- ICH GCP
- US Clinical Trials Registry
- Clinical Trial NCT06195371
Impact of CASP3 Gene in Chemoresistance
February 24, 2024 updated by: Gehad Salah El-Din shaker
The Impact of CASP3 Gene in Chemoresistant Breast Cancer
- This study aims to evaluate the abnormalities of CASP3 gene in chemo resistance in breast cancer by FISH technique. evaluate the abnormalities of CASP3 gene in chemo resistance in breast cancer by FISH technique.
- Detect CASP3 gene abnormality relation to survival, chemoresponse & chemoresistance.
- Correlate CASP3 gene abnormalities with available clinicopathological data of breast cancer patients.
Study Overview
Status
Not yet recruiting
Conditions
Detailed Description
Breast cancer (BC) is the most common malignant tumor in women and the biggest threat to the health of women worldwide.
Breast cancer represents a significant global health challenge: it is the most commonly diagnosed cancer in the world with an estimated 2.26 million cases recorded in 2020.
Breast cancer is rarely seen in males.
The incidence of breast cancer rises rapidly over the years, ranking as the first common cancer among females worldwide, and thus posing a considerable threat to female health.
Breast cancer is the leading cause of cancer mortality among females.
Although historically considered to be a disease of largely developed countries, over half of breast cancer diagnoses and two-thirds of breast cancer related deaths occurred in the less developed regions of the world in 2020.Being a highly prevalent cancer type, breast cancer is observed in both developing and developed countries with different causes and factors of progression.
Adopting new life styles, industrialization, globalization, increased life expectancy, pollution etc are the leading causes of cancer.
According to 2018 statistics, every year around 1.2 million new cases of breast cancer were diagnosed.
The GLOBACON report of 2018 concluded that breast cancer was the most frequently identified cancer type and leading cause of cancer related death in majority of countries.
Major part of breast related cancer is linked with the expression of estrogen receptors and their treatment is related with the disease prognosis.
The rate of breast cancer mortality can be reduced down to a limit by early diagnosis; timely treatment and management .
The commonly used chemotherapeutic drugs include doxorubicin (DOX), paclitaxel and cyclophosphamide.
However, the efficiency of chemotherapy is greatly limited by primary and acquired drug resistance .
Chemotherapy is widely accepted as traditional treatment method in spite of the obstacle of chemotherapy resistance.
The important mechanisms that may lead to drug resistance include alteration in expression of ABC transporters gene family, damage of topoisomerase enzyme, mutation in DNA repair genes, induced apoptosis by genetic imbalance and alteration in signalling pathways of NF alpha etc.
All these worsen the condition of breast cancer making chemotherapy a failure in most cases.
According to Yaghoubi et al., 2015, the cells which already acquired drug resistance show cross resistance to anti proliferative nature of anti-oestrogen drugs which have crucial role in breast cancer treatment .Caspase-3, a cysteine-aspartic acid protease, has recently attracted much attention .
Caspase-3 is a protein (also called CPP32 or apopain), encoded by the CASP3 gene; which is located in the 4q34 with size 2635 bp.
It mediates apoptosis in response to chemotherapy, but losing caspase 3 activity causes cell survival and induces drug resistance through apoptotic pathway in breast cancer .Caspase-3 has been identified as a key mediator of apoptosis, activated in apoptotic cells by both extrinsic (death ligands) and intrinsic (mitochondrial) pathways.
It also has several nonapoptotic functions such as involving in tissue differentiation, regeneration, and neural development.
Nonconforming activation of caspase-3 can lead to tumorigenesis instead of inducing the programmed cell death.Recent progress in caspase research indicates that caspases-3 is a prominent enzyme not only in apoptotic flux but also in nonapoptotic processes such as tissue differentiation, tissue regeneration, and neural development.
Study Type
Observational
Enrollment (Estimated)
60
Contacts and Locations
This section provides the contact details for those conducting the study, and information on where this study is being conducted.
Study Contact
- Name: Gehad Salah E-Din Shaker
- Phone Number: 01007293809
- Email: ghafez113@gmail.com
Participation Criteria
Researchers look for people who fit a certain description, called eligibility criteria. Some examples of these criteria are a person's general health condition or prior treatments.
Eligibility Criteria
Ages Eligible for Study
- Child
- Adult
- Older Adult
Accepts Healthy Volunteers
N/A
Sampling Method
Non-Probability Sample
Study Population
female patients with breast cancer
Description
Inclusion Criteria:
- Newly diagnosed patients of breast cancer admitted to South Egypt Cancer Institute at different stages of the disease
Exclusion Criteria:
- Other malignant diseases-Male breast cancer .
Study Plan
This section provides details of the study plan, including how the study is designed and what the study is measuring.
How is the study designed?
Design Details
What is the study measuring?
Primary Outcome Measures
Outcome Measure |
Measure Description |
Time Frame |
|---|---|---|
|
- Evaluation of casp3 gene abnormalities by fluorescence in situ hybridization in patients with breast cancer
Time Frame: baseline
|
Evaluation of casp3 gene abnormalities by fluorescence in situ hybridization in patients with breast cancer
|
baseline
|
Secondary Outcome Measures
Outcome Measure |
Measure Description |
Time Frame |
|---|---|---|
|
- correlation between casp3 gene and response to Chemotherapy.
Time Frame: baseline
|
correlation between casp3 gene and response to Chemotherapy.
|
baseline
|
Collaborators and Investigators
This is where you will find people and organizations involved with this study.
Sponsor
Collaborators
Publications and helpful links
The person responsible for entering information about the study voluntarily provides these publications. These may be about anything related to the study.
General Publications
- Fu W, Song J, Li H. Breviscapine reverses doxorubicin resistance in breast cancer and its related mechanisms. Thorac Cancer. 2023 Sep;14(27):2785-2792. doi: 10.1111/1759-7714.15072. Epub 2023 Aug 16.
- Wilkinson L, Gathani T. Understanding breast cancer as a global health concern. Br J Radiol. 2022 Feb 1;95(1130):20211033. doi: 10.1259/bjr.20211033. Epub 2021 Dec 14.
- Xu F, Xia T, Xu QT, Zhang X, Huang YZ, Sun X, Shi L, Zhou XJ, Wei JF, Ding Q. RBMS2 Chemosensitizes Breast Cancer Cells to Doxorubicin by Regulating BMF Expression. Int J Biol Sci. 2022 Feb 7;18(4):1724-1736. doi: 10.7150/ijbs.66480. eCollection 2022.
- Yaghoubi A, Ghojazadeh M, Abolhasani S, Alikhah H, Khaki-Khatibi F. Correlation of Serum Levels of Vitronectin, Malondialdehyde and Hs- CRP With Disease Severity in Coronary Artery Disease. J Cardiovasc Thorac Res. 2015;7(3):113-7. doi: 10.15171/jcvtr.2015.24.
- Asadi M, Taghizadeh S, Kaviani E, Vakili O, Taheri-Anganeh M, Tahamtan M, Savardashtaki A. Caspase-3: Structure, function, and biotechnological aspects. Biotechnol Appl Biochem. 2022 Aug;69(4):1633-1645. doi: 10.1002/bab.2233. Epub 2021 Aug 22.
- Jakubowska K, Guzinska-Ustymowicz K, Famulski W, Cepowicz D, Jagodzinska D, Pryczynicz A. Reduced expression of caspase-8 and cleaved caspase-3 in pancreatic ductal adenocarcinoma cells. Oncol Lett. 2016 Mar;11(3):1879-1884. doi: 10.3892/ol.2016.4125. Epub 2016 Jan 19.
- Shalini S, Dorstyn L, Dawar S, Kumar S. Old, new and emerging functions of caspases. Cell Death Differ. 2015 Apr;22(4):526-39. doi: 10.1038/cdd.2014.216. Epub 2014 Dec 19.
Study record dates
These dates track the progress of study record and summary results submissions to ClinicalTrials.gov. Study records and reported results are reviewed by the National Library of Medicine (NLM) to make sure they meet specific quality control standards before being posted on the public website.
Study Major Dates
Study Start (Estimated)
May 1, 2024
Primary Completion (Estimated)
November 1, 2026
Study Completion (Estimated)
December 1, 2026
Study Registration Dates
First Submitted
December 23, 2023
First Submitted That Met QC Criteria
December 23, 2023
First Posted (Actual)
January 8, 2024
Study Record Updates
Last Update Posted (Actual)
February 28, 2024
Last Update Submitted That Met QC Criteria
February 24, 2024
Last Verified
October 1, 2023
More Information
Terms related to this study
Additional Relevant MeSH Terms
Other Study ID Numbers
- CASP3 gene in breast cancer
Drug and device information, study documents
Studies a U.S. FDA-regulated drug product
No
Studies a U.S. FDA-regulated device product
No
This information was retrieved directly from the website clinicaltrials.gov without any changes. If you have any requests to change, remove or update your study details, please contact register@clinicaltrials.gov. As soon as a change is implemented on clinicaltrials.gov, this will be updated automatically on our website as well.
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