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Researchers
Make Cancer Advancement
Scientists
have created mice that are immune to some of the most common types
of breast cancer, a development they say brings science a step
closer to developing drugs to precisely block the spread of breast
cancer in humans.
The research
involves a protein linked to half of all human breast cancers.
The bioengineered mice lack that protein, which some tumors need
to grow.
Though it
could take years to develop a drug therapy targeting the protein,
the findings are dramatic proof that certain breast cancers can
occur only when the protein is present, said Christopher Widnell,
scientific program director of the Atlanta-based American Cancer
Society.
``This work
is taking us to the next phase, where you can actually start designing
intelligent treatments for individual tumors,'' said Widnell,
who wasn't involved in the research.
The Dana-Farber
Cancer Institute scientists who conducted the research aren't
suggesting that humans be bioengineered to resist breast cancers.
Instead, they hope their findings will inspire more research to
target the protein using drugs.
They produced
the cancer-resistant mice by building on earlier success in engineering
mice that don't express the protein cyclin D1, one of many proteins
that regulate cell growth. Because cyclin D1 is found in abnormally
high amounts in half of human breast cancers, it has become the
focus of much scientific scrutiny.
The Dana-Farber
scientists wanted to test whether eliminating the protein in mice
prone to certain breast cancers could keep them cancer-free.
The researchers
bred the mice engineered to not express cyclin D1 with four other
types of laboratory mice, each prone to different types of breast
cancer, and monitored their offspring for signs of cancer. Two
of the resulting cross-breeds were immune to the type of breast
cancer for which they carried a gene.
Piotr Sicinski,
a Dana-Farber researcher, said the findings clearly show two cancer
genes called Neu and Ras can only turn normal cells into cancer
cells by sending signals through the cyclin D1 protein.
The fact the
mice with the two other cancer genes, called Wnt-1 and Myc, developed
breast cancers means those cancer genes are capable of signaling
though other cell-regulating proteins, Sicinski said.
The research
appears in Thursday's issue of the journal Nature.
Sicinski said
he and his colleagues want to see other researchers try to target
cyclin D1 using existing cancer-blocking drugs.
He suggested
pairing drugs that target a protein partner of the cell-regulating
proteins that include cyclin D1 with Genentech's breast cancer
drug, Herceptin, which aims to block the Neu cancer gene. That
cancer gene has been linked to about 30 percent of human breast
cancers.
``If you had
a way to take out cyclin D1 you could completely unplug the (cancer
gene) pathways from the cell cycle machinery without compromising
the patient's health,'' Sicinski said.
In an accompanying
Nature commentary, two Danish scientists said that when more is
known about the cellular changes that the Neu and Ras cancer genes
induce through cyclin D1, physicians might be able to create molecular
profiles of breast cancer patients to target their unique mix
of tumors.
``It might
one day be possible to provide tailor-made treatments,'' say Jiri
Bartek and Jiri Lukas of the Institute of Cancer Biology, Danish
Cancer Society, Copenhagen.
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On the Net:
The journal
Nature: http://www.nature.com
Dana-Farber
Cancer Institute: http://www.danafarber.org
Reference
Source 102
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