To grow or not to grow, That is the question

Neoplasms represent uncontrolled growth of cells, and usually come to clinical attention because of the symptoms and/or clinical signs they elicit. A growing number of studies examining the natural history of neoplasms show that particular types can exhibit highly variable growth patterns.[18] Some neoplasms continue to grow and become malignant, while others spontaneously stop growing or even regress. As imaging and screening protocols have become more widespread and sophisticated, asymptomatic/incidental neoplasms are increasingly being found.[21] Recent evidence, including autopsy series or imaging studies, reveal the existence This article may be cited as: Kliot T, Ince Y, Tihan T, Wilson M, Kliot M. To grow or not to grow, That is the question. Surg Neurol Int 2013;4:S407-10. Available FREE in open access from: http://www.surgicalneurologyint.com/text.asp?2013/4/2/407/120882

[1]  K. Fukunaga,et al.  Neurofibromatosis Type I Tumor Suppressor Neurofibromin Regulates Neuronal Differentiation via Its GTPase-activating Protein Function toward Ras* , 2003, Journal of Biological Chemistry.

[2]  A. Lund,et al.  Optic gliomas in children with neurofibromatosis type 1 , 1991, European Journal of Pediatrics.

[3]  C. Johannessen,et al.  A negative feedback signaling network underlies oncogene-induced senescence. , 2006, Cancer cell.

[4]  F. Tamanoi,et al.  The catalytic domain of the neurofibromatosis type 1 gene product stimulates ras GTPase and complements ira mutants of S. cerevisiae , 1990, Cell.

[5]  T. Wilt.  The Prostate Cancer Intervention Versus Observation Trial: VA/NCI/AHRQ Cooperative Studies Program #407 (PIVOT): design and baseline results of a randomized controlled trial comparing radical prostatectomy with watchful waiting for men with clinically localized prostate cancer. , 2012, Journal of the National Cancer Institute. Monographs.

[6]  J. Barnholtz-Sloan,et al.  CBTRUS statistical report: Primary brain and central nervous system tumors diagnosed in the United States in 2006-2010. , 2013, Neuro-oncology.

[7]  L. Parada,et al.  Neurofibromin, a tumor suppressor in the nervous system. , 2001, Experimental cell research.

[8]  J. Mulvihill,et al.  Long-term follow-up of von Recklinghausen neurofibromatosis. Survival and malignant neoplasms. , 1986, The New England journal of medicine.

[9]  G. Thomas,et al.  Germline loss-of-function mutations in SPRED1 cause a neurofibromatosis 1–like phenotype , 2007, Nature Genetics.

[10]  C. Kruchko,et al.  CBTRUS statistical report: primary brain and central nervous system tumors diagnosed in the United States in 2005-2009. , 2012, Neuro-oncology.

[11]  H. Völzke,et al.  Potentially relevant incidental findings on research whole-body MRI in the general adult population: frequencies and management , 2013, European Radiology.

[12]  J. Shay,et al.  BRAFE600-associated senescence-like cell cycle arrest of human naevi , 2005, Nature.

[13]  J. Charrow,et al.  Natural history of optic pathway tumors in children with neurofibromatosis type 1: a longitudinal study. , 1994, The Journal of pediatrics.

[14]  M. Barbacid,et al.  Tumour biology: Senescence in premalignant tumours , 2005, Nature.

[15]  S. Lowe,et al.  Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4a , 1997, Cell.

[16]  H. Stein,et al.  Oncogene-induced senescence as an initial barrier in lymphoma development , 2005, Nature.

[17]  L. Cantley,et al.  Ras, PI(3)K and mTOR signalling controls tumour cell growth , 2006, Nature.

[18]  S. Ozonoff,et al.  Cognitive impairment in neurofibromatosis type 1. , 1999, American journal of medical genetics.

[19]  V. Riccardi,et al.  Penetrance of von Recklinghausen neurofibromatosis: a distinction between predecessors and descendants. , 1988, American journal of human genetics.

[20]  K. Hoffmann,et al.  Differentially expressed genes in neurofibromatosis 1-associated neurofibromas and malignant peripheral nerve sheath tumors , 2004, Acta Neuropathologica.

[21]  D. Viskochil,et al.  Molecular, Genetic, and Cellular Pathogenesis of Neurofibromas and Surgical Implications , 2006, Neurosurgery.

[22]  P. O'Connell,et al.  Genomic organization of the neurofibromatosis 1 gene (NF1). , 1995, Genomics.

[23]  Shlomi Constantini,et al.  Pediatric incidental brain tumors: a growing treatment dilemma. , 2012, Journal of neurosurgery. Pediatrics.

[24]  P. O’Connell,et al.  The GAP-related domain of the neurofibromatosis type 1 gene product interacts with ras p21 , 1990, Cell.

[25]  B. McManus,et al.  Cardiovascular disease in neurofibromatosis 1: Report of the NF1 Cardiovascular Task Force , 2002, Genetics in Medicine.

[26]  Jason A. Koutcher,et al.  Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis , 2005, Nature.

[27]  L. Kluwe,et al.  Growth dynamics of plexiform neurofibromas: a retrospective cohort study of 201 patients with neurofibromatosis 1 , 2012, Orphanet Journal of Rare Diseases.