Cancer Medicine (Mar 2023)

Post‐kidney transplant cancers: Racial and ethnic differences in sun‐exposed skin versus non‐sun‐exposed anogenital skin

  • Kotaro Takeda,
  • Carolann Risley,
  • Aisha Kousar,
  • Kimberly P. Briley,
  • Karyn Prenshaw,
  • Rajesh Talluri,
  • Kim R. Geisinger,
  • Lorita M. Rebellato

DOI
https://doi.org/10.1002/cam4.5431
Journal volume & issue
Vol. 12, no. 6
pp. 7348 – 7355

Abstract

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Abstract Background Transplant recipients have a 2‐ to 4‐fold increased risk of developing malignancies over the general population. Cancer is the second most common cause of death for recipients. The magnitude of the risk depends on the cancer type and increases in viral‐related malignancies. Skin cancer is the most common. However, data in most cancer registries is limited to cutaneous melanomas, thereby limiting the epidemiologic examination of cancer risk in non‐melanoma skin cancer. Our goal was to evaluate post‐kidney transplant cancer cases and sites in our population to guide screening recommendations. Methods Between 2009 and 2015, a retrospective study of adult kidney recipients transplanted at East Carolina University was conducted. The first cancer diagnosis after transplant through February 18, 2020, was captured and analyzed. Patient demographics, cancer sites, and histological diagnoses were analyzed and compared. p16 immunohistochemistry was used as a surrogate marker for high‐risk human papillomavirus (HPV) infection. Results Retrospectively, kidney transplant recipients were analyzed (N = 439), the majority were non‐Hispanic Black (NHB) individuals, 312 (71.1%), and 127 (28.9%) were non‐Hispanic White (NHW) individuals. Of these, 59 (13.4%) developed a posttransplant malignancy, with the majority on sun‐exposed skin found in NHW. NHB had all anogenital/mucosa skin cancers on non‐sun‐exposed skin. Of these detected in NHB, all were squamous cell carcinomas, with five out of six (83.3%) being positive for p16. Conclusions Posttransplant malignancy differed significantly by race, site, and potential source of etiology. The majority of malignancies are likely explained by acceleration of precursor lesions from prior exposure to ultraviolet rays or HPV.

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