Hot Papers

M. Schuermann, M. Neuberg, J.B. Hunter, T. Jenuwein, et al., "The leucine repeat motif in Fos protein mediates complex formation with Jun/AP-1 and is required for transformation," Cell, 56, 507-16, 10 February 1989. M. Neuberg, M. Schuermann, J.B. Hunter, R. Müller, "Two functionally different regions in Fos are required for the sequence-specific DNA interaction of the Fos/Jun protein complex," Nature, 338, 589-90, 13 April 1989. Manfred Neuberg (Institut für Molekularbiologie und Tumorforschung, Phillipps- Universität Marburg, W.Ger.): "The results published in these articles provided evidence that the regularly spaced leucines in Fos and Jun are structurally important features for dimerization of the two proteins, as proposed in the leucine zipper model by W.H. Landschulz, P.F. Johnson, and S.L. McKnight. (Science, 240:1759-64, 1988). We could show that dimerization of Fos and Jun is a prerequisite for DNA binding of the protein complex to the TPA responsive element (TRE) previously characterized as an important DNA motive in TPA-inducible promoters. We could localize two stretches of basic amino acids in the Fos protein involved in the recognition of the symmetrical TRE-DNA motive. "A similar structure was found in the Jun protein, which led us to propose a model for the recognition of the TPA responsive element. In this model, each of the symmetrical half-sites of the DNA motive is thought to be recognized by the basic DNA binding domains of Fos and Jun, appropriately positioned via the leucine zipper." B. Fisher, C. Redmond, N.V. Dimitrov, D. Bowman, et al., "A randomized clinical trial evaluating sequential methotrexate and fluorouracil in the treatment of patients with node-negative breast cancer who have estrogen-receptor- negative tumors," New England Journal of Medicine, 320, 473-8, 23 February 1989. B. Fisher, J. Constantino, C. Redmond, R. Poisson, et al., "A randomized clinical trial evaluating tamoxifen in the treatment of patients with node-negative breast cancer who have estrogen-receptor- positive tumors," New England Journal of Medicine, 320, 479-84, 23 February 1989. Bernard Fisher (National Surgical Adjuvant Breast and Bowel Project, Pittsburgh): "Our two papers demonstrate the benefit from postoperative systemic therapy in breast cancer patients with negative axillary lymph nodes. In the past, such treatment was considered inappropriate for these patients, because it was erroneously believed that their prognosis was highly favorable and that exposing them to the potential risks of therapy would be unjustifiable. "In one of our studies, we observed for the first time that premenopausal and postmenopausal patients with negative nodes and estrogen- receptor-negative tumors could benefit from chemotherapy that did not contain an alkylating agent, and that this therapy could be given with highly acceptable toxicity. The other clinical trial, which focused on node-negative patients with estrogen-receptor- positive tumors, compared the outcome of one group receiving tamoxifen, an anti-estrogen, with another receiving placebo. Findings from this study demonstrated that the benefit from tamoxifen in premenopausal as well as postmenopausal patients is unequivocal. "Both of these studies have resulted in dialogue among researchers regarding the magnitude of a benefit that justifies the use of adjuvant chemotherapy. The studies have also demonstrated the need for the discovery of `markers' that will identify in advance those patients who are most likely to benefit from therapy and those who are not. Both trials have failed to identify any subgroup of patients that did not benefit from either of the therapies." S.J. Baker, E.R. Fearon, J.M. Nigro, S.R. Hamilton, et al., "Chromosome 17 deletions and p53 gene mutations in colorectal carcinomas," Science, 244, 217-21, 14 April 1989. Suzanne J. Baker (The Oncology Center, Johns Hopkins University School of Medicine, Baltimore): "A segment of one of the two copies of chromosome 17 was found to be lost in many colorectal cancers. This loss suggested that a critical gene (`suppressor gene') within the lost region was involved in the formation of the tumors. It was shown that the deleted segment of chromosome 17 encompassed a gene called p53, which had previously been implicated in virally induced animal tumors. Detailed analysis of the remaining p53 genes in colorectal cancers showed that they contained single base-pair mutations, strongly supporting a role for this gene in these cancers. Thus, this work connected classic research on experimental tumor systems with clinically important human cancers." C.L. Kane, P.A. Lee, N. Read, "Motion of a single hole in a quantum antiferromagnet," Physical Review B, 39, 6880-97, 1 April 1989. Charles Kane (IBM Thomas J. Watson Research Center, Yorktown Heights, N.Y.): "The interplay between doping and magnetism is a central issue in current theories of the high-temperature superconductors. The undoped compounds are generically antiferromagnetic insulators (such as La2CuO4), and many of the fascinating properties of these materials emerge when they are doped with holes. The holes are believed to be the charge carriers in these materials, and the presence of superconducting properties depends crucially on their concentration. In order to understand the normal and ultimately superconducting properties of these materials, it is therefore important to understand the nature of holes moving in an antiferromagnetic background. "In this paper we formulate a quasiparticle theory of a single hole in a quantum antiferromagnet. We find that the mass of a hole is enhanced, since it tends to disturb the antiferromagnetic order as it moves. This quasiparticle theory for a single hole is a useful starting point for treating the more complicated and realistic problem of a finite density of holes, which would be the case in a doped antiferromagnetic material."

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