An observational study in Gallbladder Cancer, sponsored by Banaras Hindu University. Recruiting at 1 site in India. Open to participants aged 18 Years to 99 Years. Per ClinicalTrials.gov, last updated 2024-08-13.
Sponsored by Banaras Hindu University · Observational
Evidence suggests distinct models of molecular and pathologic progression, and a growing body of genetics data points to a heterogeneous collection of underlying mutations in key oncogenes and tumor suppressor genes. Although tumor genetics have been used to tailor individual treatment regimens and guide clinical decision making in other cancers, these principles have not been applied in gallbladder malignancy. Recent clinical trials with targeted therapies seem promising, although the relationships between subsets of patients with positive responses to therapy and tumor genetics remain unexplored.
Gallbladder carcinoma (GBC) is the most common type of biliary tract carcinoma and the third commonest digestive tract malignancy in India. GBC arises in the setting of chronic inflammation and the commonest source is cholesterol gallstones (in more than 75% patients). Other causes of chronic inflammation include primary sclerosing cholangitis, ulcerative colitis, liver flukes, chronic Salmonella typhi and paratyphi infections, and Helicobacter infection. Many other factors have also been identified such as ingestion of certain chemicals, exposures through water pollution, heavy metals and radiation exposure. Only a small fraction of GBC are associated with hereditary syndromes like Gardner syndrome, neurofibromatosis type I and hereditary non-polyposis colon cancer.
Of the multiple molecular alterations observed in GBC, it has not yet been possible to pinpoint which ones are the "driver" genes or controllers of the neoplastic process and to differentiate them from the "passenger" genes, those observed mainly in sporadic malignant tumors like GBC in which epigenetic alterations predominate. The most frequently mutated genes in GBC are: TP53 (41%), CDKN2A (28%) KRAS (19%), TERT (8%), CTNNB1 (8%) and PI3K (7%). The signalling pathway of the ERBB family is one of the most frequently mutated in GBC. These receptors participate in regulating cell proliferation, differentiation and survival. Their amplification mainly translates into protein over expression. The receptor HER2/NEU, after dimerization activates a large variety of downstream pathways such as RAS-RAF-MEK-ERK1/2 or PI3k-AKT-MTOR with great influence on cell proliferation. On the other hand, PTEN (phosphatase and tensin homolog) is a tumor suppressor gene that encodes a protein with phosphatase function that inactivates substrates like PI3K The absence of the PTEN functional protein permits the activation of PI3k with an even greater intensity than the activating mutation of PI3K itself. The uncontrolled production of PIP3 is one of the most important effectors of the PI3K/AKT pathway with mTOR stimulating protein synthesis that regulate apoptosis. The immunohistochemical expression of the PTEN protein is considered a good way to evaluate the functional state of the gene.
255 studies on the registry are indexed under Gallbladder Neoplasms; 61 are open to participants now.
This study's planned enrollment of 100 is below the median of 230 across 54 observational studies indexed under Gallbladder Neoplasms.
Browse Gallbladder Neoplasms studies →Banaras Hindu University is the lead sponsor of 21 studies on the registry; 2 are open to participants now.
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Patients with histologically confirmed diagnosis of gallbladder cancer irrespective of stage, being treated with palliative or curative intent with standard of care for that stage of carcinoma of the gallbladder
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Exclusion Criteria:
Patients with confirmed diagnosis of gallbladder cancer
Diagnostic Test: Next generation sequencing
NGS is carried out on DNA isolated from paraffin embedded tissue
Response to treatment
Response to treatment in terms of chemotherapy
Time frame: 1 year
Overall Survival
Survival of patients from the date of diagnosis to closure of study or death which ever is earlier
Time frame: 5 year
PFS
Progression free survival from the date of diagnosis to progression of disease
Time frame: 5 yers
RFS
Recurrence free Survival from the date of diagnosis to occurrence of recurrence or metastasis
Time frame: 5 year
Plan to share: Yes — Anonymized data will be made available on reasonable request
Supporting information: Study protocol, Statistical analysis plan, Informed consent form, Clinical study report, Analytic code
Time frame: 3 months
Access criteria: Request
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Banaras Hindu University