Fighting Breast Cancer With “Two-Headed” Antibody
A small, antibody-like molecule created by researchers at Fox Chase Cancer Center can successfully attack two separate molecules on the surface of cancer cells at the same time, halting the growth of breast cancer cells in laboratory tests, the researchers say. The molecule, nickname “ALM,” might be a means of slowing cancer spread or, as the researchers believe, a guidance system for delivering more aggressive drugs directly to cancer cells. Their findings appear in this month’s British Journal of Cancer.
Unlike naturally occurring antibodies, which only bind to one specific target at a time, ALM is bispecific, meaning it attaches to two separate targets simultaneously. ALM’s targets are two signaling proteins, ErbB2 and ErbB3, which connect to form a growth-promoting complex on the surface of many cancer cells, including head and neck cancer and drug-resistant breast cancer.
“ALM grabs the ErbB2-ErbB3 complex strongly with both hands, as it were, providing a solid grip on the tumor and blocking the transmission of a growth signal within the cell,” said lead investigator Matthew Robinson, PhD, an associate member of Fox Chase and a researcher in the Fox Chase Head and Neck Cancer Keystone Program. “Potentially, it can become a platform for delivering therapeutics directly to cancer cells or a way of detecting the presence and location of individual tumors.”
ErbB2 and ErbB3 are the protein products of two known cancer-related genes, Her2 and Her3, respectively. In normal cells, the ErbB family of proteins has a role in regulating cell growth and survival. Some cancerous cells overproduce copies of ErbB2 and ErbB3, and these excess proteins can bind to each other in a way that generates further cancer-promoting growth signals within a cell. While it is possible that the bound receptor proteins might be found on normal cells, cancer cells possess up to 18 times more of these receptors.
“Because tumors that express the ErbB2-ErbB3 complex are highly aggressive and prone to relapse after initial treatment, this subset of cancer is associated with metastasis and poor patient outcome,” Robinson says.
ALM was developed over many years at Fox Chase in the laboratory of co-author Greg Adams, PhD, in collaboration with James Marks, MD, PhD, of the University of California, San Francisco, and Louis Weiner, MD, a former Fox Chase senior member and current director of the Lombardi Comprehensive Cancer Center at Georgetown University. The Adams lab created ALM by taking the active anti-ErbB2 portion from one antibody and linking it with the anti-ErbB3 portion from another.
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For the first time in a clinical study, researchers of the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch and the Charité - Universitätsmedizin Berlin, Germany, have tested a new technology enabling them to transfer genetic material directly into a tumor by means of high pressure. As Assistant Professors Wolfgang Walther, together with Professor Peter M. Schlag report in Clinical Cancer Research (Vol. 14, Nr. 22, pp. 7545-7553)*, their results show that jet injection delivers genes into the tumor tissue safely and in a targeted manner. The application was well tolerated by all 17 patients enrolled in this study. No adverse events were experienced.
Oslo Cancer Cluster today signed a groundbreaking strategic agreement with the Toulouse Cancéropole and Cancer-Bio-Santé Cluster which will lead to an integrated effort to become the leading cancer centers in Europe for developing new cancer therapies. The signatories were Philippe Douste-Blazy, President of Cancéropole Toulouse Association, former mayor of Toulouse and former French foreign minister, Jean-Pierre Saintouil, CEO of Toulouse Cancer-Bio-Santé Cluster and Bjarte Reve, CEO of Oslo Cancer Cluster NCE. It also contained an initial series of key initiatives to be implemented over the next two years, including a joint response to the next cancer calls of the EU -Innovative Medicines Initiative.
The finding: Researchers at the University of Michigan Comprehensive Cancer Center have found a genetic marker that controls an enzyme present in aggressive and metastatic cancer. The study suggests an absence of microRNA-101 is related to high expression of the protein EZH2, which was previously shown to be active in metastatic cancers. MicroRNA’s are molecules that help regulate gene expression. miR-101 is one of few miRNA’s shown to play such an important role in the development of cancer.
Using a new approach that combines scientific technologies to hunt down genetic changes involved in cancer, researchers have discovered 13 tumor suppressor genes that, when mutated, can lead to liver cancers. Twelve of those genes had never been linked to cancer before, according to the report published online in the journal Cell, a Cell Press publication, on November 13th.
There has been much speculation over the last few years about whether cell phones increase the risk of developing a brain tumor. Research has not conclusively answered this question, which has left consumers confused. The majority of studies that have been published in scientific journals do not have sufficient evidence to show that cell phones increase the risk of brain tumors. The problem is that cell phone technology is in its infancy, so none of these studies could analyze long-term risks. This unknown is a particular issue for children, who will face a lifetime of cell phone usage. While the cell phone/brain tumor connection remains inconclusive, the American Association of Neurological Surgeons (AANS) cautions that cell phones present plenty of other risks to people’s neurological health, as illustrated by these few real-life scenarios:
An intra cellular pathway not previously linked to breast cancer is driving a sub-type of the disease that is highly lethal and disproportionately over-represented in African American women. The pathway regulates how cells identify and destroy proteins and represents a class of genes called proteasome targeting complexes. The work shows that basal cancer cells degrade the tumor suppressor gene p27 by making a new type of proteasome targeting complex. The gene p27 is one of a handful of proteins that are expressed in normal cells and act to prevent rapid cell growth, which is indicative of cancer. Beyond chemotherapy, no specific therapeutic target has been identified for this sub-type of cancer, found in between 12 to 15 percent of breast cancers in the general population and up to 25 percent of cases in African American women.
UroToday.com - The molecular mechanisms underlying development of androgen-independent growth of prostate cancer are largely unknown, and no effective therapies for hormone-refractory prostate cancer exist at present. One of the key problems in conducting studies to identify growth factors and signaling pathways that can replace androgens in the growth control of prostate cancer cells is the lack of androgen receptor (AR)-positive human prostate cancer cell lines that are regulated by androgens and tumorigenic in nude mice.
A $3.8 million Innovator Award, from the Department of Defense, is being granted over five years to an internationally renowned cancer researcher at the University of California, Santa Barbara.
UroToday.com - Can we meaningfully separate inflammatory pseudotumor (a term used since 1937 1 from inflammatory myofibroblastic tumor (IMT, a term introduced in 1990 for lung lesions 2 and from sarcoma?