Hace pocos días afirmaban en un artículo, que la psicología en torno al cáncer es una pseudoterapia para la comunidad científica y me quedé perpleja, como imagino que os habréis quedado vosotros al leer esta afirmación. Luego al releer el artículo y ver quién lo había escrito, me dí cuenta de que donde dice “comunidad científica” debería decir “circulo escéptico o santa inquisición”. ¿¿Cómo no van a ser importantes las emociones y los sentimientos en el cáncer?? Es de sentido común, no? Somos seres sintientes y no modelos matemáticos.
Hoy, quiero hablaros de la influencia del estrés en el cáncer y en concreto del papel que juegan en las metástasis. Cuando me diagnosticaron la enfermedad, desde el momento de la intervención hasta que me dieron los resultados definitivos (3 semanas) viví un periodo de miedo y estrés intenso… no podía dormir, no podía pensar con claridad, no paraba de llorar y fantasear con una muerte próxima. .. Cuando por fin la patóloga hizo el informe todo parecían buenas noticias… carcinoma de células transicionales del ovario encapsulado con lavado peritoneal negativo, lo que hacía presuponer que era un estadio Ia (el más leve)… al día siguiente me palpo las metástasis vaginales… algo sorprendente y que se sale de la evolución típica de la enfermedad. 3 semanas antes de aparecer estas metástasis en la RNM no había nada que hiciera sospechar su presencia y de repente aparecen esas lesiones. Al día siguiente tras palpar las metástasis me realizan un PET TAC y aparecen más metástasis en pulmón y hueso. Aquí, ya me quedo hecha polvo como podéis imaginar. Mi oncólogo me propone empezar quimio y yo empiezo con mi cambio de alimentación, a hacer ejercicio y tratar ese estrés…. 1 mes y medio después, nuevo PET y ya no hay enfermedad. Increíble, ¿no? Pero cierto, muy cierto. Aquí tenéis las pruebas médicas . Después de contaros mi caso vamos a ver que dice la ciencia sobre el tema, en concreto sobre estrés y cáncer de ovario…. Sé que puede ser un post muy técnico, pero está redactado así, para que aquellos que aún son escépticos y creen que las emociones no influyen en la enfermedad se convenzan. En breve, os traigo el artículo con un lenguaje más sencillo y divulgativo, hoy se trata de callar a los que hablan de pseudociencia cuando nos referimos a las emociones y al cáncer.
La principal causa de muerte por cáncer es la metástasis la cual no suele desaparecer con el tratamiento convencional. Estudios clínicos y epidemiológicos en los últimos 30 años han identificado factores psicosociales como el estrés, la depresión crónica y la falta de apoyo social como factores de riesgo para la progresión del cáncer y la aparición de metástasis. La evidencia de la función que los factores psicosociales pueden jugar en la iniciación del cáncer es limitada , pero si hay evidencia para establecer vínculo y relación entre factores psicológicos como el estrés, la depresión y el aislamiento social y la progresión de la enfermedad. La cronicidad de los sentimientos negativos, manifestada por un estado de ánimo deprimido o un sentimiento de desesperanza, parece tener una fuerte relación con este vinculo.
El apoyo social se refiere a la satisfacción percibida de un individuo con las relaciones sociales y se cree que juega un papel importante en la amortiguación psicológica y la respuesta al estrés biológico. Varios estudios han relacionado altos niveles de apoyo social con mejores resultados clínicos en pacientes con cáncer. Por ejemplo, en pacientes con cáncer de mama, el apoyo social se ha relacionado con una mayor supervivencia en varios estudios a gran escala, aunque se observaron resultados negativos en algunos estudios. Colectivamente, la evidencia ha demostrado que el estrés y factores psicosociales específicos se asocian con elementos claves de la cascada metastásica tanto en modelos animales como humanos.
- Respuesta neuroendocrina mediada por estrés Estrés y el SNC
El estrés es un proceso complejo que incluye factores ambientales y psicosociales que inician una cascada de procesos tanto en el sistema nervioso periférico como en el SNC . El estrés puede ser agudo (de corta duración) o crónico (repetitivo o que ocurre durante un período prolongado de tiempo). Bajo condiciones de estrés crónico, el cuerpo permanece en un estado constante de ‘overdrive’, con efectos deletéreos sobre la regulación de los sistemas de respuesta al estrés, así como efectos negativos sobre otros órganos. Se sabe que tanto la norepinefrina (NE) como la epinefrina (E) están elevadas en individuos con estrés agudo o crónico . Además, los niveles de dopamina (DA) se incrementan en el cerebro durante el estrés agudo . Sin embargo, bajo estrés crónico, los niveles de DA son inferiores como consecuencia de la disminución de la liberación de DA [31]. Una variedad de estresores, incluyendo un trauma severo, un divorcio, un proceso de duelo, así como un episodio de depresión o aislamiento social, se han asociado con alteraciones en varias hormonas neuroendocrinas, en particular, catecolaminas y cortisol.
Se cree que la respuesta al estrés fisiológico es uno de los mediadores probables de los efectos de los factores psicosociales en la progresión del cáncer. La respuesta global al estrés implica la activación de varios sistemas corporales incluyendo el sistema nervioso autónomo y el eje hipotalámico-pituitario-suprarrenal (HPA). La respuesta de “lucha o huida” es provocada por la producción de mediadores como NE y E del sistema nervioso simpático (SNS) y la médula suprarrenal. La respuesta de HPA incluye la liberación de la hormona liberadora de corticotropina por parte del hipotálamo, que induce la secreción de la hormona adrenocorticotrófica de la pituitaria anterior, resultando en la liberación de glucocorticoides (GC) como el cortisol de la corteza suprarrenal. Factores neuroendocrinos adicionales que también se modulan después de un periodo de estrés, incluyendo DA, prolactina, NGF, sustancia P y oxitocina .
- Papel de los mediadores neuroendocrinos en los órganos periféricos.
Los mediadores neuroendocrinos pueden modular la función celular en el tejido periférico y esto estar relacionado con el inicio y la progresión del cáncer. Por ejemplo, los neurotransmisores del SNS (es decir, NE y E) desempeñan papeles fisiológicamente relevantes en la regulación del microambiente de los órganos periféricos. El ovario proporciona un ejemplo que es altamente relevante para los cánceres del sistema reproductivo. Las concentraciones totales de catecolaminas son sustancialmente más altas en los ovarios que en el plasma Por otra parte, los niveles de catecolaminas en los ovarios se sabe que se incrementan en respuesta al estrés. Del mismo modo, las catecolaminas están presentes en niveles más altos en el microambiente de la médula ósea .
Se ha demostrado que las catecolaminas suprimen la mielopoyesis tanto in vivo como in vitro en presencia de carboplatino.
Los efectos de las catecolaminas están mediados por los receptores adrenérgicos (ADR), que son las clases más ampliamente estudiadas de los receptores acoplados a la proteína G.
Los receptores β-adrenérgicos (ADRB) median muchos efectos de las catecolaminas en las células y se han identificado en varios tipos de células cancerosas, incluyendo las células de cáncer de mama y de ovario. ADRBs son receptores-proteína G acoplados cuya función primaria es la transmisión de información desde el entorno extracelular al interior de la célula.
tanto NE y E se elevan de manera sostenida en el ovario y otros tejidos peritoneales en los modelos preclínicos de estrés crónico [61]. Estos aumentos hormonales se relacionaron con una mayor carga tumoral, al parecer debida a un aumento de la angiogénesis. Parece que el estrés crónico promueve la angiogénesis en los tumores ováricos malignos.
Los glucocorticoides son una clase de hormonas esteroides que se unen al receptor GC (GCR), que está presente en casi todas las células animales vertebradas. GCs son parte del mecanismo de retroalimentación que modula la actividad inmune y las respuestas inflamatorias. Las dosis farmacológicas de GCs se usan con frecuencia para tratar condiciones que son causadas por un sistema inmune hiperactivo. GC también interfieren con diversos mecanismos anormales en las células cancerosas, por lo que se utilizan en dosis altas para tratar ciertas neoplasias .
El cortisol es el GC humano más importante. Es esencial para la vida y regula una variedad de importantes funciones cardiovasculares, metabólicas, inmunológicas y homeostáticas. EL cortisol es secretado por la corteza suprarrenal en respuesta al estrés . El apoyo social y la reducción del estrés se asocian con menores niveles de cortisol. Una serie de estudios han demostrado que el estrés puede alterar los ritmos circadianos neuroendocrinos en formas que favorecen el crecimiento tumoral y la metástasis. Del mismo modo, el trabajo nocturno, que se sabe que perturba los ritmos endocrinos, se considera un factor de riesgo para los cánceres de mama y colorrectal .
- Efectos del estrés sobre las metástasis del cáncer
La metástasis es un proceso complejo que requiere varios pasos para desarrollarse, incluyendo angiogénesis, proliferación, invasión, embolización y evasión de la vigilancia del sistema inmune
La evidencia muestra que la respuesta al estrés puede afectar a muchas partes de esta cascada.
El estrés favorece la angiogénesis, la proliferación celular, la migración e invasión de las células tumores.
- Efectos de estrés sobre la respuesta inmune
Se sabe que el sistema nervioso central, el sistema endocrino y el sistema inmunitario interactúan entre sí y, por lo tanto, los cambios en cualquier sistema pueden tener efectos en los otros sistemas. El SNC modula la inmunidad tanto a través de la liberación de GCs a través del eje HPA como a través de la liberación de catecolaminas a través del sistema nervioso autónomo. Varios factores implicados en la respuesta al estrés están implicados en la activación o disminución de la respuesta inmune, lo que puede jugar un papel determinante para que las células tumorales escapen a la detección y eliminación por parte de las células inmunitarias.
- Glucocorticoides y respuesta inmune
Los glucocorticoides son esenciales para la regulación de respuestas inmunes e inflamatorias. Las concentraciones fisiológicas de GCs en el rango de 350-950 nmol / l, como ocurren durante el estrés físico o psicológico, resultan en la modulación de la transcripción de genes implicados en la respuesta inflamatoria, mientras que las dosis farmacológicas (concentraciones mayores que fisiológicas [> 1 μmol /L]) resultan en una supresión de la respuesta inflamatoria Del mismo modo, durante situaciones de estrés crónico, se ha demostrado que los niveles elevados de GC son inmunosupresores, lo que conduce a una mayor susceptibilidad a la infección viral, cicatrización prolongada de la herida o disminución de la producción de anticuerpos después de la vacunación . Los pacientes con cáncer de mama con mayores concentraciones diarias de cortisol diurna también mostraron inmunidad suprimida frente a los antígenos comúnmente encontrados, lo que sugiere una disminución de la respuesta inmune celular. Dentro del sistema inmunológico, las células T y B, los neutrófilos, los monocitos y los macrófagos llevan todos GCRs, lo que permite la regulación por GC tanto de las respuestas inmunes celulares como humorales . Además, GCs puede inducir la apoptosis en monocitos, macrófagos y linfocitos T , proporcionando más pruebas de su capacidad para regular la función inmune normal.
Conclusiones
El estilo de vida moderno que asocia por lo general estrés crónico se ha asociado con la patogénesis de muchas enfermedades, incluido el cáncer. El estrés crónico activa vías de señalización específicas en las células cancerosas y en el microambiente tumoral, dando lugar al crecimiento ya la progresión del tumor. Elucidar estas vías es esencial para el desarrollo de nuevos enfoques para bloquear los efectos deletéreos de la biología del estrés en el crecimiento del cáncer y metástasis.
Perspectiva futura
Los estilos de vida contemporáneos y el ambiente de las sociedades modernas parecen inducir trastornos relacionados con el estrés. Con respecto a la patogénesis del cáncer, hay evidencia creciente y convincente de las implicaciones biológicas y clínicas de las influencias psicosociales y emocionales.
Se ha demostrado que los bloqueadores beta bloquean muchos de los efectos deletéreos del estrés. Si bien algunos estudios clínicos han demostrado menor incidencia de cáncer entre los pacientes tratados con β-bloqueadores, en otros, el riesgo de cáncer era neutral.
Los estudios sugieren que las intervenciones conductuales y farmacológicas orientadas a manejar el estrés de los enfermos con cáncer puede tener efectos sobre la progresión tumoral.
Resumen
■ La evidencia apunta a un papel prominente del estrés crónico en el crecimiento del cáncer y la metástasis.
■ El sistema nervioso simpático y la activación del eje hipotálamo-hipofisario-suprarrenal, junto con hormonas relacionadas, tienen impactos funcionales y biológicamente significativos en el microambiente tumoral.
■ Las vías de señalización del receptor β-adrenérgico afectan directamente a las células cancerosas. Las hormonas de estrés (por ejemplo, norepinefrina y epinefrina) estimulan la angiogénesis, la migración celular y la invasión, conduciendo a un aumento del crecimiento y progresión del tumor.
■ La dopamina retrasa el crecimiento tumoral inhibiendo la angiogénesis.
■ Los glucocorticoides inhiben la apoptosis de células cancerosas inducida por la quimioterapia y aumentan la supervivencia de la célula cancerosa.
■ Se están desarrollando intervenciones farmacológicas y bio-conductuales integradas para modular la influencia del sistema neuroendocrino en el microambiente del tumor y crear en base a esto terapias contra el cáncer más exitosas.
Texto extraído de:
Moreno-Smith, Myrthala, Susan K Lutgendorf, and Anil K Sood. “Impact of Stress on Cancer Metastasis.” Future oncology (London, England) 6.12 (2010): 1863–1881. PMC. Web. 30 May 2017
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55. Badino GR, Novelli A, Girardi C, et al. Evidence for functional β-adrenoceptor subtypes in CG-5 breast cancer cell. Pharmacol. Res 1996;33(4–5):255–260. [PubMed: 8938018]
56. Lutgendorf SK, Cole S, Costanzo E, et al. Stress-related mediators stimulate vascular endothelial growth factor secretion by two ovarian cancer cell lines. Clin. Cancer Res 2003;9(12):4514–4521. [PubMed: 14555525]
57. McDonald PH, Lefkowitz RJ. β-arrestins: new roles in regulating heptahelical receptors functions. Cell Signal 2001;13(10):683–689. [PubMed: 11602178]
58. Dixon RA, Kobilka BK, Strader DJ, et al. Cloning of the gene and cDNA for mammalian β– adrenergic receptor and homology with rhodopsin. Nature 1986;321(6065):75–79. [PubMed: 3010132]
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84. Tjurmina OA, Armando I, Saavedra JM, et al. Exaggerated adrenomedullary response to immobilization in mice with targeted disruption of the serotonin transporter gene. Endocrinology 2002;143(12):4520–4526. [PubMed: 12446578]
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133. Simon WE, Albrecht M, Trams G, et al. In vitro growth promotion of human mammary carcinoma cells by steroid hormones, tamoxifen, and prolactin. J. Natl Cancer Inst 1984;73(2): 313–321. [PubMed: 6589426]
134. Boudreau N, Bissell MJ. Extracellular matrix signaling: integration of form and function in normal and malignant cells. Curr. Opin. Cell. Biol 1998;10(5):640–646. [PubMed: 9818175]
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136. Hynes RO. Integrins: versatility, modulation, and signaling in cell adhesion. Cell 1992;69(1):11– 25. [PubMed: 1555235]
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138. Kawasaki H, Springett GM, Mochizuki N, et al. A family of cAMP-binding proteins that directly activate Rap1. Science 1998;282(5397):2275–2279. [PubMed: 9856955]
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141. Enserink JM, Price LS, Methi T, et al. The cAMP–Epac–Rap1 pathway regulates cell spreading and cell adhesion to laminin-5 through the α3β1 integrin but not the α6β4 integrin. J. Biol. Chem 2004;279(43):44889–44896. [PubMed: 15302884]
142. Yang EV, Bane CM, MacCallum RC, et al. Stress-related modulation of matrix metalloproteinase expression. J. Neuroimmunol 2002;133(1–2):144–150. [PubMed: 12446017]
143. Wu W, Yamaura T, Murakami K, et al. Involvement of TNF-α in enhancement of invasion and metastasis of colon 26-L5 carcinoma cells in mice by social isolation stress. Oncol. Res 1999;11(10):461–469. [PubMed: 10850887]
144. Entschladen F, Lang K, Drell TL, et al. Neurotransmitters are regulators for the migration of tumor cells and leukocytes. Cancer Immunol. Immunother 2002;51(9):467–482. [PubMed: 12357318]
145. Masur K, Niggemann B, Zanker KS, et al. Norepinephrine-induced migration of SW 480 colon carcinoma cells is inhibited by β-blockers. Cancer Res 2001;61(7):2866–2869. [PubMed: 11306460]
146. Joseph J, Niggemann B, Zaenker KS, et al. The neurotransmitter γ-aminobutyric acid is an inhibitory regulator for the migration of SW 480 colon carcinoma cells. Cancer Res 2002;62(22): 6467–6469. [PubMed: 12438237]
147. Sood AK, Bhatty R, Kamat AA, et al. Stress hormone-mediated invasion of ovarian cancer cells. Clin. Cancer Res 2006;12(2):369–375. [PubMed: 16428474]
148. Drell T, Joseph J, Lang K, et al. Effects of neurotransmitters on the chemokinesis and chemotaxis of MDA-MB-468 human breast carcinoma cells. Breast Cancer Res. Treat 2003;80(1):63–70. [PubMed: 12889599]
149. Pollard J. Tumour-educated macrophages promote tumour progression and metastasis. Nat. Rev. Cancer 2004;4:71–78. [PubMed: 14708027]
150. Coussens LM, Werb Z. Inflammation and cancer. Nat. Rev. Cancer 2002;420:860–867.
151. Chan AS, Ng LW, Poon LS, Chan WW, Wong YH. Dopaminergic and adrenergic toxicities on SK-N-MC human neuroblastoma cells are mediated through G protein signaling and oxidative stress. Apoptosis 2007;12:167–179. [PubMed: 17136323]
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156. Zhang C, Kolb A, Buchler P, et al. Corticosteroid co-treatment induces resistance to chemotherapy in surgical resections, xenografts and established cell lines of pancreatic cancer. BMC Cancer 2006;6:61. [PubMed: 16539710]
157. Bekasi S, Zalatnai A. Overexpression of glucocorticoid receptor in human pancreatic cancer and in xenografts. An immunohistochemical study. Pathol. Oncol. Res 2009;15(4):561–566. [PubMed: 19253003]
158. Zhang C, Kolb A, Mattern J, et al. Dexamethasone desensitizes hepatocellular and colorectal tumours toward cytotoxic therapy. Cancer Lett 2006;242(1):104–111. [PubMed: 16338063]
159. Zhang C, Beckermann B, Kallifatidis G, et al. Corticosteroids induce chemotherapy resistance in the majority of tumour cells from bone, brain, breast, cervix, melanoma and neuroblastoma. Int. J. Oncol 2006;29(5):1295–1301. [PubMed: 17016664]
160. Zhang C, Marme A, Wenger T, et al. Glucocorticoid-mediated inhibition of chemotherapy in ovarian carcinomas. Int. J. Oncol 2006;28(2):551–558. [PubMed: 16391812]
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163. Dave JR, Anderson SM, Saviolakis GA, et al. Chronic sustained stress increases levels of anterior pituitary prolactin mRNA. Pharmacol. Biochem. Behav 2000;67(3):423–431. [PubMed: 11164069]
164. Almeida SA, Petenusci SO, Franci JA, et al. Chronic immobilization-induced stress increases plasma testosterone and delays testicular maturation in pubertal rats. Andrologia 2000;32(1):7– 11. [PubMed: 10702860]
165. Young WS 3rd, Lightman SL. Chronic stress elevates enkephalin expression in the rat paraventricular and supraoptic nuclei. Brain Res. Mol. Brain Res 1992;13(1–2):111–117. [PubMed: 1349719]
166. Glavin GB, Szabo S. Dopamine in gastrointestinal disease. Dig. Dis. Sci 1990;35(9):1153–1161. [PubMed: 2202571]
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168. Thaker PH, Sood AK. Neuroendocrine influences on cancer biology. Semin. Cancer Biol 2007;18:164–170. [PubMed: 18201896]
169. Basu S, Nagy JA, Pal S, et al. The neurotransmitter dopamine inhibits angiogenesis induced by vascular permeability factor/vascular endothelial growth factor. Nat. Med 2001;7(5):569–574. [PubMed: 11329058]
170. Teunis MA, Kavelaars A, Voest E, et al. Reduced tumor growth, experimental metastasis formation, and angiogenesis in rats with a hyperreactive dopaminergic system. FASEB J 2002;16(11):1465–1467. [PubMed: 12205050]
171. Chakroborty D, Sarkar C, Basu B, et al. Catecholamines regulate tumor angiogenesis. Cancer Res 2009;69(9):3727–3730. [PubMed: 19383906]
172. Basu S, Sarkar C, Chakroborty D, et al. Ablation of peripheral dopaminergic nerves stimulates malignant tumor growth by inducing vascular permeability factor/vascular endothelial growth factor-mediated angiogenesis. Cancer Res 2004;64:5551–5555. [PubMed: 15313889]
154. Herr I, Ucur E, Herzer K, et al. Glucocorticoid cotreatment induces apoptosis resistance toward cancer therapy in carcinomas. Cancer Res 2003;63(12):3112–3120. [PubMed: 12810637]
155. Wu W, Chaudhuri S, Brickley DR, et al. Microarray analysis reveals glucocorticoid-regulated survival genes that are associated with inhibition of apoptosis in breast epithelial cells. Cancer Res 2004;64(5):1757–1764. [PubMed: 14996737]
156. Zhang C, Kolb A, Buchler P, et al. Corticosteroid co-treatment induces resistance to chemotherapy in surgical resections, xenografts and established cell lines of pancreatic cancer. BMC Cancer 2006;6:61. [PubMed: 16539710]
157. Bekasi S, Zalatnai A. Overexpression of glucocorticoid receptor in human pancreatic cancer and in xenografts. An immunohistochemical study. Pathol. Oncol. Res 2009;15(4):561–566. [PubMed: 19253003]
158. Zhang C, Kolb A, Mattern J, et al. Dexamethasone desensitizes hepatocellular and colorectal tumours toward cytotoxic therapy. Cancer Lett 2006;242(1):104–111. [PubMed: 16338063]
159. Zhang C, Beckermann B, Kallifatidis G, et al. Corticosteroids induce chemotherapy resistance in the majority of tumour cells from bone, brain, breast, cervix, melanoma and neuroblastoma. Int. J. Oncol 2006;29(5):1295–1301. [PubMed: 17016664]
160. Zhang C, Marme A, Wenger T, et al. Glucocorticoid-mediated inhibition of chemotherapy in ovarian carcinomas. Int. J. Oncol 2006;28(2):551–558. [PubMed: 16391812]
161. Zhang C, Wenger T, Mattern J, et al. Clinical and mechanistic aspects of glucocorticoid-induced chemotherapy resistance in the majority of solid tumors. Cancer Biol. Ther 2007;6(2):278–287. [PubMed: 17224649]
162. Sood AK, Armaiz-Pena GN, Halder J, et al. Adrenergic modulation of focal adhesion kinase protects human ovarian cancer cells from anoikis. J. Clin. Invest 2010;120(5):1515–1523. [PubMed: 20389021]
163. Dave JR, Anderson SM, Saviolakis GA, et al. Chronic sustained stress increases levels of anterior pituitary prolactin mRNA. Pharmacol. Biochem. Behav 2000;67(3):423–431. [PubMed: 11164069]
164. Almeida SA, Petenusci SO, Franci JA, et al. Chronic immobilization-induced stress increases plasma testosterone and delays testicular maturation in pubertal rats. Andrologia 2000;32(1):7– 11. [PubMed: 10702860]
165. Young WS 3rd, Lightman SL. Chronic stress elevates enkephalin expression in the rat paraventricular and supraoptic nuclei. Brain Res. Mol. Brain Res 1992;13(1–2):111–117. [PubMed: 1349719]
166. Glavin GB, Szabo S. Dopamine in gastrointestinal disease. Dig. Dis. Sci 1990;35(9):1153–1161. [PubMed: 2202571]
167. Mezey E, Eisenhofer G, Hansson S, et al. Dopamine produced by the stomach may act as a paracrine/autocrine hormone in the rat. Neuroendocrinology 1998;67(5):336–348. [PubMed: 9641616]
168. Thaker PH, Sood AK. Neuroendocrine influences on cancer biology. Semin. Cancer Biol 2007;18:164–170. [PubMed: 18201896]
169. Basu S, Nagy JA, Pal S, et al. The neurotransmitter dopamine inhibits angiogenesis induced by vascular permeability factor/vascular endothelial growth factor. Nat. Med 2001;7(5):569–574. [PubMed: 11329058]
170. Teunis MA, Kavelaars A, Voest E, et al. Reduced tumor growth, experimental metastasis formation, and angiogenesis in rats with a hyperreactive dopaminergic system. FASEB J 2002;16(11):1465–1467. [PubMed: 12205050]
171. Chakroborty D, Sarkar C, Basu B, et al. Catecholamines regulate tumor angiogenesis. Cancer Res 2009;69(9):3727–3730. [PubMed: 19383906]
172. Basu S, Sarkar C, Chakroborty D, et al. Ablation of peripheral dopaminergic nerves stimulates malignant tumor growth by inducing vascular permeability factor/vascular endothelial growth factor-mediated angiogenesis. Cancer Res 2004;64:5551–5555. [PubMed: 15313889]
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El contenido del presente sitio web es de carácter general y tiene una finalidad meramente informativa, sin que se garantice plenamente el acceso a todos los contenidos, ni su exhaustividad, corrección, vigencia o actualidad, ni su idoneidad o utilidad para un objetivo específico.
Toda la información que se ofrece a través de esta página web no sustituye, en ningún caso, un asesoramiento sanitario cualificado.
La Asociación de Oncología Integrativa declina toda responsabilidad sobre las consecuencias que un mal uso de este contenido pueda tener en la salud de los pacientes. Así mismo se recomienda que los pacientes comuniquen a su oncólogo convencional qué terapias complementarias les acompañan durante los tratamientos convencionales.