Archives

  • 2019-10
  • 2020-07
  • 2020-08
  • br Conflict of interest statement br References br

    2020-08-12


    Conflict of interest statement 
    References
    [8] Cochran AJ, Balda BR, Starz H, Bachter D, Krag DN, Cruse CW, et al. The Augsburg Consensus. Techniques of lymphatic mapping, sentinel lymphadenectomy, and completion lymphadenectomy in cutaneous malignancies. Cancer 2000;89(2):
    None declared.
    [28] Murali R, Cochran AJ, Cook MG, Hillman JD, Karim RZ, Moncrieff M, et al. Interobserver reproducibility of histologic parameters of melanoma deposits in sentinel lymph nodes: im-plications for management of patients with melanoma. Cancer 2009;115(21):5026e37. https://doi.org/10.1002/cncr.24298.
    [29] van Akkooi AC, Spatz A, Eggermont AM, Mihm M, Cook MG. Expert opinion in melanoma: the sentinel node; EORTC Mela-noma Group recommendations on practical methodology of the measurement of the microanatomic location of metastases and metastatic tumour burden. Eur J Cancer 2009;45(16):2736e42. https://doi.org/10.1016/j.ejca.2009.08.015. 
    [34] Scolyer RA, Li LX, McCarthy SW, Shaw HM, Stretch JR, Sharma R, et al. Micromorphometric features of positive sentinel lymph nodes predict involvement of nonsentinel nodes in patients with melanoma. Am J Clin Pathol 2004;122(4):532e9. https: //doi.org/10.1309/TDWJTR15TDM1TG7Q.
    [39] van Akkooi AC, Nowecki ZI, Voit C, Scha¨fer-Hesterberg G, Michej W, de Wilt JH, et al. Minimal sentinel node (SN) tumor burden according to the Rotterdam criteria is the most important prognostic factor for survival in melanoma patients. A multi-center study in 388 patients with positive sentinel nodes. Ann Surg
    [40] Riber-Hansen R, Hamilton-Dutoit SJ, Steiniche T. Nodal distri-bution, stage migration due to diameter measurement and the prognostic significance of metastasis volume in melanoma sentinel lymph nodes: a validation study. APMIS 2014;122(10):968e75. https://doi.org/10.1111/apm.12240.
    [41] Rao UN, Ibrahim J, Flaherty LE, Richards J, Kirkwood JM. Implications of microscopic satellites of the primary and extrac-apsular lymph node spread in patients with high-risk melanoma: pathologic corollary of Eastern Cooperative Oncology Group Trial E1690. J Clin Oncol 2002;20(8):2053e7. https: //doi.org/10.1200/JCO.2002.08.024.
    Contents lists available at ScienceDirect
    Environmental Research
    journal homepage: www.elsevier.com/locate/envres
    Analyses of temporal and spatial patterns of glioblastoma multiforme and T other 13826-64-7 cancer subtypes in relation to mobile phones using synthetic counterfactuals
    Frank de Vocht
    Population Health Sciences, Bristol Medical School, University of Bristol, Canynge Hall, 39 Whatley Road, Bristol BS8 2PS, UK
    Keywords:
    Brain cancer
    Glioblastoma multiforme
    GBM
    Mobile phones
    Cellphones
    Timeseries
    Bayesian
    Structural timeseries 
    This study assesses whether temporal trends in glioblastoma multiforme (GBM) in different brain regions, and of different malignant and benign (including acoustic neuroma and meningioma) subtypes in the temporal lobe, could be associated with mobile phone use. Annual 1985–2005 incidence of brain cancer subtypes for England were linked to population-level covariates. Bayesian structural timeseries were used to create 2006–2014 counterfactual trends, and differences with measured newly diagnosed cases were interpreted as causal effects. Increases in excess of the counterfactuals for GBM were found in the temporal (+38% [95% Credible Interval -7%,78%]) and frontal (+36% [-8%,77%]) lobes, which were in agreement with hypothesised temporal and spatial mechanisms of mobile phone usage, and cerebellum (+59% [-0%,120%]). However, effects were pri-marily present in older age groups, with largest effects in 75 + and 85 + groups, indicating mobile phone use is unlikely to have been an important putative factor. There was no evidence of an effect of mobile phone use on incidence of acoustic neuroma and meningioma. Although 1985–2014 trends in GBM in the temporal and frontal lobes, and probably cerebellum, seem consistent with mobile phone use as an important putative factor, age-group specific analyses indicate that it is unlikely that this correlation is causal.
    1. Background
    Although both the incidence of certain types of brain cancers (Khurana et al., 2009; De Vocht, 2016; De Vocht et al., 2011; Zada et al., 2012; Yang et al., 2017) and use of mobile phones (and other wireless technology) (Khurana et al., 2009) have been increasing over the last 2 decades, and despite extensive research it remains unclear whether this is a question of causation or correlation (Sienkiewicz et al., 2017). Based on all available evidence at the time, The International Agency for Research on Cancer (IARC) concluded in 2011 that exposure to radiofrequency radiation (RF) in the frequency range 30 kHz to 300 GHz, which includes the frequencies used by mobile phones (Cardis et al., 2011), should be classified as 2B (possibly carcinogenic to hu-mans) taking into account positive associations between glioma and acoustic neuroma, and exposure to RF-EMF from wireless phones (Baan et al., 2011). Results from the National Toxicology Program (NTP) in rats seem to support this, with results suggesting an increased incidence of malignant glioma, as well as schwannomas of the heart in male, but not female, rats after whole-body averaged Specific Absorption Rate