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Researchers discover a family of Liver
Cancer genes
Newswise — An interdisciplinary team of researchers at Stony
Brook University Medical Center has
identified a family of genes linked to the
development of liver cancer.
Principal Investigator Wadie F. Bahou, M.D., Professor of
Medicine and Genetics, and colleagues
discovered in a mouse model that the loss of
one specific gene (Iqgap2) in this family
causes Hepatocellular carcinoma (HCC).
They also found that when another member of the gene family
(Iqgap1) is turned on, a more aggressive
form of the disease occurs. Their findings
are reported in the March issue of
Molecular and Cellular Biology.
Dr. Bahou says that the findings regarding the two genes
demonstrate that both genes could serve as a
basis for developing important targets for
early diagnosis and/or treatment of HCC.
The disease accounts for more than 80 percent of all liver
cancer in humans, which causes death in
500,000 to 1 million adults annually
worldwide. Treatment for advanced HCC is
often ineffective.
A recently approved chemotherapy drug developed to treat
metastatic liver cancer provides disease
stabilization but not a cure.
“This is an exciting development in the field of cancer
research, as there is a tremendous need for
targeted therapies for liver cancer,”
emphasizes Dr. Bahou.
“The data resulting from our research provides important
insights into genes that may predispose to
HCC development,” he adds, further noting
that the model is a valuable tool for
testing therapeutic agents aimed at curing
liver cancer.
Dr. Bahou explains that to date attempts to treat liver
cancer have been difficult without
appropriate animal models of disease.
He says that the model generated by the Stony Brook team is
the closest to human disease because: 1) The
disease closely resembles human HCC
microscopically; 2) does not require
intervention from outside sources, such as
chemically induced cancer models; 3) is
associated with a reproducible and very high
incidence of HCC, and 4) is strictly limited
to HCC.
With expertise ranging from hematology/oncology, genetics,
pharmacology and pathology, the team
detailed their results in an article titled
“Development of Hepatocellular Carcinoma in
Iqgap2-Deficient Mice Is Iqgap1-dependent.”
They collectively found that Iqgap1 and Iqgap2 have
functionally divergent roles in
hepatocellular carcinogenesis.
When they removed the Iqgap2 gene using sophisticated genetic
techniques, the mice developed HCC. This
result confirmed that Iqgap2 has a
fundamentally important protective role
against the development of liver cancer.
When mice retained Iqgap1, the cousin gene of Iqgap2, the
animals developed more advanced disease.
Further experimentation showed that inactivation of Iqgap1 in
the mouse liver limits the aggressiveness of
HCC caused by Iqgap2 deficiency.
According to Dr. Bahou, the researchers are currently
conducting similar genetic analyses in human
liver cancer. Co-investigators of the mouse
study include lead author Valentina A.
Schmidt, Ph.D., Department of Medicine;
Carmine S. Chiariello, Ph.D., Program in
Genetics; Encarnación Capilla, Ph.D.,
Department of Pharmaological Sciences, and
Frederick Miller, M.D., Department of
Pathology. The research was supported by the
National Institutes of Health.
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