From Leiomyoma to Leiomyosarcoma: Role of Obesity
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2017, Vol 1, Issue 1
Abstract
Leiomyoma and leiomyosarcome (LMS) appear as two stages of tumor progression process of a transformed smooth muscle cell. Obesity is a well-established risk factor of leiomyoma. The connection between both of them are not well understood. The involvement of obesity in this transformation needs more investigation to be highlighted. Here, we discussed from a tumor immunology perspective, by focusing on the microenvironment immunosuppression that, probably, allows LMS to escape the antitumor immune response. Leiomyoma are benign monoclonal tumor arising from the smooth muscle cell of the myometrium. Leiomyoma are the most common indication for gynecologic surgery in the U.S. and accounts for around 350,000 hysterectomies and 30,000 myomectomies per year [1]. Common symptoms of leiomyoma are heavy and prolonged menstrual bleeding, pelvic pain, dysmenorrheal, urinary incontinence, sexual dysfunction, lower back pain, and sub fertility as well as pregnancy complications [2]. Cumulative exposure to estrogen and progesterone is believed to be a major etiologic factor [3], and may influence the hormonal milieu. Leiomyosarcoma (LMS) is a rare tumor that represents 1% of described uterine tumors. However, at the diagnosis LMS mimics the phenotype of leiomyoma. At the pathological level, the difference between leiomyoma and LMS are resumed in the presence of infiltrative borders, coagulative necrosis and nuclear atypia [4-5]. Obesity is a major established risk factor of malignancies promotion and growth increase that can lead to metastasis. The fat tissue produces and releases adipokines and hormones like a lymphatic organ, which increases the risk of leiomyoma and certainly LMS [6]. The question is, why doesn’t leiomyoma progress to LMS? Are there biomarkers able to establish the possible connection between both entities? The answers to those questions will help the development of clinical management for both diseases. The connection between leiomyoma and LMS is not clear [7-8]. Studies of the transformation process from benign tumor, such as leiomyoma, to full tumorigenic phenotype exhibited by LMS are needed. Based on our cumulated experiences in the field of tumor immunology, immunosuppression is the key of tumor progression and metastasis. We know that inflammation is promoted in leiomyoma, but not enough to lead to the LMS stage, maybe due to the involvement of steroid hormones: Estrogen and/or Progesterone signaling alteration. To highlight this area, the characterization of the immune signature in leiomyoma and LMS needs more investigation to establish possible links that will explain their connection.
Authors and Affiliations
Abdeljabar El Andaloussi
Keywords
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- EP ID EP566589
- DOI 10.26717/BJSTR.2017.01.000106
- Views 203
- Downloads 0
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