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NCI CANCERLIT^® Search: Ataxia Telangiectasia - September 2002

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National Cancer Institute^®
Ultima Vez Modificado: 1 de septiembre del 2002

The Saccharomyces cerevisiae MEC1 gene, which encodes a homolog of the human ATM gene product, is required for G1 arrest following radiation
The ATM homologue MEC1 is required for phosphorylation of replication protein A in yeast.
MEC1-dependent redistribution of the Sir3 silencing protein from telomeres to DNA double-strand breaks.
Checkpoints: it takes more than time to heal some wounds.
Atm heterozygous mice are more sensitive to radiation-induced cataracts than are their wild-type counterparts.
Correction of radiation sensitivity in ataxia telangiectasia cells by a truncated I kappa B-alpha.
Impaired regulation of nuclear factor-kappaB results in apoptosis induced by gamma radiation.
The ATM protein is required for sustained activation of NF-kappaB following DNA damage.
Functional link between BLM defective in Bloom's syndrome and the ataxia-telangiectasia-mutated protein, ATM.
Mice heterozygous for mutation in Atm, the gene involved in ataxia-telangiectasia, have heightened susceptibility to cancer.
ATM heterozygosity and cancer risk.
Mammalian mutants defective in the response to ionizing radiation-induced DNA damage.
The role of Ataxia telangiectasia and the DNA-dependent protein kinase in the p53-mediated cellular response to ionising radiation.
Cell cycle checkpoints and DNA repair in Nijmegen breakage syndrome.
Essential and perilous: V(D)J recombination and DNA damage checkpoints in lymphocyte precursors.
Replication-mediated DNA damage by camptothecin induces phosphorylation of RPA by DNA-dependent protein kinase and dissociates RPA:DNA-PK
The controlling role of ATM in homologous recombinational repair of DNA damage.
Genetic interactions between ATM and the nonhomologous end-joining factors in genomic stability and development.

1
UI - 8824640
AU - Siede W; Allen JB; Elledge SJ; Friedberg EC
TI - The Saccharomyces cerevisiae MEC1 gene, which encodes a homolog of the human ATM gene product, is required for G1 arrest following radiation treatment.
SO - J Bacteriol 1996 Oct;178(19):5841-3
AD - Division of Cancer Biology, Department of Radiation Oncology and Winship Cancer Center, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
The Saccharomyces cerevisiae gene MEC1 represents a structural homolog of the human gene ATM mutated in ataxia telangiectasia patients. Like human ataxia telangiectasia cell lines, mec1 mutants are defective in G2 and S-phase cell cycle checkpoints in response to radiation treatment. Here we show an additional defect in G1 arrest following treatment with UV light or gamma rays and map a defective arrest stage at or upstream of START in the yeast cell cycle.

2
UI - 8986766
AU - Brush GS; Morrow DM; Hieter P; Kelly TJ
TI - The ATM homologue MEC1 is required for phosphorylation of replication protein A in yeast.
SO - Proc Natl Acad Sci U S A 1996 Dec 24;93(26):15075-80
AD - Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Replication protein A (RPA) is a highly conserved single-stranded DNA-binding protein, required for cellular DNA replication, repair, and recombination. In human cells, RPA is phosphorylated during the S and G2 phases of the cell cycle and also in response to ionizing or ultraviolet radiation. Saccharomyces cerevisiae exhibits a similar pattern of cell cycle-regulated RPA phosphorylation, and our studies indicate that the radiation-induced reactions occur in yeast as well. We have examined yeast RPA phosphorylation during the normal cell cycle and in response to environmental insult, and have demonstrated that the checkpoint gene MEC1 is required for the reaction under all conditions tested. Through examination of several checkpoint mutants, we have placed RPA phosphorylation in a novel pathway of the DNA damage response. MEC1 is similar in sequence to human ATM, the gene mutated in patients with ataxia-telangiectasia (A-T). A-T cells are deficient in multiple checkpoint pathways and are hypersensitive to killing by ionizing radiation. Because A-T cells exhibit a delay in ionizing radiation-induced RPA phosphorylation, our results indicate a functional similarity between MEC1 and ATM, and suggest that RPA phosphorylation is involved in a conserved eukaryotic DNA damage-response pathway defective in A-T.

3
UI - 10367890
AU - Mills KD; Sinclair DA; Guarente L
TI - MEC1-dependent redistribution of the Sir3 silencing protein from telomeres to DNA double-strand breaks.
SO - Cell 1999 May 28;97(5):609-20
AD - Massachusetts Institute of Technology, Department of Biology, Cambridge 02139, USA.
The yeast Sir2/3/4p complex is found in abundance at telomeres, where it participates in the formation of silent heterochromatin and telomere maintenance. Here, we show that Sir3p is released from telomeres in response to DNA double-strand breaks (DSBs), binds to DSBs, and mediates their repair, independent of cell mating type. Sir3p relocalization is S phase specific and, importantly, requires the DNA damage checkpoint genes MEC1 and RAD9. MEC1 is a homolog of ATM, mutations in which cause ataxia telangiectasia (A-T), a disease characterized by various neurologic and immunologic abnormalities, a predisposition for cancer, and a cellular defect in repair of DSBs. This novel mode by which preformed DNA repair machinery is mobilized by DNA damage sensors may have implications for human diseases resulting from defective DSB repair.

4
UI - 11137027
AU - Rhind N; Russell P
TI - Checkpoints: it takes more than time to heal some wounds.
SO - Curr Biol 2000 Dec 14-28;10(24):R908-11
AD - The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA. rhind@scripps.edu
The S-phase DNA damage checkpoint seems to provide a twist on the checkpoint theme. Instead of delaying replication and allowing repair as a consequence, it may activate repair and delay replication as a consequence.

5
UI - 12119422
AU - Worgul BV; Smilenov L; Brenner DJ; Junk A; Zhou W; Hall EJ
TI - Atm heterozygous mice are more sensitive to radiation-induced cataracts than are their wild-type counterparts.
SO - Proc Natl Acad Sci U S A 2002 Jul 23;99(15):9836-9
AD - Eye Radiation and Environmental Research Laboratory and Center for Radiological Research, Columbia University, College of Physicians and Surgeons, New York, NY 10032, USA.
It is important to know whether the human population includes genetically predisposed radiosensitive subsets. In vitro studies have shown that cells from individuals homozygous for ataxia telangiectasia (A-T) are much more radiosensitive than cells from unaffected individuals. Although cells heterozygous for the ATM gene (ATM(+/-)) may be slightly more radiosensitive in vitro, it remained to be determined whether the greater susceptibility of ATM(+/-) cells translates into an increased sensitivity for late effects in vivo, though there is a suggestion that radiotherapy patients that are heterozygous for the ATM gene may be more at risk of developing late normal tissue damage. We chose cataractogenesis in the lens as a means to assay for the effects of ATM deficiency in a late-responding tissue. One eye of wild-type, Atm heterozygous and homozygous knockout mice was exposed to 0.5-, 1.0-, 2.0-, or 4.0-Gy x rays. The animals were followed weekly for cataract development by conventional slit-lamp biomicroscopy. Cataract development in the animals of all three groups was strongly dependent on dose. The lenses of homozygous mice were the first to opacify at any given dose. Most important in the present context is that cataracts appeared earlier in the heterozygous versus wild-type animals. The data suggest that ATM heterozygotes in the human population may also be radiosensitive. This may influence the choice of individuals destined to be exposed to higher than normal doses of radiation, such as astronauts, and may also suggest that radiotherapy patients who are ATM heterozygotes could be predisposed to increased late normal tissue damage.

6
UI - 7777860
AU - Jung M; Zhang Y; Lee S; Dritschilo A
TI - Correction of radiation sensitivity in ataxia telangiectasia cells by a truncated I kappa B-alpha.
SO - Science 1995 Jun 16;268(5217):1619-21
AD - Department of Radiation Medicine, Georgetown University School of Medicine, Washington, DC 20007, USA.
Cells from patients with ataxia telangiectasia (AT) are hypersensitive to ionizing radiation and are defective in the regulation of DNA synthesis. A complementary DNA that corrects the radiation sensitivity and DNA synthesis defects in fibroblasts from an AT group D patient was isolated by expression cloning and shown to encode a truncated form of I kappa B-alpha, an inhibitor of the nuclear factor kappa B (NF-kappa B) transcriptional activator. The parental AT fibroblasts expressed large amounts of the I kappa B-alpha transcript and showed constitutive activation of NF-kappa B. The AT fibroblasts transfected with the truncated I kappa B-alpha expressed normal amounts of the I kappa B-alpha transcript and showed regulated activation of NF-kappa B. These results suggest that aberrant regulation of NF-kappa B and I kappa B-alpha contribute to the cellular defect in AT.

7
UI - 9611098
AU - Jung M; Zhang Y; Dimtchev A; Dritschilo A
TI - Impaired regulation of nuclear factor-kappaB results in apoptosis induced by gamma radiation.
SO - Radiat Res 1998 Jun;149(6):596-601
AD - Department of Radiation Medicine, Georgetown University Medical Center, Washington, DC 20007, USA.
Recent studies have shown that activation of nuclear factor-kappaB (NF-kappaB) is critical for cell survival. Cells from patients with ataxia telangiectasia (AT) have an impaired NF-kappaB response to ionizing radiation. AT cells also exhibit inappropriate regulation of apoptosis. We report here that expression of a dominant negative form of IkappaB-alpha, an inhibitor of NF-kappaB, protects AT fibroblasts from apoptosis induced by gamma radiation, but it enhances apoptosis in normal fibroblasts. Furthermore, the process leading to apoptosis may involve caspase 3-mediated cleavage of IkappaB-alpha. These data suggest that regulation of NF-kappaB may play an important role in programmed cell death induced by DNA damage in AT cells.

8
UI - 10327072
AU - Piret B; Schoonbroodt S; Piette J
TI - The ATM protein is required for sustained activation of NF-kappaB following DNA damage.
SO - Oncogene 1999 Apr 1;18(13):2261-71
AD - Laboratory of Fundamental Virology and Immunology, University of Liege, CHU, Belgium.
Cells lacking an intact ATM gene are hypersensitive to ionizing radiation and show multiple defects in the cell cycle-coupled checkpoints. DNA damage usually triggers cell cycle arrest through, among other things, the activation of p53. Another DNA-damage responsive factor is NF-kappaB. It is activated by various stress situations, including oxidative stress, and by DNA-damaging compounds such as topoisomerase poisons. We found that cells from Ataxia Telangiectasia patients exhibit a defect in NF-kappaB activation in response to treatment with camptothecin, a topoisomerase I poison. In AT cells, this activation is shortened or suppressed, compared to that observed in normal cells. Ectopic expression of the ATM protein in AT cells increases the activation of NF-kappaB in response to camptothecin. MO59J glioblastoma cells that do not express the DNA-PK catalytic subunit respond normally to camptothecin. These results support the hypothesis that NF-kappaB is a DNA damage-responsive transcription factor and that its activation pathway by DNA damage shares some components with the one leading to p53 activation.

9
UI - 12034743
AU - Beamish H; Kedar P; Kaneko H; Chen P; Fukao T; Peng C; Beresten S;
TI - Gueven N; Purdie D; Lees-Miller S; Ellis N; Kondo N; Lavin MF Functional link between BLM defective in Bloom's syndrome and the ataxia-telangiectasia-mutated protein, ATM.
SO - J Biol Chem 2002 Aug 23;277(34):30515-23
AD - Queensland Cancer Fund Research Laboratories, The Queensland Institute of Medical Research, P. O. Royal Brisbane Hospital, Herston, Brisbane, Qld 4029, Australia.
Chromosome aberrations, genomic instability, and cancer predisposition are hallmarks of a number of syndromes in which the defective genes recognize and/or repair DNA damage or are involved in some aspect of DNA processing. We report here direct interaction between BLM, mutated in Bloom's Syndrome (BS), and ATM, mutated is ataxia-telangiectasia, and we have mapped the sites of interaction. Full-length BLM cDNA corrected sister chromatid exchange (SCE) and radiosensitivity in BS cells. Mitotic phosphorylation of BLM was partially dependent on ATM, and phosphorylation sites on BLM were identified. A phosphospecific antibody against one of these sites (Thr-99) revealed radiation-induced phosphorylation, which was defective in ataxia-telangiectasia cells. Stable cell lines expressing phosphorylation site mutants failed to correct radiosensitivity in BS cells but corrected SCE. These mutants also sensitized normal control cells to radiation and increased radiation-induced chromosome aberrations but did not cause SCE numbers to increase. These data suggest that ATM and BLM function together in recognizing abnormal DNA structures by direct interaction and that these phosphorylation sites in BLM are important for radiosensitivity status but not for SCE frequency.

10
UI - 12195425
AU - Spring K; Ahangari F; Scott SP; Waring P; Purdie DM; Chen PC; Hourigan
TI - K; Ramsay J; McKinnon PJ; Swift M; Lavin MF Mice heterozygous for mutation in Atm, the gene involved in ataxia-telangiectasia, have heightened susceptibility to cancer.
SO - Nat Genet 2002 Sep;32(1):185-90
AD - Queensland Institute of Medical Research, PO Royal Brisbane Hospital, Herston, 4029, Australia.
Ataxia-telangiectasia is characterized by radiosensitivity, genome instability and predisposition to cancer. Heterozygous carriers of ATM, the gene defective in ataxia-telangiectasia, have a higher than normal risk of developing breast and other cancers. We demonstrate here that Atm 'knock-in' (Atm-Delta SRI) heterozygous mice harboring an in-frame deletion corresponding to the human 7636del9 mutation show an increased susceptibility to developing tumors. In contrast, no tumors are observed in Atm knockout (Atm(+/-)) heterozygous mice. In parallel, we report the appearance of tumors in 6 humans from 12 families who are heterozygous for the 7636del9 mutation. Expression of ATM cDNA containing the 7636del9 mutation had a dominant-negative effect in control cells, inhibiting radiation-induced ATM kinase activity in vivo and in vitro. This reduces the survival of these cells after radiation exposure and enhances the level of radiation-induced chromosomal aberrations. These results show for the first time that mouse carriers of a mutated Atm that are capable of expressing Atm have a higher risk of cancer. This finding provides further support for cancer predisposition in human ataxia-telangiectasia carriers.

11
UI - 12205473
AU - Concannon P
TI - ATM heterozygosity and cancer risk.
SO - Nat Genet 2002 Sep;32(1):89-90

12
UI - 7739608
AU - Zdzienicka MZ
TI - Mammalian mutants defective in the response to ionizing radiation-induced DNA damage.
SO - Mutat Res 1995 May;336(3):203-13
AD - MGC-Department of Radiation Genetics and Chemical Mutagenesis, University of Leiden, The Netherlands.

13
UI - 8808686
AU - Jongmans W; Artuso M; Vuillaume M; Bresil H; Jackson SP; Hall J
TI - The role of Ataxia telangiectasia and the DNA-dependent protein kinase in the p53-mediated cellular response to ionising radiation.
SO - Oncogene 1996 Sep 19;13(6):1133-8
AD - Unit of Mechanisms of Carcinogenesis, International Agency for Research on Cancer, Lyon, France.
The DNA-dependent protein kinase (DNA-PK), whose catalytic subunit shows structural similarities to the Ataxia telangiectasia (AT) gene product (ATM), has also been implicated in the p53-mediated signal transduction pathway that activates the cellular response to DNA damage produced by ionizing radiation. DNA-PK activity however was not found to be related to the transcriptional induction of WAFl/CIP1(p2l) in AT lymphoblastoid cell lines, following treatment with ionizing radiation. Normal protein and transcription levels of Ku70 and Ku80, as well as DNA-PK activity, were found in six different AT cell lines, 1-4 h following exposure to ionizing radiation, timepoints where reduced and delayed transcriptional induction of WAF1/CIP1 (p21) was observed. WAF1/CIP1 (p21) was found to be transcriptionally induced by p53 in normal cell lines over this same time period following exposure to ionizing radiation. These results suggest that despite the findings that in vitro DNA-PK may phosphorylate p53, in vivo it would not appear to play a central role in the activation of p53 as a transcription factor nor can it substitute for the ATM gene product in the cellular response following exposure to ionizing radiation.

14
UI - 9000041
AU - Sullivan KE; Veksler E; Lederman H; Lees-Miller SP
TI - Cell cycle checkpoints and DNA repair in Nijmegen breakage syndrome.
SO - Clin Immunol Immunopathol 1997 Jan;82(1):43-8
AD - Children's Hospital of Philadelphia, Pennsylvania 19104, USA.
Nijmegen breakage syndrome is characterized by a variable T cell and B cell immunodeficiency, growth failure, and an increased risk of malignancy. It is inherited in an autosomal recessive manner and is biochemically related to ataxia-telangiectasia. Cells from a patient with Nijmegen breakage syndrome were unable to arrest cell cycle progression after exposure to ionizing radiation, and BrdU incorporation into newly synthesized DNA was uninhibited, demonstrating that these cells have an aberrant response to radiation exposure. Although gross chromosomal breakage was observed, dinucleotide repeat segments were stable over time, suggesting that other types of DNA stability were not affected. DNA-PK activity, which is mediated by a protein related to the ataxia-telangiectasia gene product and is intimately involved in DNA repair and VDJ recombination, was normal in cells from an NBS patient. Therefore, cells from patients with Nijmegen breakage syndrome have an abnormal response to radiation exposure similar to that seen in ataxia-telangiectasia.

15
UI - 9200331
AU - Danska JS; Guidos CJ
TI - Essential and perilous: V(D)J recombination and DNA damage checkpoints in lymphocyte precursors.
SO - Semin Immunol 1997 Jun;9(3):199-206
AD - Hospital for Sick Children Research Institute, Toronto, ON, Canada.
V(D)J recombination generates a diverse array of antigen-binding specificities, but breakage and re-joining of DNA segments have grave implications for the maintenance of genomic stability and oncogenic risk. Exposure of eukaryotic cells to genotoxic agents activates a DNA damage checkpoint that induces cell-cycle arrest and DNA repair, or apoptosis. We discuss several lines of evidence implicating DNA-dependent protein kinase (DNA-PK), and the gene mutated in ataxia telangiectasia (ATM), two mammalian homologues of yeast DNA damage-checkpoint genes, in regulating the response to intrinsic DNA damage that occurs during V(D)J recombination.

16
UI - 10064605
AU - Shao RG; Cao CX; Zhang H; Kohn KW; Wold MS; Pommier Y
TI - Replication-mediated DNA damage by camptothecin induces phosphorylation of RPA by DNA-dependent protein kinase and dissociates RPA:DNA-PK complexes.
SO - EMBO J 1999 Mar 1;18(5):1397-406
AD - Laboratory of Molecular Pharmacology, Division of Basic Sciences, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4255, USA.
Replication protein A (RPA) is a DNA single-strand binding protein essential for DNA replication, recombination and repair. In human cells treated with the topoisomerase inhibitors camptothecin or etoposide (VP-16), we find that RPA2, the middle-sized subunit of RPA, becomes rapidly phosphorylated. This response appears to be due to DNA-dependent protein kinase (DNA-PK) and to be independent of p53 or the ataxia telangiectasia mutated (ATM) protein. RPA2 phosphorylation in response to camptothecin required ongoing DNA replication. Camptothecin itself partially inhibited DNA synthesis, and this inhibition followed the same kinetics as DNA-PK activation and RPA2 phosphorylation. DNA-PK activation and RPA2 phosphorylation were prevented by the cell-cycle checkpoint abrogator 7-hydroxystaurosporine (UCN-01), which markedly potentiates camptothecin cytotoxicity. The DNA-PK catalytic subunit (DNA-PKcs) was found to bind RPA which was replaced by the Ku autoantigen upon camptothecin treatment. DNA-PKcs interacted directly with RPA1 in vitro. We propose that the encounter of a replication fork with a topoisomerase-DNA cleavage complex could lead to a juxtaposition of replication fork-associated RPA and DNA double-strand end-associated DNA-PK, leading to RPA2 phosphorylation which may signal the presence of DNA damage to an S-phase checkpoint mechanism. Keywords: camptothecin/DNA damage/DNA-dependent protein kinase/RPA2 phosphorylation

17
UI - 10654944
AU - Morrison C; Sonoda E; Takao N; Shinohara A; Yamamoto K; Takeda S
TI - The controlling role of ATM in homologous recombinational repair of DNA damage.
SO - EMBO J 2000 Feb 1;19(3):463-71
AD - Bayer Chair Department of Molecular Immunology and Allergology, Faculty of Medicine, Kyoto University, Japan.
The human genetic disorder ataxia telangiectasia (A-T), caused by mutation in the ATM gene, is characterized by chromosomal instability, radiosensitivity and defective cell cycle checkpoint activation. DNA double-strand breaks (dsbs) persist in A-T cells after irradiation, but the underlying defect is unclear. To investigate ATM's interactions with dsb repair pathways, we disrupted ATM along with other genes involved in the principal, complementary dsb repair pathways of homologous recombination (HR) or non-homologous end-joining (NHEJ) in chicken DT40 cells. ATM(-/-) cells show altered kinetics of radiation-induced Rad51 and Rad54 focus formation. Ku70-deficient (NHEJ(-)) ATM(-/-) chicken DT40 cells show radiosensitivity and high radiation-induced chromosomal aberration frequencies, while Rad54-defective (HR(-)) ATM(-/-) cells show only slightly elevated aberration levels after irradiation, placing ATM and HR on the same pathway. These results reveal that ATM defects impair HR-mediated dsb repair and may link cell cycle checkpoints to HR activation.

18
UI - 11248063
AU - Sekiguchi J; Ferguson DO; Chen HT; Yang EM; Earle J; Frank K; Whitlow S;
TI - Gu Y; Xu Y; Nussenzweig A; Alt FW Genetic interactions between ATM and the nonhomologous end-joining factors in genomic stability and development.
SO - Proc Natl Acad Sci U S A 2001 Mar 13;98(6):3243-8
AD - The Center for Blood Research, Harvard Medical School, Boston, MA 02115, USA.
DNA ligase IV (Lig4) and the DNA-dependent protein kinase (DNA-PK) function in nonhomologous end joining (NHEJ). However, although Lig4 deficiency causes late embryonic lethality, deficiency in DNA-PK subunits (Ku70, Ku80, and DNA-PKcs) does not. Here we demonstrate that, similar to p53 deficiency, ataxia-telangiectasia-mutated (ATM) gene deficiency rescues the embryonic lethality and neuronal apoptosis, but not impaired lymphocyte development, associated with Lig4 deficiency. However, in contrast to p53 deficiency, ATM deficiency enhances deleterious effects of Lig4 deficiency on growth potential of embryonic fibroblasts (MEFs) and genomic instability in both MEFs and cultured progenitor lymphocytes, demonstrating significant differences in the interplay of p53 vs. ATM with respect to NHEJ. Finally, in dramatic contrast to effects on Lig4 deficiency, ATM deficiency causes early embryonic lethality in Ku- or DNA-PKcs-deficient mice, providing evidence for an NHEJ-independent role for the DNA-PK holoenzyme.

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NCI CANCERLIT^® Search: Ataxia Telangiectasia - September 2002

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