Daily Archives: December 12, 2014

PUBLIC RELEASE DATE:

11-Dec-2014

Contact: Michael Petr michael.petr@insilicomedicine.com InSilico Medicine, Inc. @InSilicoMeds

BALTIMORE, December 11, 2014 - Insilico Medicine along with scientists from Vision Genomics and Howard University shed light on AMD disease, introducing the opportunity for eventual diagnostic and treatment options.

The scientific collaboration between Vision Genomics, Inc., Howard University, and Insilico Medicine, Inc., has revealed encouraging insight on the AMD disease using an interactome analysis approach. Resources such as publicly available gene expression data, Insilico Medicine's original algorithm OncoFinderTM, and AMD MedicineTM from Vision Genomics allowed discovery of signaling pathways activated during AMD disease.

"We are thrilled to collaborate with Alex Zhavoronkov and Evgeny Makarev, and their team at InSilico Medicine. Big Data analysis is part of the future of medicine, and with our technique of signaling pathway activation analysis, we will decipher the genetic network alterations that lead to age-related macular degeneration (AMD), and eventually human aging itself", said Antonei Benjamin Csoka, PhD, CEO of Vision Genomics, LLC, and Assistant Professor at Howard University.

The research publication titled "Pathway activation profiling reveals new insights into Age-related Macular Degeneration and provides avenues for therapeutic interventions" was accepted by one of aging research's top-rated journals "Aging", detailing these findings and methodology. This study not only validates the efficacy of interactome analysis within aging, but also allows the investigation of cellular populations within AMD models.

"We are happy to collaborate with Antonei Benjamin Csoka's teams at both Vision Genomics and Howard University on this exciting project. Coupling Big Data with advanced signaling pathway activation analysis may help find new therapeutic approaches for age-related macular degeneration (AMD), a disease that holds many keys to understanding human aging", said Evgeny Makarev, PhD, Director of Aging Research at Insilico Medicine.

On December 9th Insilico Medicine, Inc announced the appointment of 2013 Nobel Laureate in Chemistry, Michael Levitt, to its Scientific Advisory Board. Dr. Levitt's background in computational modeling focused on understanding protein folding processes and molecular interactions, may turn to be extremely valuable for compound discovery related to AMD and other age-related diseases. The concept utilized by Insilico Medicine involves identifying the difference between several signaling states on a tissue-specific level, be it health and disease, or young and old, and evaluating a large number of drugs and drug combinations that can modulate the difference using advanced parametric and machine-learned algorithms. "To create more value from our predictions we will need to identify compounds that are even more effective than top-scoring drugs and that would require multi-scale modeling of macromolecules, the field pioneered by Dr. Michael Levitt ", said Alex Zhavoronkov, PhD, CEO of Insilico Medicine, Inc. Insilico Medicine continues to be represented from top institutions, including Stanford University, Johns Hopkins University, and New York University. With this broad range of expertise, Insilico and its collaborators will pursue AMD disease further and utilize the newly discovered activated pathways as a foundation.

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New discoveries in age-related macular degeneration revealed in industry and academia

Targeted therapies are a growing and groundbreaking field in cancer care in which drugs or other substances are designed to interfere with genes or molecules that control the growth and survival of cancer cells. Now, scientists at Virginia Commonwealth University Massey Cancer Center and VCU Institute of Molecular Medicine (VIMM) have identified a novel interaction between a microRNA and a gene that could lead to new therapies for the most common and deadly form of brain tumor, malignant glioma.

In a study recently published in the journal Neuro-Oncology, a team of scientists led by Luni Emdad, M.B.B.S., Ph.D., and Paul B. Fisher, M.Ph., Ph.D., provided the first evidence of an important link between a specific microRNA, miR-184, and a cancer promoting gene, SND1, in the regulation of malignant glioma. miR-184 is known to suppress tumor development by regulating a variety of genes involved in cancer growth, while SND1 has been shown to play a significant role in the development of breast, colon, prostate and liver cancers. Through a variety of preclinical experiments, the team demonstrated that increasing the expression of miR-184 slows the growth and invasive characteristics of glioma cells through direct regulation of SND1. Additionally, they showed that reduced levels of SND1 led to reduced levels of STAT3, a gene that has been shown to promote the most lethal characteristics of brain cancer.

"Patients suffering from brain tumors are in desperate need of improved therapies," says Fisher, Thelma Newmeyer Corman Endowed Chair in Cancer Research and co-leader of the Cancer Molecular Genetics research program at VCU Massey Cancer Center, chairman of the Department of Human and Molecular Genetics at VCU School of Medicine and director of the VIMM. "We're hopeful that this new understanding of the relationship between miR-184 and SND1 ultimately will lead to the development of new drugs that reduce SND1 expression and improve patient outcomes."

Prior studies have shown that levels of miR-184 are unusually low in tissue samples from patients with malignant gliomas. Using advanced computer analysis techniques designed to study and process biological data, the researchers identified SND1 among a handful of other genes that miR-184 helps regulate. Knowing SND1 is implicated in a variety of cancers and having previously defined its role in liver cancer, Emdad, Fisher and their colleagues explored this relationship further. They confirmed low levels of miR-184 expression in human glioma tissue samples and cultured cell lines as well as an increase in the expression of SND1 compared to normal brain tissue. Using data from a large public brain tumor database called REMBRANDT, the researchers confirmed that patients with lower levels of SND1 survived longer than those with elevated SND1 expression.

"We still have a long way to go and many challenges to overcome before we will have therapies that are ready for clinical use, but this is a significant first step in the process," says Emdad, member of the Cancer Molecular Genetics research program at Massey, assistant professor in the VCU Department of Human and Molecular Genetics and member of the VIMM. "Future studies will aim to explore the relationship between SND1 and STAT3, identify additional microRNAs that may be relevant to malignant glioma and explore the effects of drugs that block SND1 expression in more advanced preclinical models."

Story Source:

The above story is based on materials provided by Virginia Commonwealth University. Note: Materials may be edited for content and length.

Excerpt from:
Important gene interaction defined that drives aggressive brain cancer