Bladder CancerNCT07657299
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
An observational study of Bladder Cancer and Bladder Cancer Recurrence, run by Ain Shams University at 1 site in Egypt.
Trial summary
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. Read more about this study
- Who is it for?
- Any age
- Conditions the study is for
- Bladder Cancer, Bladder Cancer Recurrence
- How many people
- 30 participants
- Where
- 1 siteEgypt
- Study dates
- 1 Apr 2022to 1 Jun 2024
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages Any age
- All sexes
- No healthy volunteers
- Child, Adult, Older adult
Study population: * Inclusion Criteria: 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 * Exclusion Criteria: 1. Age at the time of cancer diagnosis > 70 years 2. Patients diagnosed with MIBC 3. Patients with concomitant upper urinary tracts tumors 4. Patients with concomitant prostatic tumors 5. Patients diagnosed with TCC T1 who did not received full induction, or maintenance doses BCG 6. Patients showed BCG toxicity signs 7. Patients diagnosed with TCC T1 who did not underwent 2nd look TURBT 8. Patients with known genetic/congenital disorder that may interfere with/or increase risk of BC; 9. Patients with history of chemotherapy or pelvic radiations for other tumor treatment than BC
Who may be able to join
- 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
- Exclusion Criteria:
- Age at the time of cancer diagnosis > 70 years
- Patients diagnosed with MIBC
- Patients with concomitant upper urinary tracts tumors
Show all 16Show fewer
- 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
Who cannot join
None listed.
Trial locations and contacts
1 site in 1 country.
About this study
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.
Read the detailed description
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].
The current standard treatment of patients with non-muscle-invasive bladder cancer (NMIBC) is complete removal of the visible tumor burden by transurethral resection (TUR), and the prognosis of such patients is generally favorable, achieving 5-year survival rates greater than 80% [7].
However, the high probability of intravesical recurrence in patients undergoing TUR has been reported to range between 30% and 80% in patients with NMIBC [7-8]. Intensive efforts, therefore, have been made to identify factors precisely predicting the clinical course of NMIBC following TUR, which are of great utility in planning both postoperative adjuvant therapy and follow-up schedule in an individual patient.
Of patients with BC 50% to 55% present with Ta tumors, for which recurrence is the main clinical issue, occurring in up to 80% [9-10].
However, for the 20% to 25% of patients presenting with T1 tumors, progression is the main clinical concern, occurring in up to 45% [9-10]. Progression to or presentation with muscle invasive disease (stage T2-4) represents the critical step in the disease course of bladder cancer, Necessitating more radical and aggressive therapies, including surgery, chemotherapy or radiotherapy, and carrying a 5-year survival rate of only 27% to 50% [10].
These aggressive therapies represent relatively crude approaches with significant morbidity and mortality [11].
Cadherins are the main mediators of cell-cell adhesion in epithelial tissues; E-cadherin is an important transmembrane glycoprotein of epithelial cell adhesion. It is also an inhibitor of tumor invasion and metastasis. It plays an important role in maintaining cell morphology, cell movement, and adhesion function [12].
E-cadherin needs β-catenin to mediate and participate in its physiological function. β-catenin is an E-cadherin-related protein. The intracellular domain of E-cadherin is connected with β-catenin to form a β-catenin/E-cadherin complex, which is transported to the cell membrane through the cytoplasm and inserted into the cell membrane to maintain the polarity and stability of epithelial cells [13].
In the process of tumorigenesis, the abnormality of β-catenin affects the stability of the β-catenin/E-cadherin complex, which leads to a decrease in cell junction density and the loss of cell contact inhibition function. In the development of tumors, it manifests as invasion and metastasis [13-14].
Furthermore, the abnormal expression of Cadherins (cadherin switching) has been shown to promote a more invasive and malignant phenotype of cancer, and possibly even acts as the principal mediator of invasion and metastasis in BC [15].
SOX (SRY-related HMG-box) family of transcription factors involved In organogenesis of various organs. One of the candidate is located at the chromosome 6p22 locus is Sox4 [16],
SOX4 gene expression is upregulated in many cancer types, and it's increase activity contributes to cellular transformation, cell survival, and metastasis [17].
SOX family of proteins are found in all metazoans, and high expression of SOX4 has been used to recognize the presence of CSCs. This approach has been applied in some studies of TCC [18].
The cancer stem cells (CSCs) hypothesis is based on the observation of many cancers, including bladder cancer, are driven by a subpopulation of tumor-initiating cells (popularly known as CSCs) and promote tumor growth. In addition, CSCs are resistant to chemotherapy and radiation treatments, which potentially explains the limitations of curing human malignancies [19].
Down-regulation of SOX4 led to mesenchymal-to-epithelial transition (MET) and inhibition of cell migration. Of note, knockdown of SOX4 reduced sphere formation, aldehyde-dehydrogenase-high (ALDH) cell population and potential of tumor formation. Furthermore, immunohistochemistry (IHC) analysis of human bladder tumor tissue microarrays (TMAs) indicated that high SOX4 expression correlated with advanced tumor stages and poorer survival of urinary bladder cancer patients. Providing the first evidence, that SOX4 may act as an oncogene [20].
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.
- Conditions
- Bladder Cancer, Bladder Cancer Recurrence
- Keywords
- β-catenin, E-cadherin, NMIBC, progression, recurrence, SOX4
- Medical subject headings
- Urinary Bladder Neoplasms, Non-Muscle Invasive Bladder Neoplasms, Disease Progression, Recurrence
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| 30 patients who treated with transurethral resection of bladder tumor finally diagnosed with NMIBC | * Inclusion Criteria: 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 * Exclusion Criteria: 1. Age at the time of cancer diagnosis > 70 years 2. Patients diagnosed with MIBC 3. Patients with concomitant upper urinary tracts tumors 4. Patients with concomitant prostatic tumors 5. Patients diagnosed with TCC T1 who did not received full induction, or maintenance doses BCG 6. Patients showed BCG toxicity signs 7. Patients diagnosed with TCC T1 who did not underwent 2nd look TURBT 8. 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, |
What is being measured
The primary outcome is the main question the study is designed to answer.
This study aims to develop correlation regarding the alternation in the expression of E-cadherin, β-catenin and SOX4 in determining the recurrence and/or progression and their prognostic value in NMIBC TCC.
This study aims to develop correlation regarding the alternation in the expression of E-cadherin, β-catenin and SOX4 in determining the recurrence and/or progression and their prognostic value in NMIBC TCC.
Measured: 2 years
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted18 Jun 2026
- Study start1 Apr 2022
- Primary completion1 Jun 2024
- Study completion1 Jun 2024
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (20)Papers the sponsor has linked to this study.
- Other trials for Bladder CancerStudies of the same condition, open and under way.
- More trials run by Ain Shams UniversityThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case-control
- Time perspective
- Retrospective
- Enrolment
- 30 participants (actual)
Sponsor and investigators
- Lead sponsor
- Ain Shams University
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07657299
- Sponsor's protocol ID
- FMASU MS 332/2022
- Other IDs
- URO 37 12 28
- Status last verified
- Jan 2026
- First submitted
- 13 Jun 2026
- Last updated
- 18 Jun 2026
- Results posted
- No
- Data monitoring committee
- Yes
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided
Publications
Du Y, Spence SE, Jenkins NA, Copeland NG. Cooperating cancer-gene identification through oncogenic-retrovirus-induced insertional mutagenesis. Blood. 2005 Oct 1;106(7):2498-505. doi: 10.1182/blood-2004-12-4840. Epub 2005 Jun 16.
PubMed 15961513Chan KS, Espinosa I, Chao M, Wong D, Ailles L, Diehn M, Gill H, Presti J Jr, Chang HY, van de Rijn M, Shortliffe L, Weissman IL. Identification, molecular characterization, clinical prognosis, and therapeutic targeting of human bladder tumor-initiating cells. Proc Natl Acad Sci U S A. 2009 Aug 18;106(33):14016-21. doi: 10.1073/pnas.0906549106. Epub 2009 Aug 4.
PubMed 19666525Ojha R, Singh SK, Bhattacharyya S, Dhanda RS, Rakha A, Mandal AK, Jha V. Inhibition of grade dependent autophagy in urothelial carcinoma increases cell death under nutritional limiting condition and potentiates the cytotoxicity of chemotherapeutic agent. J Urol. 2014 Jun;191(6):1889-98. doi: 10.1016/j.juro.2014.01.006. Epub 2014 Jan 15.
PubMed 24440234Tiwari N, Tiwari VK, Waldmeier L, Balwierz PJ, Arnold P, Pachkov M, Meyer-Schaller N, Schubeler D, van Nimwegen E, Christofori G. Sox4 is a master regulator of epithelial-mesenchymal transition by controlling Ezh2 expression and epigenetic reprogramming. Cancer Cell. 2013 Jun 10;23(6):768-83. doi: 10.1016/j.ccr.2013.04.020.
PubMed 23764001Lioubinski O, Muller M, Wegner M, Sander M. Expression of Sox transcription factors in the developing mouse pancreas. Dev Dyn. 2003 Jul;227(3):402-8. doi: 10.1002/dvdy.10311.
PubMed 12815626Yilmaz M, Christofori G. EMT, the cytoskeleton, and cancer cell invasion. Cancer Metastasis Rev. 2009 Jun;28(1-2):15-33. doi: 10.1007/s10555-008-9169-0.
PubMed 19169796Kashibuchi K, Tomita K, Schalken JA, Kume H, Takeuchi T, Kitamura T. The prognostic value of E-cadherin, alpha-, beta- and gamma-catenin in bladder cancer patients who underwent radical cystectomy. Int J Urol. 2007 Sep;14(9):789-94. doi: 10.1111/j.1442-2042.2007.01830.x.
PubMed 17760743Umbas R, Isaacs WB, Bringuier PP, Xue Y, Debruyne FM, Schalken JA. Relation between aberrant alpha-catenin expression and loss of E-cadherin function in prostate cancer. Int J Cancer. 1997 Aug 22;74(4):374-7. doi: 10.1002/(sici)1097-0215(19970822)74:43.0.co;2-s.
PubMed 9291424Bringuier PP, Umbas R, Schaafsma HE, Karthaus HF, Debruyne FM, Schalken JA. Decreased E-cadherin immunoreactivity correlates with poor survival in patients with bladder tumors. Cancer Res. 1993 Jul 15;53(14):3241-5.
PubMed 8324734Lorusso V, Silvestris N. Systemic chemotherapy for patients with advanced and metastatic bladder cancer: current status and future directions. Ann Oncol. 2005 May;16 Suppl 4:iv85-89. doi: 10.1093/annonc/mdi914. No abstract available.
PubMed 15923437Wallace DM, Bryan RT, Dunn JA, Begum G, Bathers S; West Midlands Urological Research Group. Delay and survival in bladder cancer. BJU Int. 2002 Jun;89(9):868-78. doi: 10.1046/j.1464-410x.2002.02776.x.
PubMed 12010230van Rhijn BW, Burger M, Lotan Y, Solsona E, Stief CG, Sylvester RJ, Witjes JA, Zlotta AR. Recurrence and progression of disease in non-muscle-invasive bladder cancer: from epidemiology to treatment strategy. Eur Urol. 2009 Sep;56(3):430-42. doi: 10.1016/j.eururo.2009.06.028. Epub 2009 Jun 26.
PubMed 19576682Millan-Rodriguez F, Chechile-Toniolo G, Salvador-Bayarri J, Palou J, Vicente-Rodriguez J. Multivariate analysis of the prognostic factors of primary superficial bladder cancer. J Urol. 2000 Jan;163(1):73-8. doi: 10.1016/s0022-5347(05)67975-x.
PubMed 10604317Oosterlinck W. The management of superficial bladder cancer. BJU Int. 2001 Jan;87(2):135-40. doi: 10.1046/j.1464-410x.2001.00948.x. No abstract available.
PubMed 11167630Aine M, Eriksson P, Liedberg F, Hoglund M, Sjodahl G. On Molecular Classification of Bladder Cancer: Out of One, Many. Eur Urol. 2015 Dec;68(6):921-3. doi: 10.1016/j.eururo.2015.07.021. Epub 2015 Jul 26.
PubMed 26215606
Study at a glance
From the registry record, last updated by the sponsor on 18 Jun 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- 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
- ClinicalTrials.gov ID
- NCT07657299
- Acronym / sponsor ID
- FMASU MS 332/2022
- Conditions
- Bladder Cancer, Bladder Cancer Recurrence
- Keywords
- β-catenin, E-cadherin, NMIBC, progression, recurrence, SOX4
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 30 participants (actual)
- Lead sponsor
- Ain Shams UniversityUniversity, hospital or other
- Study start
- 1 Apr 2022 (actual)
- Primary completion
- 1 Jun 2024 (actual)
- Study completion
- 1 Jun 2024 (actual)
- First posted
- 18 Jun 2026 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
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.
Detailed description
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].
The current standard treatment of patients with non-muscle-invasive bladder cancer (NMIBC) is complete removal of the visible tumor burden by transurethral resection (TUR), and the prognosis of such patients is generally favorable, achieving 5-year survival rates greater than 80% [7].
However, the high probability of intravesical recurrence in patients undergoing TUR has been reported to range between 30% and 80% in patients with NMIBC [7-8]. Intensive efforts, therefore, have been made to identify factors precisely predicting the clinical course of NMIBC following TUR, which are of great utility in planning both postoperative adjuvant therapy and follow-up schedule in an individual patient.
Of patients with BC 50% to 55% present with Ta tumors, for which recurrence is the main clinical issue, occurring in up to 80% [9-10].
However, for the 20% to 25% of patients presenting with T1 tumors, progression is the main clinical concern, occurring in up to 45% [9-10]. Progression to or presentation with muscle invasive disease (stage T2-4) represents the critical step in the disease course of bladder cancer, Necessitating more radical and aggressive therapies, including surgery, chemotherapy or radiotherapy, and carrying a 5-year survival rate of only 27% to 50% [10].
These aggressive therapies represent relatively crude approaches with significant morbidity and mortality [11].
Cadherins are the main mediators of cell-cell adhesion in epithelial tissues; E-cadherin is an important transmembrane glycoprotein of epithelial cell adhesion. It is also an inhibitor of tumor invasion and metastasis. It plays an important role in maintaining cell morphology, cell movement, and adhesion function [12].
E-cadherin needs β-catenin to mediate and participate in its physiological function. β-catenin is an E-cadherin-related protein. The intracellular domain of E-cadherin is connected with β-catenin to form a β-catenin/E-cadherin complex, which is transported to the cell membrane through the cytoplasm and inserted into the cell membrane to maintain the polarity and stability of epithelial cells [13].
In the process of tumorigenesis, the abnormality of β-catenin affects the stability of the β-catenin/E-cadherin complex, which leads to a decrease in cell junction density and the loss of cell contact inhibition function. In the development of tumors, it manifests as invasion and metastasis [13-14].
Furthermore, the abnormal expression of Cadherins (cadherin switching) has been shown to promote a more invasive and malignant phenotype of cancer, and possibly even acts as the principal mediator of invasion and metastasis in BC [15].
SOX (SRY-related HMG-box) family of transcription factors involved In organogenesis of various organs. One of the candidate is located at the chromosome 6p22 locus is Sox4 [16],
SOX4 gene expression is upregulated in many cancer types, and it's increase activity contributes to cellular transformation, cell survival, and metastasis [17].
SOX family of proteins are found in all metazoans, and high expression of SOX4 has been used to recognize the presence of CSCs. This approach has been applied in some studies of TCC [18].
The cancer stem cells (CSCs) hypothesis is based on the observation of many cancers, including bladder cancer, are driven by a subpopulation of tumor-initiating cells (popularly known as CSCs) and promote tumor growth. In addition, CSCs are resistant to chemotherapy and radiation treatments, which potentially explains the limitations of curing human malignancies [19].
Down-regulation of SOX4 led to mesenchymal-to-epithelial transition (MET) and inhibition of cell migration. Of note, knockdown of SOX4 reduced sphere formation, aldehyde-dehydrogenase-high (ALDH) cell population and potential of tumor formation. Furthermore, immunohistochemistry (IHC) analysis of human bladder tumor tissue microarrays (TMAs) indicated that high SOX4 expression correlated with advanced tumor stages and poorer survival of urinary bladder cancer patients. Providing the first evidence, that SOX4 may act as an oncogene [20].
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.
Study design
- Observational model
- Case-control
- Time perspective
- Retrospective
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| 30 patients who treated with transurethral resection of bladder tumor finally diagnosed with NMIBC | – | –* Inclusion Criteria: 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 * Exclusion Criteria: 1. Age at the time of cancer diagnosis > 70 years 2. Patients diagnosed with MIBC 3. Patients with concomitant upper urinary tracts tumors 4. Patients with concomitant prostatic tumors 5. Patients diagnosed with TCC T1 who did not received full induction, or maintenance doses BCG 6. Patients showed BCG toxicity signs 7. Patients diagnosed with TCC T1 who did not underwent 2nd look TURBT 8. 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, |
Who may qualify
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child, Adult, Older adult
- Study population
- * Inclusion Criteria: 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 * Exclusion Criteria: 1. Age at the time of cancer diagnosis > 70 years 2. Patients diagnosed with MIBC 3. Patients with concomitant upper urinary tracts tumors 4. Patients with concomitant prostatic tumors 5. Patients diagnosed with TCC T1 who did not received full induction, or maintenance doses BCG 6. Patients showed BCG toxicity signs 7. Patients diagnosed with TCC T1 who did not underwent 2nd look TURBT 8. Patients with known genetic/congenital disorder that may interfere with/or increase risk of BC; 9. Patients with history of chemotherapy or pelvic radiations for other tumor treatment than BC
Key inclusion criteria (16 listed)
- 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
- Exclusion Criteria:
- Age at the time of cancer diagnosis > 70 years
- Patients diagnosed with MIBC
Key exclusion criteria (0 listed)
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
This study aims to develop correlation regarding the alternation in the expression of E-cadherin, β-catenin and SOX4 in determining the recurrence and/or progression and their prognostic value in NMIBC TCC.
Time frame: 2 years
This study aims to develop correlation regarding the alternation in the expression of E-cadherin, β-catenin and SOX4 in determining the recurrence and/or progression and their prognostic value in NMIBC TCC.
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 18 Jun 2026.
- Background: PubMed 15961513Du Y, Spence SE, Jenkins NA, Copeland NG. Cooperating cancer-gene identification through oncogenic-retrovirus-induced insertional mutagenesis. Blood. 2005 Oct 1;106(7):2498-505. doi: 10.1182/blood-2004-12-4840. Epub 2005 Jun 16.
- Background: PubMed 19666525Chan KS, Espinosa I, Chao M, Wong D, Ailles L, Diehn M, Gill H, Presti J Jr, Chang HY, van de Rijn M, Shortliffe L, Weissman IL. Identification, molecular characterization, clinical prognosis, and therapeutic targeting of human bladder tumor-initiating cells. Proc Natl Acad Sci U S A. 2009 Aug 18;106(33):14016-21. doi: 10.1073/pnas.0906549106. Epub 2009 Aug 4.
- Background: PubMed 24440234Ojha R, Singh SK, Bhattacharyya S, Dhanda RS, Rakha A, Mandal AK, Jha V. Inhibition of grade dependent autophagy in urothelial carcinoma increases cell death under nutritional limiting condition and potentiates the cytotoxicity of chemotherapeutic agent. J Urol. 2014 Jun;191(6):1889-98. doi: 10.1016/j.juro.2014.01.006. Epub 2014 Jan 15.
- Background: PubMed 23764001Tiwari N, Tiwari VK, Waldmeier L, Balwierz PJ, Arnold P, Pachkov M, Meyer-Schaller N, Schubeler D, van Nimwegen E, Christofori G. Sox4 is a master regulator of epithelial-mesenchymal transition by controlling Ezh2 expression and epigenetic reprogramming. Cancer Cell. 2013 Jun 10;23(6):768-83. doi: 10.1016/j.ccr.2013.04.020.
- Background: PubMed 12815626Lioubinski O, Muller M, Wegner M, Sander M. Expression of Sox transcription factors in the developing mouse pancreas. Dev Dyn. 2003 Jul;227(3):402-8. doi: 10.1002/dvdy.10311.
- Background: PubMed 19169796Yilmaz M, Christofori G. EMT, the cytoskeleton, and cancer cell invasion. Cancer Metastasis Rev. 2009 Jun;28(1-2):15-33. doi: 10.1007/s10555-008-9169-0.
- Background: PubMed 17760743Kashibuchi K, Tomita K, Schalken JA, Kume H, Takeuchi T, Kitamura T. The prognostic value of E-cadherin, alpha-, beta- and gamma-catenin in bladder cancer patients who underwent radical cystectomy. Int J Urol. 2007 Sep;14(9):789-94. doi: 10.1111/j.1442-2042.2007.01830.x.
- Background: PubMed 9291424Umbas R, Isaacs WB, Bringuier PP, Xue Y, Debruyne FM, Schalken JA. Relation between aberrant alpha-catenin expression and loss of E-cadherin function in prostate cancer. Int J Cancer. 1997 Aug 22;74(4):374-7. doi: 10.1002/(sici)1097-0215(19970822)74:43.0.co;2-s.
- Background: PubMed 8324734Bringuier PP, Umbas R, Schaafsma HE, Karthaus HF, Debruyne FM, Schalken JA. Decreased E-cadherin immunoreactivity correlates with poor survival in patients with bladder tumors. Cancer Res. 1993 Jul 15;53(14):3241-5.
- Background: PubMed 15923437Lorusso V, Silvestris N. Systemic chemotherapy for patients with advanced and metastatic bladder cancer: current status and future directions. Ann Oncol. 2005 May;16 Suppl 4:iv85-89. doi: 10.1093/annonc/mdi914. No abstract available.
- Background: PubMed 12010230Wallace DM, Bryan RT, Dunn JA, Begum G, Bathers S; West Midlands Urological Research Group. Delay and survival in bladder cancer. BJU Int. 2002 Jun;89(9):868-78. doi: 10.1046/j.1464-410x.2002.02776.x.
- Background: PubMed 19576682van Rhijn BW, Burger M, Lotan Y, Solsona E, Stief CG, Sylvester RJ, Witjes JA, Zlotta AR. Recurrence and progression of disease in non-muscle-invasive bladder cancer: from epidemiology to treatment strategy. Eur Urol. 2009 Sep;56(3):430-42. doi: 10.1016/j.eururo.2009.06.028. Epub 2009 Jun 26.
- Individual participant dataSharing planned: Undecided
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Muscle Invasive Bladder Urothelial Carcinoma, Muscle Invasive Renal Pelvis Urothelial Carcinoma
RecruitingPhase 3
A Clinical Trial of Sacituzumab Tirumotecan (Sac-TMT, MK-2870) and Pembrolizumab (MK-3475A) in Participants With Bladder Cancer (MK-2870-055)
Bladder Cancer
Active, not recruitingPhase 2/3
A Study of CTX-009 in Combination With Paclitaxel in Adult Patients With Unresectable Advanced, Metastatic or Recurrent Biliary Tract Cancers (COMPANION-002)
Biliary Tract Cancer, Cholangiocarcinoma
Recruiting
Effect of Cyclic Sighing Breathing Exercise on CRBD, Pain, and Sleep Quality in Patients Undergoing TUR
Transurethral Resection of Bladder Tumor, Transurethral Resection of the Prostate (TURP)
Recruiting
The Vanguard Study: Testing a New Way to Screen for Cancer
Bladder Carcinoma, Breast Carcinoma
Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
The record lists no contact. Use the official record to reach the sponsor.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Bladder Cancer and Bladder Cancer Recurrence, run by Ain Shams University at 1 site in Egypt.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 16 inclusion and 0 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 18 Jun 2026. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Egypt. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
This study aims to develop correlation regarding the alternation in the expression of E-cadherin, β-catenin and SOX4 in determining the recurrence and/or progression and their prognostic value in NMIBC TCC. (time frame: 2 years). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT07657299, which also lists 20 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 18 Jun 2026.