Latest studies on the causes of the endometrial cancer focus on the effects of estrogen and progesterone; however, they do not demonstrate any evidence of the possible influence of inflammation, inhibited by biosynthesis expressions in the uterus. The research proves that DRUG A consumption decreases a risk of endometrial cancer among women with obesity correlated with anti-inflammation medications.
The research approved by the Human Research Committee of the Brigham and Women’s Hospital Boston, calculated consumption of the DRUG A in amount of 1 tablet per week biennially since 1976 and included 82,971 female participants. Between 1980 and 2004 studies included participants with menopausal status, PMH, weight diabetes, oral contraceptive consumption and BMI rate. The primary analysis was based on the relative risk of endometrial cancer among consumers and non-consumers of DRUG A and divided into 5-year age category. The listed risk factors were also determiners in the study of the variation of the PMH use, oral contraceptive use, parity, menopausal or smoking status and DRUG A effectiveness according to these conditions.Want an expert to write a paper for you Talk to an operator now
The study carried out between 1980 and 2004 calculated 747 incidence cases among which participants diagnosed with endometrial cancer were 98 with premenopausal status and 645 with postmenopausal status. These figures include 268 participants with BMI rate of 30 kg/m² and 286 PMH non-consumers. Numbers of the incidence cases in DRUG A use were generally similar. The results have also shown that BMI rate was higher among participants who consumed seven or more tablets of DRUG A per week. Other results varied by BMI and PMH use and showed that non-consumers of DRUG A and non-obese women did not have endometrial cancer reduction.
The finding of the research demonstarted endometrial cancer reduction among 35 % DRUG A consumers with BMI rate of 30 kg/m² who has never used PMH. Anti-inflammation medications such as ENZYME-1 and ENZYME-2 increase production of prostaglandin E2 and with DRUG A or DRUG B consumption help to repair gene expression, regulate cell cycle and control apoptosis. Obesity, as a risk factor of the endometrial cancer, is grounded on the production of estrogens, which induce endometrial cell spreading and carcinogenesis. In addition, previous inflammation may result into retention of the pre-cancer clones of endometrium, which basement membrane can be broken down by the current carcinogenic promoters.
The effect of ENZYME-1 may supersede the incomplete sloughing of the pre-cancer clones in non-obese DRUG A consumers. Studies suggest the maximal effectiveness of DRUG A use is achieved in the short period with the highest dose. DRUG C use included relatively few cases and proved to lack a systematic anti-inflammatory effect; however, it has structural similarity to steroids and can lower follicular levels of hormones. The risks and benefits of DRUG A use among obese women, who have the highest risk of the endometrial cancer, should be confirmed by the further researches.