A Possible Screening for the Development of Uterine Cancer in Obesity
Location
CSU 253/4/5
Start Date
4-4-2011 1:30 PM
End Date
4-4-2011 3:00 PM
Student's Major
Biological Sciences
Student's College
Science, Engineering and Technology
Mentor's Name
Steven Mercurio
Mentor's Department
Biological Sciences
Mentor's College
Science, Engineering and Technology
Description
Constant growth and shedding of the uterine lining in women has made them prone to mutations and cancer, especially in obesity. Obese women and animals have also shown increased sensitivity of their estrogen receptors. To test the hypothesis that obese female mice challenged with estrogen would have increased cancer gene expression and reduced risk in the presence of a medication that reduced blood vessel formation, female mice were fed a normal diet compared to others fed a high fat diet for 15 weeks, given that medication (Avastin®) for the first 10 days, and challenged with a dose of estrogen 6 hours prior to sampling. The uterus of each mouse was examined at the end of the treatment period and frozen under liquid nitrogen. It was already noticed the whole mouse and uterine weights of Avastin®-treated mice were lower than their untreated controls, whether high fat or low fat. Some uteri appeared necrotic. Using these uterus samples, I looked for development of the c-MYC gene to find the effect of obesity versus Avastin®. Mice were analyzed by a gene kit using a real-time PCR machine. A kit was used to examine m-RNA sequences indicating c-MYC expression. Their development was seen by fluorescence labeling of the new gene transcripts. It already appeared that the medication had profound effects, especially on animals that were not obese and that pretreatment for cancer was unwarranted. However, development of this gene assay may have proven to be a good marker for developing reproductive cancer in women.
A Possible Screening for the Development of Uterine Cancer in Obesity
CSU 253/4/5
Constant growth and shedding of the uterine lining in women has made them prone to mutations and cancer, especially in obesity. Obese women and animals have also shown increased sensitivity of their estrogen receptors. To test the hypothesis that obese female mice challenged with estrogen would have increased cancer gene expression and reduced risk in the presence of a medication that reduced blood vessel formation, female mice were fed a normal diet compared to others fed a high fat diet for 15 weeks, given that medication (Avastin®) for the first 10 days, and challenged with a dose of estrogen 6 hours prior to sampling. The uterus of each mouse was examined at the end of the treatment period and frozen under liquid nitrogen. It was already noticed the whole mouse and uterine weights of Avastin®-treated mice were lower than their untreated controls, whether high fat or low fat. Some uteri appeared necrotic. Using these uterus samples, I looked for development of the c-MYC gene to find the effect of obesity versus Avastin®. Mice were analyzed by a gene kit using a real-time PCR machine. A kit was used to examine m-RNA sequences indicating c-MYC expression. Their development was seen by fluorescence labeling of the new gene transcripts. It already appeared that the medication had profound effects, especially on animals that were not obese and that pretreatment for cancer was unwarranted. However, development of this gene assay may have proven to be a good marker for developing reproductive cancer in women.
Recommended Citation
Lamoreux, Jennifer L.. "A Possible Screening for the Development of Uterine Cancer in Obesity." Undergraduate Research Symposium, Mankato, MN, April 4, 2011.
https://cornerstone.lib.mnsu.edu/urs/2011/poster-session-C/9
