Predictive Value of E-cadherin, β-catenin and SOX4 in Recurrence and/or Progression of Non-muscle Invasive Urinary Bladder Transitional Cell Carcinoma. A Retrospective Study
试验速览
- 阶段
- 不适用
- 状态
- 已完成
- 入组人数
- 30
- 试验地点
- 1
研究概览
简要总结
Bladder cancer is common tumor in which recurrence and/or progression in patients undergoing TUR has been reported to range between 30% and 80% in patients with NMIBC TCC.
With evidence of E-cadherin, β-catenin and SOX4 playing a role in the development of tumors, it manifests as invasion and metastasis.
In this study, we hope to develop the correlation regarding the alternation in the expression of E-cadherin, β-catenin and Sox4 in determining the recurrence, progression and up staging and their prognostic value in NMIBC.
详细描述
Bladder cancer (BC) is one of the most common genitourinary malignancies worldwide. [1]
The incidence of BC increases with age, with a high incidence among those 50-70 years old. The incidence of BC in males is three- to four-times higher than that in females [2]. The etiology and pathogenesis of BC are complex, with both internal genetic factors and external environmental factors. Smoking and occupational exposure to aromatic amine chemicals (such as aniline, 2-aminobiphenyl, 2-naphthalene, 1-naphthalamines etc.) are the two major risk factors for BC [3].
At present, some studies suggest that the abnormal function of intercellular adhesion molecules is highly correlated with the invasion of surrounding tissues and distant organ metastasis of BC [4].
BC is typically grouped into two main pathological classes non-muscular invasive bladder cancer (NMIBC) which is further sub classified according to histological grade (low or high), and muscular invasive bladder cancer (MIBC) according to the European Association of Urology (EAU) guidelines. BC can also be divided into several types-transitional cell carcinoma (TCC), squamous epithelial carcinoma, and adenocarcinoma-among which over 90% are TCC [5].
While histological and pathological grading and staging systems exist for some time, recent advances in genomic sequencing have lent insight into molecular characterizations that stratify patients into various subtypes based on genetic markers, such as amplifications, mutations and deletions [6].
研究设计
- 研究类型
- Observational
- 观察模型
- Case Control
- 时间视角
- Retrospective
入排标准
- 性别
- All
- 接受健康志愿者
- 否
入选标准
- •1. The patients were treated with transurethral resection of bladder tumor finally diagnosed with NMIBC TCC by pathological examination.
- •2. The controls were normal bladder tissues. Or patients diagnosed with cystitis or dysplasia on pathological examination
排除标准
- •Age at the time of cancer diagnosis > 70 years
- •Patients diagnosed with MIBC
- •Patients with concomitant upper urinary tracts tumors
- •Patients with concomitant prostatic tumors
- •Patients diagnosed with TCC T1 who did not received full induction, or maintenance doses BCG
- •Patients showed BCG toxicity signs
- •Patients diagnosed with TCC T1 who did not underwent 2nd look TURBT
- •Patients with known genetic/congenital disorder that may interfere with/or increase risk of BC;
- •Bladder exstrophy.
- •Rb1: An altered form of Rb1, retinoblastoma gene, is associated with cancer of the eye in infants, and may increase your bladder cancer risks.
- •Cowden disease: This syndrome, linked to an abnormal form of the gene PTEN, may trigger breast cancer and thyroid cancer, and increases the risk of bladder cancer.
- •Lynch syndrome: This genetic condition, also known as hereditary non-polyposis colorectal cancer, is usually tied to colon and endometrial cancer. However, this syndrome may also increase the risk of bladder cancer and cancer of the ureter.
- •Patients with history of chemotherapy or pelvic radiations for other tumor treatment than BC