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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleDisplayedQuote" id="dsq0005"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall"><span class="elsevierStyleItalic">The sleep of a laborer is sweet&#44; whether they eat little or much&#44; but as for the rich&#44; their abundance permits them no sleep&#46;</span></p><span class="elsevierStyleSource">Ecclesiastes 5&#58;12</span></span></p><p id="par0010" class="elsevierStylePara elsevierViewall">The quantity and quality of sleep has always been a concern for mankind&#44; and it is known to be essential for sustaining life in general and human life in particular&#46; All patients with acute and chronic disease suffer altered sleep patterns&#46; Cancer patients&#44; in particular&#44; suffer fatigue and difficulties falling or staying asleep&#46; This editorial does not address this topic&#44; but instead discusses the influence of primary sleep-disordered breathing on the development of cancer&#44; and the role of the respiratory medicine specialist now and in the future&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">The circadian rhythm is an essential biological function in all living beings&#44; and determines physiological changes and behavior over a 24-h period&#46; In mammals&#44; the circadian &#8220;pacemaker&#8221; is located in the suprachiasmatic nucleus &#40;SCN&#41; in the hypothalamus&#46; Circadian rhythms are genetically determined&#44; and preliminary studies have reported the presence of certain genetic polymorphisms that might determine disorders in the sleep&#8211;wake pattern&#46; Epigenetic modifications in key genes for circadian regulation have been reported in shift workers and individuals exposed to high levels of light at night&#44; modifications that simultaneously alter the transcription of regulatory genes related with susceptibility to cancer&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> Epidemiological studies performed in these workers have found an association between the risk of cancer&#44; particularly breast cancer&#44;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> and shift work&#46; The intermediary mechanisms that might explain the relationship between shift work and the risk of cancer are unknown&#46; Melatonin is known to have anti-oncogenic effects&#44; and <span class="elsevierStyleItalic">in vitro</span> studies have shown it to increase expression of the PER2 gene which&#44; among other things&#44; reduces the production of &#946;-catenine&#46; This protein increases cyclin-D levels&#44; activating the proliferation of neoplastic cells&#46; Various melatonin receptors affecting tumor physiology have been described in breast cancer tumor cells&#46; In both male and female shift workers&#44; melatonin levels at night and in 24-h urine are reduced and fluctuate much less than in day-time workers&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">3</span></a> This finding would support the laboratory studies mentioned above&#44; but to date no causal relationship has been identified between melatonin and the risk of cancer&#44; and no interventional trials been performed with melatonin in animals or in humans&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Sleep duration&#44; whether too short or too long&#44; and its relationship with the risk of cancer&#44; has been evaluated in some population studies&#44; with inconsistent results&#46; Instead of studying real &#8220;sleep time&#8221;&#44; which is difficult to establish since it is based on reported questionnaires&#44; it is easier to study sleep fragmentation &#40;SF&#41; and its relationship with the risk of cancer&#46; In animal models in which SF was induced while preserving sleep time and eliminating the potential effect of intermittent hypoxia &#40;IH&#41;&#44; the degree of SF was determined to be associated with greater proliferation rates and tumor development&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a> In another animal study&#44; Almendros et al&#46; evaluated the effect of IH&#44; but this time the effect of SF was eliminated&#46; They showed clearly that IH was associated with a faster melanoma growth rate and an early and more intense development of distant metastasis&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> To date&#44; no experimental studies have been conducted to evaluate the relative importance of these 2 intermediate mechanisms &#40;SF and IH&#41; in the same animal model&#46; What intermediate mechanisms might favor oncogenesis induced by SF and IH&#63; Recent experiments in rat models have shown that IH did not induce direct dysplastic changes&#44; but instead changed the polarity of the macrophages&#44; transforming them into a less immunocompetent phenotype &#40;M2&#41; that would allow greater tumor proliferation&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a> M2 macrophages also were elevated in animal models of SF&#44; in this case increasing toll-like receptor 4 expression&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a> It seems&#44; then&#44; that the 2 main components of obstructive sleep apnea &#40;OSA&#41;&#44; SF and IH&#44; cause changes in innate immunity&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Confirmation of these phenomena in humans would suggest that anticancer surveillance and neoplastic growth control phenomena are less effective in patients with OSA&#46; The Spanish Sleep Group demonstrated almost simultaneously with the Wisconsin group that untreated OSA patients had a greater incidence of cancer&#44;<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">7&#44;8</span></a> providing epidemiological data to support the results of the <span class="elsevierStyleItalic">in vitro</span> research&#46; However&#44; a Canadian population study was unable to confirm this association&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> Interested readers can consult the excellent review by Martinez-Garcia on this subject that appeared recently in Archivos de Bronconeumolog&#237;a&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">What are the clinical implications of these studies on the relationship between sleep and cancer&#63; In my opinion&#44; no robust studies establishing the relationship between the amount and the quality of sleep and cancer have yet been published&#46; For now&#44; we must insist on the need for good sleep hygiene and avoid treatments that alter natural sleep&#46; As respiratory medicine specialists&#44; we are in the front line of treating patients with OSA&#46; There is still no evidence to establish a causal relationship between OSA and cancer&#44; so there is no need to actively investigate for cancer the first time we see a patient with OSA&#44; nor do we need to change our current therapeutic practice&#46; However&#44; the available information obliges us to be more alert to the potential risk of cancer as a comorbidity in OSA patients and to monitor them regularly&#44; but without causing alarm&#46;</p></span>"
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Editorial
Sleep and Cancer
Sueño y cáncer
José M. Marína,b
a Hospital Universitario Miguel Servet, IIS Aragón, Zaragoza, Spain
b CIBER Enfermedades Respiratorias (CIBERES), Spain
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    "titulo" => "Sleep and Cancer"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleDisplayedQuote" id="dsq0005"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall"><span class="elsevierStyleItalic">The sleep of a laborer is sweet&#44; whether they eat little or much&#44; but as for the rich&#44; their abundance permits them no sleep&#46;</span></p><span class="elsevierStyleSource">Ecclesiastes 5&#58;12</span></span></p><p id="par0010" class="elsevierStylePara elsevierViewall">The quantity and quality of sleep has always been a concern for mankind&#44; and it is known to be essential for sustaining life in general and human life in particular&#46; All patients with acute and chronic disease suffer altered sleep patterns&#46; Cancer patients&#44; in particular&#44; suffer fatigue and difficulties falling or staying asleep&#46; This editorial does not address this topic&#44; but instead discusses the influence of primary sleep-disordered breathing on the development of cancer&#44; and the role of the respiratory medicine specialist now and in the future&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">The circadian rhythm is an essential biological function in all living beings&#44; and determines physiological changes and behavior over a 24-h period&#46; In mammals&#44; the circadian &#8220;pacemaker&#8221; is located in the suprachiasmatic nucleus &#40;SCN&#41; in the hypothalamus&#46; Circadian rhythms are genetically determined&#44; and preliminary studies have reported the presence of certain genetic polymorphisms that might determine disorders in the sleep&#8211;wake pattern&#46; Epigenetic modifications in key genes for circadian regulation have been reported in shift workers and individuals exposed to high levels of light at night&#44; modifications that simultaneously alter the transcription of regulatory genes related with susceptibility to cancer&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> Epidemiological studies performed in these workers have found an association between the risk of cancer&#44; particularly breast cancer&#44;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> and shift work&#46; The intermediary mechanisms that might explain the relationship between shift work and the risk of cancer are unknown&#46; Melatonin is known to have anti-oncogenic effects&#44; and <span class="elsevierStyleItalic">in vitro</span> studies have shown it to increase expression of the PER2 gene which&#44; among other things&#44; reduces the production of &#946;-catenine&#46; This protein increases cyclin-D levels&#44; activating the proliferation of neoplastic cells&#46; Various melatonin receptors affecting tumor physiology have been described in breast cancer tumor cells&#46; In both male and female shift workers&#44; melatonin levels at night and in 24-h urine are reduced and fluctuate much less than in day-time workers&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">3</span></a> This finding would support the laboratory studies mentioned above&#44; but to date no causal relationship has been identified between melatonin and the risk of cancer&#44; and no interventional trials been performed with melatonin in animals or in humans&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Sleep duration&#44; whether too short or too long&#44; and its relationship with the risk of cancer&#44; has been evaluated in some population studies&#44; with inconsistent results&#46; Instead of studying real &#8220;sleep time&#8221;&#44; which is difficult to establish since it is based on reported questionnaires&#44; it is easier to study sleep fragmentation &#40;SF&#41; and its relationship with the risk of cancer&#46; In animal models in which SF was induced while preserving sleep time and eliminating the potential effect of intermittent hypoxia &#40;IH&#41;&#44; the degree of SF was determined to be associated with greater proliferation rates and tumor development&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a> In another animal study&#44; Almendros et al&#46; evaluated the effect of IH&#44; but this time the effect of SF was eliminated&#46; They showed clearly that IH was associated with a faster melanoma growth rate and an early and more intense development of distant metastasis&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> To date&#44; no experimental studies have been conducted to evaluate the relative importance of these 2 intermediate mechanisms &#40;SF and IH&#41; in the same animal model&#46; What intermediate mechanisms might favor oncogenesis induced by SF and IH&#63; Recent experiments in rat models have shown that IH did not induce direct dysplastic changes&#44; but instead changed the polarity of the macrophages&#44; transforming them into a less immunocompetent phenotype &#40;M2&#41; that would allow greater tumor proliferation&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a> M2 macrophages also were elevated in animal models of SF&#44; in this case increasing toll-like receptor 4 expression&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a> It seems&#44; then&#44; that the 2 main components of obstructive sleep apnea &#40;OSA&#41;&#44; SF and IH&#44; cause changes in innate immunity&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Confirmation of these phenomena in humans would suggest that anticancer surveillance and neoplastic growth control phenomena are less effective in patients with OSA&#46; The Spanish Sleep Group demonstrated almost simultaneously with the Wisconsin group that untreated OSA patients had a greater incidence of cancer&#44;<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">7&#44;8</span></a> providing epidemiological data to support the results of the <span class="elsevierStyleItalic">in vitro</span> research&#46; However&#44; a Canadian population study was unable to confirm this association&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> Interested readers can consult the excellent review by Martinez-Garcia on this subject that appeared recently in Archivos de Bronconeumolog&#237;a&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">What are the clinical implications of these studies on the relationship between sleep and cancer&#63; In my opinion&#44; no robust studies establishing the relationship between the amount and the quality of sleep and cancer have yet been published&#46; For now&#44; we must insist on the need for good sleep hygiene and avoid treatments that alter natural sleep&#46; As respiratory medicine specialists&#44; we are in the front line of treating patients with OSA&#46; There is still no evidence to establish a causal relationship between OSA and cancer&#44; so there is no need to actively investigate for cancer the first time we see a patient with OSA&#44; nor do we need to change our current therapeutic practice&#46; However&#44; the available information obliges us to be more alert to the potential risk of cancer as a comorbidity in OSA patients and to monitor them regularly&#44; but without causing alarm&#46;</p></span>"
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Article information
ISSN: 15792129
Original language: English
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2024 February 55 22 77
2023 March 9 3 12
2023 February 53 24 77
2023 January 30 44 74
2022 December 45 34 79
2022 November 36 27 63
2022 October 61 43 104
2022 September 34 33 67
2022 August 32 52 84
2022 July 38 53 91
2022 June 22 39 61
2022 May 27 37 64
2022 April 37 33 70
2022 March 32 40 72
2022 February 35 32 67
2022 January 36 43 79
2021 December 23 40 63
2021 November 35 49 84
2021 October 53 53 106
2021 September 41 48 89
2021 August 32 60 92
2021 July 27 33 60
2021 June 55 69 124
2021 May 37 74 111
2021 April 107 67 174
2021 March 66 35 101
2021 February 53 32 85
2021 January 59 34 93
2020 December 54 82 136
2020 November 55 55 110
2020 October 36 29 65
2020 September 39 25 64
2020 August 36 29 65
2020 July 99 51 150
2020 June 19 21 40
2020 May 28 14 42
2020 April 33 14 47
2020 March 35 16 51
2020 February 75 25 100
2020 January 33 18 51
2019 December 51 15 66
2019 November 42 23 65
2019 October 29 14 43
2019 September 26 12 38
2019 August 27 17 44
2019 July 30 34 64
2019 June 14 11 25
2019 May 27 24 51
2019 April 34 29 63
2019 March 28 17 45
2019 February 24 25 49
2019 January 28 25 53
2018 December 42 26 68
2018 November 44 17 61
2018 October 79 21 100
2018 September 37 11 48
2018 May 22 1 23
2018 April 39 5 44
2018 March 58 3 61
2018 February 57 9 66
2018 January 120 4 124
2017 December 42 10 52
2017 November 38 13 51
2017 October 26 12 38
2017 September 31 14 45
2017 August 0 1 1
2017 April 0 2 2
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