Immune status in merkel cell carcinoma: Relationships with clinical factors and independent prognostic value.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e21509-e21509
Author(s):  
Mehran Yusuf ◽  
Jeremy T. Gaskins ◽  
Abbas Rattani ◽  
Grant McKenzie ◽  
Steven Mandish ◽  
...  

e21509 Background: Immunosuppression (IS) is not currently considered in staging for Merkel cell carcinoma (MCC). We performed an analysis of the National Cancer Database (NCDB) to investigate immune status as an independent predictor of overall survival (OS) for patients with MCC and describe the relationship between immune status and other prognostic factors. Methods: The NCDB was queried for patients diagnosed with MCC from 2010 to 2016 with known immune status. Multivariable Cox proportional hazards models were used to define factors associated with OS. Adjuvant radiation and chemotherapy were treated as time-dependent predictors to limit immortal time bias. Secondary models were constructed to assess the association between IS etiology and OS. Multivariable logistic regression models were used to characterize relationships between immune status and other factors. Multiple imputation was used to minimize missing data bias. Results: The overall cohort included 3,882 patients (3,470 patients with known immunocompetence and 412 patients with known immunosuppression). Etiologies for profound IS included chronic lymphocytic leukemia (CLL, n = 118), Other including HIV/AIDS (n = 116), solid-organ transplant (n = 106), and Non-Hodgkin Lymphoma (NHL, n = 72). 2,864 patients (73.8%) underwent surgical nodal examination. The median follow-up time was 33 months (Interquartile Range: 18 to 55 months). The 3-year OS was lower for patients with IS (44.6%, CI 39.8-49.9%) compared to immunocompetent (IC) patients (68.7%, CI 67.1-70.4%, p < .0001). IS was associated with increased adjusted mortality hazard (HR 2.36, 95% CI 2.03-2.75). Etiology of IS was associated with OS ( p = .0015) with lowest 3-year OS (32.7%, CI 24.6%-43.5%) for patients with solid-organ transplantation. IS was associated with increased odds of greater nodal burden (OR 1.70, CI 1.37-2.11) and lymphovascular invasion (OR 1.58, CI 1.23-2.03). Conclusions: Immune status was independently prognostic for OS for patients with localized MCC. Etiology of IS may be associated with differential survival outcomes. Multiple adverse prognostic factors were associated with increased likelihood of IS. Immune status and potentially etiology of IS may be useful prognostic factors to consider for future MCC staging systems.

2015 ◽  
Vol 107 (2) ◽  
pp. dju382-dju382 ◽  
Author(s):  
C. A. Clarke ◽  
H. A. Robbins ◽  
Z. Tatalovich ◽  
C. F. Lynch ◽  
K. S. Pawlish ◽  
...  

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 8590-8590
Author(s):  
Sean Donovan ◽  
Amy Weaver ◽  
Clark Otley ◽  
Richard Wayne Joseph

8590 Background: Merkel Cell Carcinoma (MCC) is an aggressive cutaneous malignancy of neuroendocrine origin associated with immunosuppression presumably through infection with Merkel Cell Polyomavirus present in >80% of patients (pts). The impact of immune status on clinical outcomes in pts with MCC is unknown. The primary objective of this study was to compare clinical characteristics and outcomes of pts with MCC who are immunosuppressed (ISP) versus non-immunosuppressed (non-ISP). Methods: We performed a retrospective chart review on pts with MCC diagnosed at the Mayo Clinic between 1981 and 2009. A dermatopathologist confirmed all cases. ISP was defined as pts diagnosed with chronic lymphocytic leukemia, HIV, solid organ transplant recipients, or chronic immunosuppressive medication. The association between ISP status and overall survival was summarized using the hazard ratio (HR) and 95% confidence interval (CI) estimated from a Cox regression model. Results: Of the 268 pts identified and included in the study, 38 (14%) were ISP. We found no differences in age, tumor size, tumor location, stage of disease, or recurrence rate in ISP vs Non-ISP. Among pts who had Stage 3-4 disease, there was no difference in the size of the primary between groups. Among pts with Stage 1-2 disease, ISP status was not significantly associated with poorer survival (HR 1.5, 95% CI 0.7-3.3). However, among pts with Stage 3-4 disease, ISP pts had significantly poorer survival compared to non-ISP pts (HR 2.7, 95% CI 1.2 - 6.2). Conclusions: Baseline clinical characteristics of pts with MCC do not differ based on immunosuppression, and outcomes do not differ in pts in regards to immunosuppression in early stage MCC (Stage 1-2). However, in pts with Stage III-IV MCC, ISP pts have a worse clinical outcome suggesting that metastatic MCC either behaves more aggressively in ISP pts either through intrinsic differences in the biology of the tumor or improved immune evasion in ISP pts. These results should be cautiously interpreted given the small number (n=12) of immunosuppressed pts with advanced stage MCC. The authors will update their data with an additional 58 patients by the date of presentation.


2009 ◽  
Vol 27 (24) ◽  
pp. 4021-4026 ◽  
Author(s):  

Purpose To expedite improved understanding, diagnosis, treatment, and prevention of Merkel cell carcinoma (MCC), a rare malignancy of cutaneous neuroendocrine cells that has a 28% 2-year mortality rate. Methods This article summarizes a workshop that discussed the state-of-the-art research and priorities for research on MCC and on a new human polyomavirus (ie, MCPyV) recently discovered in 80% of MCC tumors. Results Normal Merkel cells are widely distributed in the epidermis near the end of nerve axons and may function as mechanoreceptors or chemoreceptors. Malignant MCC cells typically stain for cytokeratin 20 as well as for other epithelial and neuroendocrine markers. MCC subtypes, which are based on histology, on cell line growth properties, and on gene expression profiles, have been reported but have not been linked to prognosis. Clinical management has been empiric. MCPyV is clonally integrated at various sites in the human genome of MCC tumors, with truncating mutations in the viral, large T antigen gene that interrupt viral replication. MCPyV seroprevalence may be high, as with previously known human polyomaviruses. MCC risk is increased 11-fold with AIDS and with other cell-mediated immune deficiencies, B-cell neoplasms, and ultraviolet radiation exposure. Conclusion Development and validation of a range quantitative polymerase chain reaction and serologic assays for detection of MCPyV, as well as an infectious clone of the virus, would clarify the fundamental biology, natural history, and epidemiology of the virus, of MCC, and of other diseases. Contingent on standardized histologic diagnosis and staging of MCC, consortia are needed to clarify the risks and benefits of sentinel lymph node biopsy, adjuvant radiation therapy, and salvage therapies; consortia are needed also for epidemiologic studies of MCC etiology.


2016 ◽  
Vol 23 (11) ◽  
pp. 3564-3571 ◽  
Author(s):  
Kelly L. Harms ◽  
Mark A. Healy ◽  
Paul Nghiem ◽  
Arthur J. Sober ◽  
Timothy M. Johnson ◽  
...  

2019 ◽  
Vol 103 (5) ◽  
pp. E47-E48
Author(s):  
Praveen Pendyala ◽  
John Byun ◽  
Sharad Goyal ◽  
James Goydos ◽  
Ann W. Silk ◽  
...  

2014 ◽  
Vol 73 (5) ◽  
pp. 531-534 ◽  
Author(s):  
Kevin W. Sexton ◽  
Stephen P. Poteet ◽  
John Bradford Hill ◽  
Alexandra Schmidt ◽  
Ashit Patel ◽  
...  

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