New drug targets for aggressive breast cancer

July 26, 2013 — Scientists at A*STAR’s Genome Institute of Singapore (GIS) led in a study that has identified genes that are potential targets for therapeutic drugs against aggressive breast cancer. These findings were reported in the July 2013 issue of PNAS.Out of the 1.5 million women diagnosed with breast cancer in the world annually, nearly one in seven of these is classified as triple negative. Patients with triple-negative breast cancer (TNBC) have tumours that are missing three important proteins that are found in other types of breast cancer. The absence of these three proteins make TNBC patients succumb to a higher rate of relapse following treatment and have lower overall survival rates. There is currently no effective therapy for TNBC.Using integrated genomic approaches, GIS scientists led by Dr. Qiang Yu, in collaboration with local and international institutions, set out to search for targets that can be affected by drugs. The scientists discovered that a protein tyrosine phosphatase[1], called UBASH3B, is overexpressed in one third of TNBC patients. UBASH3B controls the activity of an important breast cancer gene. The researchers found that deleting this gene expression markedly inhibits TNBC cell invasive growth and lung metastasis in a mouse model. They also showed that patients with TNBC tumours that have high levels of UBASH3B tend to be more likely to have early recurrence and metastasis.Lead author Dr Qiang Yu said, “The identification of target genes is always the most crucial first step towards treating a disease. …

Read more

Scientists discover molecular communication network in human stem cells

July 2, 2013 — Scientists at A*STAR’s Genome Institute of Singapore (GIS) and the Max Planck Institute for Molecular Genetics (MPIMG) in Berlin (Germany) have discovered a molecular network in human embryonic stem cells (hESCs) that integrates cell communication signals to keep the cell in its stem cell state. These findings were reported in the June 2013 issue of Molecular Cell.Human embryonic stem cells have the remarkable property that they can form all human cell types. Scientists around the world study these cells to be able to use them for medical applications in the future. Many factors are required for stem cells to keep their special state, amongst others the use of cell communication pathways.Cell communication is of key importance in multicellular organisms. For example, the coordinated development of tissues in the embryo to become any specific organ requires that cells receive signals and respond accordingly. If there are errors in the signals, the cell will respond differently, possibly leading to diseases such as cancer. The communication signals which are used in hESCs activate a chain of reactions (called the extracellular regulated kinase (ERK) pathway) within each cell, causing the cell to respond by activating genetic information.Scientists at the GIS and MPIMG studied which genetic information is activated in the cell, and thereby discovered a network for molecular communication in hESCs. They mapped the kinase interactions across the entire genome, and discovered that ERK2, a protein that belongs to the ERK signaling family, targets important sites such as non-coding genes and histones, cell cycle, metabolism and also stem cell-specific genes.The ERK signaling pathway involves an additional protein, ELK1 which interacts with ERK2 to activate the genetic information. Interestingly, the team also discovered that ELK1 has a second, totally opposite function. At genomic sites which are not targeted by ERK signaling, ELK1 silences genetic information, thereby keeping the cell in its undifferentiated state. …

Read more

Utilizzando il sito, accetti l'utilizzo dei cookie da parte nostra. maggiori informazioni

The cookie settings on this website are set to "allow cookies" to give you the best browsing experience possible. If you continue to use this website without changing your cookie settings or you click "Accept" below then you are consenting to this.

Close