2 test with a nominal value of p < 0.05 as a test for significance. Results: We identified a total of 174,605 patients who underwent a breast surgery and found a SSI rate of 2.59%. We identified a total of 137,121 patients who underwent hysterectomy and found a SSI rate of 2.58%. We identified 383 patients who underwent a combined breast surgery and hysterectomy and found a SSI rate of 2.87%. When comparing SSI rates of combined breast surgery and hysterectomy, to breast surgery or hysterectomy alone, we found no significant difference in the rates of SSI between these groups (p = .7304). We analyzed SSI rates in patients by different surgical approaches including combined breast surgery and open hysterectomy and found an SSI rate of 4.35% (p = .357), combined breast surgery and laparoscopic hysterectomy and found an SSI rate of 2.38% (p = .931), and combined breast surgery and laparoscopic assisted vaginal hysterectomy and found an SSI rate of 2.75% (p = .916). Conclusions: The rates of SSI in patients undergoing combined breast surgery and hysterectomy is not significantly different from breast surgery or hysterectomy alone. Gynecologic oncologist should coordinate with breast surgeons to perform a combined procedure in patients who require both breast surgery and hysterectomy.