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An Examination of the Current Understanding of the Biochemistry of Endometriosis
Jillian Paul
Division:
Consumer and Health Sciences
Department:
Chemistry/Public Health
Mentor:
Mickey Laux
Mentor's e-mail:
jlaux@occ.cccd.edu
Author's e-mail:
jpaul10@student.cccd.edu
Abstract:

Endometriosis is a prevalent gynecological disease often misunderstood as and reduced to “bad menstrual cramps.” Presenting in approximately 10-15% of women and characterized by the growth of endometrial tissue in the abdominal cavity, endometriosis produces varied symptoms consisting of chronic crippling pain, inflammation, gastrointestinal problems, infertility, and an overall reduction in quality of life.  The pathology of the disease is not fully known, resulting in unreliable cures, and limited treatment options. This literature review has been conducted to gain a better awareness of the current understanding of the biochemical makeup of endometrial tissue, the hormonal pathways involved, and how they compare to a healthy system.  This study involves comparing and analyzing recent research projects on the histology, biochemistry, and pathology of endometriosis. When comparing endometriosis tissue to tissue from a healthy endometrium findings include: alterations in lipids (Yie Hou Lee, et al. E1913), drastically reduced iodine levels (Feider, et al.), increased inflammation markers, the dysregulation of steroid pathways, and disruption of the immune response    (García-Gómez et al.). This review finds that endometrial tissue is not, as commonly believed, simply uterine tissue that has implanted in the abdominal cavity, but rather a mutation of that healthy tissue with a unique pathology further supported by an observed resistance to cellular death in endometriosis cells (Klemmt & Starzinski-Powitz p109).  This study indicates that as endometriosis research continues, hormonal regulation and biochemical inflammatory pathways will be important factors in finding a cause and cure of the disease as well as continuing to identify genetic markers.

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