4 Williams syndrome,” Pediatric Neuroscience, vol. 12, no. 3, pp. 188–191, 1985. [16] N. Montano, P. De Bonis, L. Lauriola et al., “Late onset cerebel- lar metastasis from oesophageal adenocarcinoma in Williams Syndrome,” Journal of Neuro-Oncology, vol. 88, no. 3, pp. 349– 351, 2008. [17] A. Meinhardt, B. Burkhardt, M. Zimmermann et al., “Phase II window study on rituximab in newly diagnosed pedi- atric mature B-cell non-Hodgkin’s lymphoma and Burkitt leukemia,” Journal of Clinical Oncology, vol. 28, no. 19, pp. 3115–3121, 2010. [18] T. Y. Flanders and W. D. Foulkes, “Pancreatic adenocarcinoma: Epidemiology and genetics,” Journal of Medical Genetics, vol. 33, no. 11, pp. 889–898, 1996. [19] M. Bayes, L. F. Magano, N. Rivera, R. Flores, and L. A. Perez Jurado, “Mutational mechanisms of williams-beuren syn- drome deletions,” American Journal of Human Genetics, vol. 73, no. 1, pp. 131–151, 2003. [20] M. C. Lowery, C. A. Morris, A. Ewart et al., “Strong corre- lation of elastin deletions, detected by FISH, with Williams syndrome: evaluation of 235 patients,” American Journal of Human Genetics, vol. 57, no. 1, pp. 49–53, 1995. [21] A. Xiao, H. Li, D. Shechter et al., “WSTF regulates the H2A.X DNA damage response via a novel tyrosine kinase activity,” Nature, vol. 457, no. 7225, pp. 57–62, 2009. [22] A. Celeste, S. Diﬁlippantonio, M. J. Diﬁlippantonio et al., “H2AX haploinsuﬃciency modiﬁes genomic stability and tumor susceptibility,” Cell, vol. 114, no. 3, pp. 371–383, 2003. [23] C. H. Bassing, H. Suh, D. O. Ferguson et al., “Histone H2AX: a dosage-dependent suppressor of oncogenic translocations and tumors,” Cell, vol. 114, no. 3, pp. 359–370, 2003. [24] A. Celeste, S. Petersen, P. J. Romanienko et al., “Genomic instability in mice lacking histone H2AX,” Science, vol. 296, no. 5569, pp. 922–927, 2002. [25] M. Davila, A. R. Frost, W. E. Grizzle, and R. Chakrabarti, “LIM kinase 1 is essential for the invasive growth of prostate epithelial cells: implications in prostate cancer,” Journal of Biological Chemistry, vol. 278, no. 38, pp. 36868–36875, 2003. [26] X. Yan, X. Zhao, M. Qian, N. Guo, X. Gong, and X. Zhu, “Characterization and gene structure of a novel retinoblastoma-protein-associated protein similar to the tran- scription regulator TFII-I,” Biochemical Journal, vol. 345, no. 3, pp. 749–757, 2000. [27] V. J. Zani, N. Asou, D. Jadayel et al., “Molecular cloning of complex chromosomal translocation t(8;14;12)(q24.1;q32.3; q24.1) in a Burkitt lymphoma cell line deﬁnes a new gene (BCL7A) with homology to caldesmon,” Blood, vol. 87, no. 8, pp. 3124–3134, 1996. [28] D. M. Jadayel, L. R. Osborne, L. J. A. Coignet et al., “The BCL7 gene family: deletion of BCL7B in Williams syndrome,” Gene, vol. 224, no. 1-2, pp. 35–44, 1998. Case Reports in Medicine