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J Pain Symptom Manage · May 2024
IDENTIFICATION OF A HIGHER RISK LYMPHEDEMA PHENOTYPE AND ASSOCIATIONS WITH CYTOKINE GENE POLYMORPHISMS.
- Christine Miaskowski, Yvette P Conley, Bruce A Cooper, Steven M Paul, Betty J Smoot, Marilyn J Hammer, Mei Fu, and Jon D Levine.
- School of Nursing, University of California, San Francisco, CA, USA; School of Medicine, University of California, San Francisco, CA, USA. Electronic address: chris.miaskowski@ucsf.edu.
- J Pain Symptom Manage. 2024 May 1; 67 (5): 375383.e3375-383.e3.
ContextBreast cancer-related lymphedema (BCRL) is chronic condition that occurs in 5% to 75% of women following treatment for breast cancer. However, little is known about the risk factors and mechanisms associated with a worse BCRL profile.ObjectivesIdentify distinct BCRL profiles in women with the condition (i.e., lower vs. higher risk phenotype) and evaluate for associations with pro- and anti-inflammatory genes.MethodsLatent class profile analysis (LCPA) was used to identify the BCRL profiles using phenotypic characteristics evaluated prior to surgery. Candidate gene analyses were done to identify cytokine genes associated with the two BCRL profiles.ResultsOf the 155 patients evaluated, 35.5% (n = 55) were in the Lower and 64.5% (n = 100) were in the Higher Risk classes. Risk factors for membership in the Higher class included: lower functional status, having sentinel lymph node biopsy, axillary lymph node dissection, mastectomy, higher number of positive lymph nodes, and receipt of chemotherapy. Polymorphisms for interleukin (IL)1-beta and IL6 were associated with membership in the Higher Risk class.ConclusionThe readily available and clinically relevant phenotypic characteristics associated with a worse BCRL profile can be used by clinicians to identify higher risk patients. If confirmed, these characteristics can be tested in predictive risk models. In addition, the candidate gene findings may guide the development of mechanistically-based interventions to decrease the risk of BCRL.Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.
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