From: Subject: Better model of deadly brain cancer Date: Thu, 27 Apr 2006 09:05:12 +0200 MIME-Version: 1.0 Content-Type: multipart/related; type="text/html"; boundary="----=_NextPart_000_0000_01C669D9.B119B6F0" X-MimeOLE: Produced By Microsoft MimeOLE V6.00.2900.2869 This is a multi-part message in MIME format. ------=_NextPart_000_0000_01C669D9.B119B6F0 Content-Type: text/html; charset="Windows-1252" Content-Transfer-Encoding: quoted-printable Content-Location: http://www.eurekalert.org/pub_releases/2006-04/hhmi-bmo042606.php Better model of deadly brain cancer

Public = release date:=20 26-Apr-2006
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Contact: Jennifer Michalowski
michalow@hhmi.org
301-215-8576Howard Hughes Medical=20 Institute

Better model of deadly brain cancer

Researchers have created a mouse model that = closely=20 mimics human medulloblastoma, the most common type of childhood brain = tumor. The=20 new model, which was created by knocking out a key component of the DNA = repair=20 machinery, will aid in exploring the genetic roots of this deadly brain = cancer.

The researchers, led by Howard Hughes Medical Institute investigator=20 Frederick W. Alt, published their findings the week of April 24, 2006, = in the=20 early online edition of the Proceedings of the National Academy of=20 Sciences. Catherine Yan, who is in Alt's laboratory at Children's = Hospital=20 Boston, was lead author of the article. Other co-authors were from = Brigham &=20 Women's Hospital, CBR Institute of Biomedical Research, Children's = Hospital and=20 Dana-Farber Cancer Institute, all of Harvard Medical School.

Although childhood cancers are rare, brain tumors are among the most = common.=20 About one out of five childhood brain tumors is medulloblastoma, an = aggressive=20 cancer of the cerebellum. Alt and his colleagues produced the mouse = model of=20 medulloblastoma by knocking out a gene called XRCC4, which = produces a=20 protein that plays an important role in stitching together the ends of = broken=20 DNA. These breaks which can occur in all cell types from exposure to = radiation,=20 chemicals, or other insults, occur specifically in the immune system = when genes=20 are snipped and rearranged to produce a vast array of antibodies. The = abnormal=20 swapping of chromosomal regions that ensues when such repair goes = awry--known as=20 chromosomal translocations--is sometimes harmless, but can contribute to = cancer=20 and other diseases.

In earlier studies, Alt and his colleagues discovered that = XRCC4 is a=20 component of nonhomologous end-joining, a process that is essential for = the=20 repair of chromosome breaks. They found that knocking out this gene in = mice led=20 to widespread death of newly generated neurons and death late in = embryonic=20 development. The researchers then combined these experiments with the=20 elimination of a gene for a sentinel protein called p53, which triggers = the=20 death of malfunctioning cells. With both p53 and XRCC4 = missing,=20 neurons survive and the mice live into early adulthood, but then die of=20 lymphomas caused by translocations of antibody genes. The researchers = noted that=20 by this time, the mice were also beginning to develop medulloblastomas.=20

After they made that observation, Alt's team wanted to zero in on the = possible role of XRCC4 deficiency in medulloblastomas. While their = earlier=20 studies involved knocking out the XRCC4 gene throughout the = animals'=20 bodies, now =93the major goal was to eliminate this protein only in the = developing=20 nervous system, so we could specifically determine whether there was a = role for=20 nonhomologous end-joining in suppressing cancers of cells besides those = of the=20 immune system,=94 he said. =93We also wanted to know whether getting rid = of both=20 XRCC4 and p53 in the nervous system would predispose the = animals=20 to neuronal tumors, and whether or not those tumors would also be = associated=20 with particular chromosomal translocations.=94

So Yan and her colleagues engineered two strains of mice in which=20 XRCC4 was knocked out only in neural progenitor cells in the = developing=20 nervous system. One strain had only the XRCC4 knockout, and the = other=20 also had a deficiency in both XRCC4 and p53. These mice = appeared=20 to develop normally without XRCC4, they found. But every mouse = lacking=20 both XRCC4 and p53 died very early of medulloblastomas.=20 Furthermore, =93those tumors strongly resembled human = medulloblastomas,=94 said Alt.

Analyzing the tumors for genetic abnormalities, Alt and his = colleagues found=20 that specific genes were frequently altered in association with = recurrent=20 chromosomal translocations--and that affected genes often were those = activated=20 or inactivated in human medulloblastomas. Thus, the tumors often showed=20 amplifications of two genes called N-myc and Cyclin D2, = which are=20 characteristic of many human neural tumors, including medulloblastomas. = The=20 animals also showed the loss of one copy of a gene called = patched, which=20 is also characteristic of some human medulloblastomas.=20

=93Only in our wildest dreams had we hoped to see these kinds of = recurrent=20 translocations,=94 said Alt. =93It's quite exciting to us that we'll be = able to=20 explore mechanistically why they happen when the basic process of = end-joining is=20 compromised.=94

Other mouse models of medulloblastoma have been created by knocking = out=20 patched or other individual genes that have been implicated in = the=20 development of medulloblastoma. However, said Alt, =93what we did was = different.=20 We created an environment in which end-joining was defective and let the = biology=20 of the cell sort out the consequences. And while in most other models = not every=20 mouse develops medulloblastomas, in our case every animal very = reproducibly=20 develops these tumors at a very young age. It's really quite intriguing, = too,=20 how this general genomic instability very specifically leads to the = selection of=20 tumor cells that have deregulated particular genes such as N-myc, = patched and Cyclin D2.=94

According to Alt, the new mouse model will prove valuable in = understanding=20 why N-myc is so frequently amplified in human tumors, including=20 neuroblastomas and medulloblastomas, and the consequences of that = amplification.=20 The model also will enable the researchers to better explore causes of = the=20 chromosomal translocations, deletions, and amplifications in neuronal = cells.

The mouse model should also be useful in testing potential treatments = for=20 medulloblastoma. Alt said that other laboratories have consulted them on = the=20 possibility of using the model for drug testing. =93This model could be = very=20 useful for such a purpose because every mouse gets tumors with an early = onset=20 and the tumors show activation or inactivation of a set of genes that is = implicated in human tumors,=94 he said. =93So, if one wants to test = therapies that=20 interfere with pathways involved in human tumors, this should be a good = model.=94=20

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