Zahid Siddik
University of Texas MD Anderson Cancer Center, TX·Pharmacology
Cisplatin is a widely used cancer drug. It works by switching on p53, a protein that tells damaged cells to die.
- Fields
Pharmacology
Medicine & Clinical Research
Biochemistry
- Topics
ovarian cancer
p53
tumor suppressor
- Grants
- 1 known grant, through Nov 2026
What they work on
- Test whether reducing MDM4, a natural inhibitor of the p53 tumor suppressor, restores basal p53 phosphorylation in cisplatin-resistant rare ovarian cancer subtype models, both in cultured cells and in animals.
- Determine whether targeting MDM4 makes resistant ovarian tumors sensitive to cisplatin again, using drug tools to measure tumor sensitivity and graphical modeling of combinations to test for synergy.
- Identify the active kinase, an enzyme that adds phosphate groups, that tags p53 once MDM4 is lowered, using biochemical and molecular tools, and assess whether it could serve as a therapy target.
More about the research
Many tumors still carry a normal, or wild-type, copy of p53, yet they resist cisplatin. A clear example is clear cell ovarian cancer, where only about 25% of patients respond and overall survival is about 10%. Rare ovarian cancer subtypes make up about 30% of ovarian cancers. About 90% of them carry wild-type p53, and they kill women at younger ages. Treatment for these subtypes is still largely trial and error.
Why it matters
Women with rare, cisplatin-resistant ovarian cancer subtypes, often diagnosed young, have poor survival and few rational treatment options. Restoring p53 activity by targeting MDM4 could lay groundwork for therapies that work together with cisplatin. Because many resistant cancers, such as mesothelioma and osteosarcoma, carry wild-type p53, the approach may apply to other tumors resistant to drugs.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Xinbin Chen
University of California-Davis, CA·Biochemistry
Determine how CDK4/6 enzymes, the RNA-binding protein RBM38 and the protein-synthesis factor eIF4G together boost mutant p53 production, and whether CDK4/6 inhibitors suppress triple-negative breast cancers partly by lowering mutant p53.
Jixin Dong
University of Nebraska Medical Center, NE·Pharmacology
Establish in animal models whether protein kinase R, an enzyme best known in antiviral immunity, determines how tumors respond to antitubulin drugs such as paclitaxel.
Sham Kakar
University of Louisville, KY·Medicine & Clinical Research
Determine the safety, tolerability and maximum tolerated dose of withaferin A, given as oral ashwagandha capsules at 2, 4 and 8 g twice daily, combined with standard liposomal doxorubicin (DOXIL) in 18 patients with platinum-resistant recurrent ovarian cancer.
The school
University of Texas MD Anderson Cancer Center: 23 labs on PI Pages, $1.4B a year on research.
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