CISMA EN LA ONCOLOGÍA: carta abierta a Mariano Barbacid

cissé africano(p.vidente) · 31 Dic 2010

CISMA EN LA ONCOLOGÍA: carta abierta a Mariano Barbacid noticiasdeabajo

Un grupo de prestigiosos oncólogos publica una CARTA ABIERTA A MARIANO BARBACID en la que cuestionan tanto lo que oficialmente se afirma del cáncer como los tratamientos que se utilizan.

Un grupo de prestigiosos oncólogos médicos e investigadores en el campo de la Oncología -básica y clínica- ha decidido enviar a través de Discovery DSALUD una Carta abierta al Dr. Mariano Barbacid -Director del Centro Nacional de Investigaciones Oncológicas (CNIO)- en la que le solicitan responda públicamente a una serie de cuestiones de vital importancia en el momento actual de la investigación del cáncer y diga si está de acuerdo en que “ha llegado la hora de hacerse un replanteamiento global sobre esta patología, muy especialmente en lo que a la manera de afrontarla se refiere dado el fracaso de los actuales tratamientos médicos en la mayoría de los tumores malignos”.
Los firmantes -miembros de la International Society for Proton Dynamics of Cancer (ISPDC) o Sociedad Internacional de la Dinámica de Protones en el Tratamiento del Cáncer (www.ispdc.net)-, son el Dr. Salvador Harguindey –del Instituto de Biología Clínica y Metabolismo (IBCM) de Vitoria y vicepresidente de la mencionada sociedad-, el Dr. Stefano Fais -Director de la Sección de Medicamentos Antitumorales del Departamento de Investigación Terapéutica y Evaluación de Medicinas del Instituto Nacional de la Salud de Roma (Italia) y presidente del ISPDC-, la Dra. Miriam L. Wahl –ex Directora del Laboratorio de pH Tumoral de la Universidad de Duke (Carolina del Norte, EEUU) y miembro de la Facultad de Medicina de la Universidad de Baltimore (EEUU)- y el *Dr. Stephan J. Reshkin* -profesor del Departamento de Fisiología General y Ambiental de la Universidad de Bari (Italia)-.

La carta –extensa y técnica- aparece íntegra en el número de Discovery DSALUD que salió a la venta el pasado viernes 24 de diciembre- y en ella se denuncia que la afirmación de que la palabra “cáncer” engloba en realidad “a más de 200 enfermedades distintas” es una aseveración que “corresponde a una visión obsoleta del cáncer que se opone frontalmente al moderno paradigma surgido en la Oncología hace escasos años”.

“(…) Cabe preguntar tanto al Dr. Barbacid como a quienes con él comparten aún la misma reduccionista y disgregadora cosmovisión oncológica –agrega la carta- qué es lo que en verdad sabe la mayoría de los investigadores en la actualidad sobre la naturaleza íntima y esencial de las enfermedades neoplásicas para sostener que el cáncer son ’200 enfermedades diferentes’. Es regla de oro de la Medicina que sólo llegando a la raíz, a lo que subyace en cualquier problema de salud, se puede acceder a una comprensión racional e interpretación correcta de una patología, paso previo imprescindible para aspirar tanto a prevenirla como a tratarla adecuadamente una vez se haya manifestado.

Sin conocer la causa o causas primarias (etiología), los mecanismos intermediarios (etiopatogenia) y la esencia íntima de una enfermedad (su naturaleza) no se puede siquiera pensar en superarla. Y eso es así muy
especialmente en este caso porque como ya dijo el padre de la bioquímica
del cáncer, Otto Warburg, sólo podremos curar lo que primero podamos entender”.

La Carta Abierta plantea a continuación numerosas preguntas al Dr. Barbacid y a quienes con él comparten su trasnochada visión del cáncer solicitando que las responda públicamente para conocimiento de médicos y medios de comunicación.

” El enfoque y paradigma conceptual asumido hasta hoy está muerto –se afirma en la carta-. Ha sido necesario replantearse todo lo que se cree saber sobre esta patología desde la raíz antes de haber conseguido poder integrar sus muchas caras y ramas dentro del árbol de la ciencia de una unidad superior, el llamado ‘paradigma emergente’”. Y se añade: “¿No se puede -o no se quiere- entender aún que ha llegado ya la hora de que los profesionales de la investigación oncológica de todo el mundo se conciencien de esta realidad y de que deben familiarizarse cuanto antes con las claves de los principales sistemas energéticos del funcionamiento besugo y específico de *todas *las células y tumores malignos?”

Más adelante se afirma: “Tal vez haya llegado la hora -o esté cada vez más cerca- de que los oncólogos básicos y clínicos consigan despertar y decidirse a plantear otras alternativas y, al mismo tiempo, hagan acopio de la necesaria inspiración, generosidad y valor para dejar de “vivir esclavizados y embobados por ese Gran Hermano de la Oncología que constituyen las grandes multinacionales farmacéuticas, entidades de dudosa ética a las que sólo les importan sus intereses económicos y cuyas dinámicas y motivaciones -muchas veces pseudocientíficas- llevan a tratar por todos los medios de comercializar medicaciones cada día más tóxicas, menos efectivas y más caras”.
La carta, que puede leerse íntegra en el número de Discovery DSALUD que se encuentra a la venta en los kioscos, termina diciendo: “En suma, los abajo firmantes postulamos un nuevo paradigma integral, unitario y radical de las enfermedades neoplásicas, por entender que todos los tumores malignos tienen más factores en común que diferencias entre ellos, tal como ha sido consensuado en el reciente I Congreso Internacional de la Sociedad para el Estudio de las Dinámicas de Protones en el Cáncer celebrado a principios de septiembre pasado en Roma (Proton Dynamics in Cancer - Your resource for Proton Dynamics in Cancer, Proton Dynamics, Chemotherapy, Radiotherapy, Antibiotics, Malignant Tumors, Cancer Cure, Cancer News, Cancer Discussions, Cancer Research). Ello “exige abandonar”, también radicalmente, “el actual modelo analítico-reduccionista y desintegrado que insiste en que la palabra cáncer designa a más de 200 enfermedades distintas que han de ser tratadas con infinidad de combinaciones farmacológicas diferentes a pesar de que a día de hoy los quimioterápicos han demostrado ser más tóxicos que eficaces”, exceptuando los tumores germinales y algunas leucemias y linfomas, neoplasias que conforman una muy reducida minoría dentro del conjunto de todos los tumores malignos. Y eso significa que persistir en el camino trillado sólo puede ahondar aún más en el mayoritario fracaso terapéutico de la Oncología Médica actual al mismo tiempo que impedir y detener todo posible avance y verdadero progreso”.

Un saludo.

Minsky Moment · 31 Dic 2010

Detector de magufada al rojo. Esa revista es la mayor patraña del mundo editorial pseudocientífico. ¡Cuidado! El cáncer es una enfermedad muy seria. Que nadie se deje llevar por estas magufadas. Es muy peligroso.

PD: Ni cisma, ni leches. Esto son cuatro ilumináos.

PutinReReloaded · 31 Dic 2010

Minsky Moment dijo:
Detector de magufada al rojo.

El fracaso de la medicina frente al cáncer no es ninguna magufada, es la realidad.

Habrá que ver la categoría de los firmantes antes de calificarlos porque sí.

Minsky Moment dijo:
¡Cuidado! El cáncer es una enfermedad muy seria.

Pues será mejor prevenirla que curarla, no te parece?

Minsky Moment · 31 Dic 2010

pilinguinReReloaded dijo:
Pues será mejor prevenirla que curarla, no te parece?

Mira, pilinguin, no vamos a entrar en una discusión sin fin como aquella del VIH de hace unos meses (¿fue contigo, no?, ya no me acuerdo bien). Es demasiado tarde hoy

. Yo solo digo que lo que se afirma ahí arriba, y en general en esa revista "médica" (ejem), son patrañas sin fundamento. El que se quiera dar por avisado, avisado está. Y hará bien en estarlo, EMHO.

Edito: La categoría de los firmantes no me dice nada. Me basta con los argumentos.

PutinReReloaded · 31 Dic 2010

Minsky Moment dijo:
Yo solo digo que lo que se afirma ahí arriba, y en general en esa revista "médica" (ejem), son patrañas sin fundamento.

Todos tenemos una opinión y un ojo ciego, poco mérito hay en ello.

Sin razonar, tu opinión de que son "patrañas sin fundamento" tampoco tiene ningún fundamento

Minsky Moment dijo:
La categoría de los firmantes no me dice nada. Me basta con los argumentos.

Si tu lo dices habrá que creer que tienes razón :bla:

quevagosoy · 31 Dic 2010

Revista dirigida por José Antonio Campoy, magufo mayor del reino, ex-director de la revista de astrología y "misterios" para catorceañeros llamada "Más allá de la ciencia", en la que, en los tiempos en que él la dirigía... ¡había una sección fija en la que un extraterrestre, de nombre Geenom, respondía a preguntas!.

Tener un conocido tan distinguido le hizo merecedor, a su propio criterio, de llenarse más el bolsillo, e incluso llegó a publicar un libro en el que contaba sus entrevistas con el extraterrestre:

Este "señor" no es más que un timador profesional engañabobos. La credibilidad de su publicación es, aproximadamente, la de los horóscopos.

PutinReReloaded · 31 Dic 2010

Así a primera vista el Dr. Stefano Fais no parece ningún magufo:

Istituto Superiore di Sanità: Stefano Fais*

ya sé que los expañoles lo valéis y tal... :bla: ... pero siempre a remolque del extranjero.

Pubblicazioni

1. Huber V, Fais S, Iero M, Lugini L, Canese P, Squarcina P, Zaccheddu A, Colone M, Arancia G, Gentile M, Seregni E, Valenti R, Ballabio G, Belli F, Leo E, Parmiani G, Rivoltini L. Human colorectal cancer cells induce T-cell death through release of proapoptotic microvesicles: role in immune escape. Gastroenterology 2005;128(7):1796-1804.
2. Fais S, De Milito A, Lozupone F. The role of FAS to ezrin association in FAS-mediated apoptosis. Apoptosis: an international journal on programmed cell death 2005;10(5):941 - 947.
3. Luciani F, Spada M, De Milito A, Molinari A, Rivoltini L, Montinaro A, Marra M, Lugini L, Logozzi M, Lozupone F, Federici C, Iessi E, Parmiani G, Arancia G, Belardelli F, Fais S. Effect of proton pump inhibitor pretreatment on resistance of solid tumors to cytotoxic drugs. Journal of the National cancer institute 2004;96(22):1702-1713.
4. Luciani F, Matarrese P, Giammarioli AM, Lugini L, Lozupone F, Federici C, Iessi E, Malorni V, Fais S. CD95/phosphorylated ezrin association underlies HIV-1 GP120/IL-2 induced susceptibility to CD95(APO-1/Fas)-mediated apoptosis of human resting CD4+T-lymphocytes. Cell death and differentiation 2004;11(5):574-582.
5. Lozupone F, Pende D, Burgio VL, Castelli C, Spada M, Venditti M, Luciani F, Lugini L, Federici C, Ramoni C, Rivoltini L, Parmiani G, Belardelli F, Rivera P, Marcenaro S, Moretta L, Fais S. Effect of human natural killer and gammadelta T cells on the growth of human autologous melanoma xenografts in SCID mice. Cancer research 2004;64(1):378-385.
6. Lozupone F, Lugini L, Matarrese P, Luciani F, Federici C, Iessi E, Margutti P, Stassi G, Malorni V, Fais S. Identification and relevance of the CD95-binding domain in the N-terminal region of Ezrin. Journal of biological chemistry 2004;279(10):9199-9207.
7. Migliaccio G, Testa U, Cometa MF, Fais S, Chistolini P, Bignami M, Agrimi U, Proietti E, Coccia EM. Linee guida sui prodotti per terapia cellulare. Notiziario dell'Istituto Superiore di Sanità 2004;17(07-08):9-14.
8. Lozupone F, Rivoltini L, Luciani F, Venditti M, Lugini L, Cova A, Squarcina P, Parmiani G, Belardelli F, Fais S. Adoptive transfer of an anti-mart1 27-35-specific CD8+ T cell clone leads to immunoselection of human melanoma antigen-loss variants in SCID mice. European journal of immunology 2003;33(2):556-566.
9. Lugini L, Lozupone F, Matarrese P, Funaro C, Luciani F, Malorni V, Rivoltini L, Castelli C, Tinari A, Piris A, Parmiani G, Fais S. Potent phagocytic activity discriminates metastatic and primary human malignant melanomas: a key role of Ezrin. Laboratory investigation 2003;83(11):1555-1567.
10. Fais S, Malorni V. Leukocyte uropod formation and membrane/cytoskeleton linkage in immune interactions. Journal of leukocyte biology 2003;73:556-563.
11. Andreola G, Rivoltini L, Castelli C, Huber V, Perego P, Deho P, Squarcina P, Accornero P, Lozupone F, Lugini L, Stringaro A, Molinari A, Arancia G, Gentile M, Parmiani G, Fais S. Induction of lymphocyte apoptosis by tumor cell secretion of FasL-bearing microvesicles. Journal of experimental medicine 2002;195(10):1303-1316.
12. Luciani F, Molinari A, Lozupone F, Calcabrini A, Lugini L, Stringaro A, Puddu P, Arancia G, Cianfriglia M, Fais S. P-glycoprotein-actin association through ERM family proteins: a role in P-glycoprotein ******** in human cells of lymphoid origin. Blood 2002;99(2):641-648.
13. Rivoltini L, Carrabba M, Huber V, Castelli C, Novellino L, Dalerba P, Mortarini R, Arancia G, Anichini A, Fais S, Parmiani G. Immunity to cancer: attack and escape in T lymphocyte-tumor cell interaction. Immunological reviews 2002;188(1):97-113.
14. Ramoni C, Luciani F, Spadaro F, Lugini L, Lozupone F, Fais S. Differential expression and distribution of ezrin, radixin and moesin in human natural killer cells. European journal of immunology 2002;32(11):3059-3065.
15. Fabbri A, Falzano L, Travaglione S, Stringaro A, Malorni V, Fais S, Fiorentini C. Rho-activating Escherichia coli cytotoxic necrotizing factor 1: macropinocytosis of apoptotic bodies in human epithelial cells. International journal of medical microbiology 2002;291(6-7):551-554.
16. Travaglione S, Falzano L, Fabbri A, Stringaro A, Fais S, Fiorentini C. Epithelial cells and expression of the phagocytic marker CD68: scavenging of apoptotic bodies amowing Rho activation. Toxicology in vitro 2002;16(4):405-411.
17. Santini SM, Lapenta C, Logozzi M, Parlato S, Spada M, Di Pucchio T, Fais S, Belardelli F. Chimeric models of SCID mice transplanted with human cells: the Hu-PBL-SCID mouse and its use in AIDS research. In: Cossarizza A, Kaplan D, ed. Cellular aspects of HIV infection New York: John Wiley & Sons Inc; 2002. p. 385-398.
18. Parlato S, Santini SM, Lapenta C, Di Pucchio T, Logozzi M, Spada M, Giammarioli AM, Malorni V, Fais S, Belardelli F. Expression of CCR-7, MIP-3beta, and Th-1 chemokines in type I IFN-induced monocyte-derived dendritic cells: importance for the rapid acquisition of potent migratory and ********al activities. Blood 2001;98(10):3022-3029.
19. Fiorentini C, Falzano L, Fabbri A, Stringaro A, Logozzi M, Travaglione S, Contamin S, Arancia G, Malorni V, Fais S. Activation of Rho GTPases by cytotoxic necrotizing factor 1 induces macropinocytosis and scavenging activity in epithelial cells. Molecular biology of the cell 2001;12(7):2061-2073.
20. Giammarioli AM, Garofalo T, Sorice M, Misasi R, Gambardella L, Gradini R, Fais S, Pavan A, Malorni V. GD3 glycosphingolipid contributes to Fas-mediated apoptosis via association with ezrin cytoskeletal protein. FEBS letters 2001;506:45-50.
21. Rizza P, Fais S, Pini C, Proietti E, Belardelli F. First international workshop on human/SCID mouse models. Journal of biological regulators and homeostatic agents 2001;15:170-174.
22. Arancia G, Molinari A, Calcabrini A, Stringaro A, Luciani F, Lozupone F, Luigini L, Puddu P, Cianfriglia M, Fais S. P-glycoprotein/actin association through erm family proteins: implication for development of multidrug resistance. In: 5. Multinational Congress on Electron Microscopy. Proceedings; September 20-25, 2001; Lecce. 2001. p. 157-158.
23. Rizza P, Fais S, Pini C, Proietti E, Belardelli F. L'impiego dei modelli animali in campo biomedico: i modelli chimerici uomo-topo. Notiziario dell'Istituto Superiore di Sanità 2001;14(10):11-15.
24. Parlato S, Giammarioli AM, Logozzi M, Lozupone F, Matarrese P, Luciani F, Falchi M, Malorni V, Fais S. CD95 (APO-1/Fas) linkage to the actin cytoskeleton through ezrin in human T lymphocytes: a novel regulatory mechanism of the CD95 apoptotic pathway. EMBO journal 2000;19(19):5123-5134.
25. Parlato S, Santini SM, Lapenta C, Spada M, Logozzi M, Rizza P, Proietti E, Belardelli F, Fais S. Primary HIV-1 infection of human CD4+ T cells passaged into SCID mice leads to selection of chronically infected cells through a massive Fas-mediated autocrine suicide of uninfected cells. Cell death and differentiation 2000;7:37-47.
26. Lozupone F, Luciani F, Venditti M, Rivoltini L, Pupa S, Parmiani G, Belardelli F, Fais S. Murine granulocytes control human tumor growth in scid mice. International journal of cancer 2000;87:569-573.
27. Fais S, Luciani F, Logozzi M, Parlato S, Lozupone F. Linkage between cell membrane proteins and actin-based cytoskeleton: the cytoskeletal-driven cellular ********s. Histology and Histopathology 2000;15:539-549.
28. Fais S. Tecniche immunocitochimiche PAP-APAAP per la identificazione di pathways differenziativi cellulari. In: Molinari A, Arancia G, ed. Le tecniche microscopiche nello studio delle caratteristiche strutturali e funzionali delle cellule in coltura Roma: Centro Stampa De Vittoria; 2000. p. 43-45.
29. Proietti E, Fais S, Belardelli F, ed. 1. International workshop. Human/scid mouse models. Abstract book. Roma: Istituto Superiore di Sanità; 2000. (ISTISAN Congressi ,00/70).
30. Fais S, Lapenta C, Santini SM, Spada M, Parlato S, Logozzi M, Rizza P, Belardelli F. Human immunodeficiency bichito type 1 strains R5 and X4 induce different pathogenic effects in hu-PBL-SCID mice, depending on the state of activation/differentiation of human target cells at the time of primary infection. Journal of virology 1999;73(8):6453-6459.
31. Lapenta C, Boirivant M, Marini L, Santini SM, Logozzi M, Viora M, Belardelli F, Fais S. Human intestinal lamina propria lymphocytes are naturally permissive to HIV-1 infection. European journal of immunology 1999;29:1202-1208 .
32. Lapenta C, Santini SM, Parlato S, Logozzi M, Spada M, Rizza P, Fais S, Proietti E, Belardelli F. The "added value" of using hu-scid mouse models for studies on the pathogenesis, therapy and prophylaxis of HIV-1 infection". In: Centro di coordinamento, organizzazione e verifica dei progetti per la lotta all'AIDS, ed. Second national research program on AIDS. Progress report. Istituto Superiore di Sanità. Rome, July 12-16,1999. Roma: Istituto Superiore di Sanità; 1999. (Rapporti ISTISAN 99/11). p.349.
33. Lapenta C, Santini SM, Proietti E, Rizza P, Logozzi M, Spada M, Parlato S, Fais S, Pitha PM, Belardelli F. Type 1 interferon is a powerful inhibitor of in vivo HIV-1 infection and preserves human CD4+ T cells from bichito-induced depletion in SCID mice transplanted with human cells. Virology 1999;263:78-88.
34. Monini P, Colombini S, Stürzl M, Goletti D, Cafaro A, Sgadari C, Buttò S, Franco M, Leone P, Fais S, Leone P, Melucci-Vigo G, Chiozzini C, Carlini F, Ascherl G, Cornali E, Zietz C, Ramazzotti E, Ensoli F, Andreoni M, Pezzotti P, Rezza G, Yarchoan R, Gallo RC, Ensoli B. Reactivation and persistence of human herpesvirus-8 infection in B cells and monocytes by Th-1 cytokines increased in Kaposi's sarcoma. Blood 1999;93(12):4044-4058.
35. Monini P, Stürzl M, Goletti D, Cafaro A, Sgadari C, Buttò S, Franco M, Leone P, Fais S, Leone P, Melucci-Vigo G, Chiozzini C, Carlini F, Andreoni M, Pezzotti P, Rezza G, Ensoli B. Reactivation and persistence of human herpesvirus-8 infection in B cells and monocytes by TH-1 cytokines increased in Kaposi's sarcoma. In: Centro di coordinamento, organizzazione e verifica dei progetti per la lotta all'AIDS, ed. Second national research program on AIDS. Progress report. Istituto Superiore di Sanità. Rome, July 12-16,1999. Roma: Istituto Superiore di Sanità; 1999. (Rapporti ISTISAN 99/11). p.326.
36. Puddu P, Fais S, Luciani F, Gherardi G, Dupuis ML, Romagnoli G, Ramoni C, Cianfriglia M, Gessani S. Interferon-gamma up-regulates expression and activity of P-glycoprotein in human peripheral blood monocyte-derived macrophages. Laboratory investigation 1999;79(10):1299-1309.
37. Rozera C, Mecchia M, Gresser I, Bandu MT, Proietti E, Venditti M, Sestili P, Santini SM, Fais S, Belardelli F, Ferrantini M. Murine interferon-alfa1 gene transduced ESb tumor cells are rejected by host-metiated mechanisms despite the resistance of the parental tumor to interferon-alfa/beta therapy. Cancer gene therapy 1999;6(3):246-253.
38. Rozera C, Mecchia M, Gresser I, Bandu MT, Proietti E, Venditti M, Sestili P, Santini SM, Fais S, Belardelli F, Ferrantini M. Murine interferon-alpha1 gene-transduced ESb tumor cells are rejected by host-mediated mechanisms despite resistance of the parental tumor to interferon-alpha/beta therapy. Cancer gene therapy 1999;6(3):246-253.
39. Lapenta C, Parlato S, Spada M, Santini SM, Rizza P, Logozzi M, Proietti E, Belardelli F, Fais S. Human lymphoblastoid CD4(+) T cells become permissive to macrophage-tropic strains of human immunodeficiency bichito type 1 after passage into severe combined immunodeficient mice through in vivo upregulation of CCR5: in vivo dynamics of CD4(+) T-cell differentiation in pathogenesis of AIDS. Journal of virology 1998;72(12):10323-10327.
40. Lapenta C, Parlato S, Spada M, Santini SM, Rizza P, Logozzi M, Proietti E, Belardelli F, Fais S. Human lymphoblastoid CD4(+) T cells become permissive to macrophage-tropic strains of human immunodeficiency bichito type 1 after passage into severe combined immunodeficient mice through in vivo upregulation of CCR5: in vivo dynamics of CD4(+) T-cell differentiation in pathogenesis of AIDS. Journal of virology 1998;72(12):10323-10327.
41. Lapenta C, Parlato S, Spada M, Santini SM, Rizza P, Logozzi M, Proietti E, Belardelli F, Fais S. Human lymphoblastoid CD4(+) T cells become permissive to macrophage-tropic strains of human immunodeficiency bichito type 1 after passage into severe combined immunodeficient mice through in vivo upregulation of CCR5: in vivo dynamics of CD4(+) T-cell differentiation in pathogenesis of AIDS. Journal of virology 1998;72(12):10323-10327.
42. Malorni V, Fais S, Fiorentini C. Morphological aspects of apoptosis. In: Boraschi D, Bossù P, Cossarizza A, ed. Apoptosis. A laboratory manual of experimental methods L'Aquila: Graphic Press; 1998. .
43. Santini SM, Spada M, Parlato S, Logozzi M, Lapenta C, Proietti E, Belardelli F, Fais S. Treatment of severe combined immunodeficiency mice with anti-murine granulocyte monoclonal antibody improves human leukocyte xenotransplantation. Transplantation 1998;65(3):416-420.
44. Fais S, Burgio VL, Capobianchi MR, Gessani S, Pallone F, Belardelli F. The biological relevance of polykaryons in the immune response. Immunology today (Reference ed.) 1997;18(11):522-527.
45. Lapenta C, Fais S, Rizza P, Spada M, Logozzi M, Parlato S, Santini SM, Pirillo MF, Belardelli F, Proietti E. U937-SCID mouse xenografts: a new model for acute in vivo HIV-1 infection suitable to test antiviral strategies. Anticancer research 1997;36(2):81-90.
46. Monini P, Goletti D, Cafaro A, Sgadari C, Stürzl M, Buttò S, Franco M, Leone P, Fais S, Leone P, Ensoli F, Fiorelli V, Sirianni MC, Ensoli B. In vivo presence and in vitro transmission of human herpesvirus-8 (HHV-8) infection B cells, T cells, and monocytes-macrophages: viral activation by inflammatory cytokines (IC). Roma: Istituto Superiore di Sanità; 1997. (Rapporti ISTISAN ,97/30). p.27.
47. Fais S, Borghi P, Gherardi G, Logozzi M, Belardelli F, Gessani S. Human immunodeficiency bichito type 1 induces cellular polarization, intercellular adhesion molecule-1 redistribution, and multinucleated giant cell generation in human primary monocytes but not in monocyte-derived macrophages. Laboratory investigation 1996;75(6):783-790.
48. Rizza P, Santini SM, Logozzi M, Lapenta C, Sestili P, Gherardi G, Lande R, Spada M, Parlato S, Belardelli F, Fais S. T-cell dys********s in hu-PBL-SCID mice infected with human immunodeficiency bichito (HIV) shortly after reconstitution: in vivo effects of HIV on highly activated human immune cells. Journal of virology 1996;70(11):7958-7964.
49. Fais S, Pallone F. Inability of normal human intestinal macrophages to form multinucleated giant cells in response to cytokines. Gut 1995;37(6):798-801.
50. Santini SM, Rizza P, Logozzi M, Sestili P, Gherardi G, Lande R, Lapenta C, Belardelli F, Fais S. The scid mouse reaction to human peripheral blood mononuclear leukocyte engraftment. Transplantation 1995;60(11):1306-1314.
51. Fais S, Maiuri L, Pallone F, De Vincenzi M, De Ritis G, Troncone R, Auricchio S. Gliadin induced changes in the expression of MHC-class II antigens by human small intestinal epithelium. Organ culture studies with coeliac disease mucosa. Gut 1992;33:472-475.

stiff upper lip · 31 Dic 2010

Pues la siguiente de la lista Miriam L. Wahl tampoco se queda corta:

No veo ningún artículo sobre la orgonita en sus publicaciones...

1. Abnormal acidification of melanoma cells induces tyrosinase retention in the early secretory pathway
Ruth Halaban
Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
J Biol Chem 277:14821-8
2. The H+-linked monocarboxylate transporter (MCT1/SLC16A1): a potential therapeutic target for high-risk neuroblastoma
Jun Fang
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
Mol Pharmacol 70:2108-15
3. Angiostatin and anti-angiogenic therapy in human disease
Miriam L Wahl
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
Recent Prog Horm Res 59:73-104
4. Intracellular acidification abrogates the heat shock response and compromises survival of human melanoma cells
Ronald A Coss
Department of Radiation Oncology, and the Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
Mol Cancer Ther 2:383-8
5. Tumor oxygenation and acidification are increased in melanoma xenografts after exposure to hyperglycemia and meta-iodo-benzylguanidine
Randy Burd
Department of Radiation Oncology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
Radiat Res 159:328-35
6. Regulation of intracellular pH in human melanoma: potential therapeutic implications
Miriam L Wahl
Department of Biochemistry and Molecular Pharmacology, Haverford College, Haverford, Pennsylvania 19041, USA
Mol Cancer Ther 1:617-28
7. Angiostatin induces intracellular acidosis and anoikis in endothelial cells at a tumor-like low pH
Miriam L Wahl
Department of Biochemistry and Molecular Pharmacology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
Endothelium 9:205-16
8. The mechanism of action of angiostatin: can you teach an old dog new tricks?
Tammy L Moser
Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
Thromb Haemost 87:394-401
9. Effects of microenvironmental extracellular pH and extracellular matrix proteins on angiostatin's activity and on intracellular pH
M L Wahl
Department of Biochemistry and Molecular Pharmacology, Thomas Jefferson University, 233 South, 10th Street, Room 226, Philadelphia, PA 19107, USA
Gen Pharmacol 35:277-85
10. An Inhibitor of the F1 subunit of ATP synthase (IF1) modulates the activity of angiostatin on the endothelial cell surface
Nick R Burwick
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
J Biol Chem 280:1740-5

Collaborators

* Somnath Mukhopadhyay
* Jun Fang
* Ulrich Rodeck
* John M Maris
* Qun Wang
* Randy Burd
* John E Biaglow
* R A Coss
* David Berd
* Ruth Halaban
* Mark W Dewhirst
* Mario Gonzalez-Gronow
* David J Adams
* Phyllis R Wachsberger
* Daniel J Kenan
* Salvatore V Pizzo
* Tammy L Moser
* Sulene L Chi
* Roderick A Capaldi
* Nick R Burwick
* Barbara D Lipes
* Yvonne M Mowery
* Susana C Hilderbrand
* Michael F Marusich
* Siqing Shan
* Carrie E Johnson
* Zhaoxi Zhong
* Bo Li
* M Sharon Stack

Detail Information
Publications14

1. Abnormal acidification of melanoma cells induces tyrosinase retention in the early secretory pathway
Ruth Halaban
Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
J Biol Chem 277:14821-8
....
2. The H+-linked monocarboxylate transporter (MCT1/SLC16A1): a potential therapeutic target for high-risk neuroblastoma
Jun Fang
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
Mol Pharmacol 70:2108-15
..Such treatment would have selectivity by virtue of the acidic milieu surrounding tumors, because MCT is increasingly active as extracellular pH decreases below 7.0 and lactic acid production increases...
3. Angiostatin and anti-angiogenic therapy in human disease
Miriam L Wahl
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
Recent Prog Horm Res 59:73-104
....
4. Intracellular acidification abrogates the heat shock response and compromises survival of human melanoma cells
Ronald A Coss
Department of Radiation Oncology, and the Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
Mol Cancer Ther 2:383-8
..This strategy could result in a therapeutic gain, because normal tissues, existing at a pHe above 7.0, would not be sensitized...
5. Tumor oxygenation and acidification are increased in melanoma xenografts after exposure to hyperglycemia and meta-iodo-benzylguanidine
Randy Burd
Department of Radiation Oncology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
Radiat Res 159:328-35
..Hyperglycemia plus MIBG has the potential to improve response to radiation therapy as well as to hyperthermia and some chemotherapies...
6. Regulation of intracellular pH in human melanoma: potential therapeutic implications
Miriam L Wahl
Department of Biochemistry and Molecular Pharmacology, Haverford College, Haverford, Pennsylvania 19041, USA
Mol Cancer Ther 1:617-28
..In most tissues, it is proposed that the NHE-1 could compensate for an inhibited MCT to prevent acidification, but in melanoma cells this did not occur. Therefore, MCT inhibitors may be particularly effective against malignant melanoma...
7. Angiostatin induces intracellular acidosis and anoikis in endothelial cells at a tumor-like low pH
Miriam L Wahl
Department of Biochemistry and Molecular Pharmacology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
Endothelium 9:205-16
..The results also implicate roles for both pH(e) and pH(i) regulation in the mechanism of angiostatin action...
8. The mechanism of action of angiostatin: can you teach an old dog new tricks?
Tammy L Moser
Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
Thromb Haemost 87:394-401
..This review will describe what is known about the mechanism of action of angiostatin from the current literature...
9. Effects of microenvironmental extracellular pH and extracellular matrix proteins on angiostatin's activity and on intracellular pH
M L Wahl
Department of Biochemistry and Molecular Pharmacology, Thomas Jefferson University, 233 South, 10th Street, Room 226, Philadelphia, PA 19107, USA
Gen Pharmacol 35:277-85
..These data indicate that substrate and pH(e) are critical parameters in the evaluation of this antiangiogenic substance, and probably for others as well...
10. An Inhibitor of the F1 subunit of ATP synthase (IF1) modulates the activity of angiostatin on the endothelial cell surface
Nick R Burwick
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
J Biol Chem 280:1740-5
..These data suggest that there is a relationship between the binding sites of IF1 and angiostatin on ATP synthase and that IF1 could be employed to modulate angiogenesis...
11. Camptothecin analogs with enhanced activity against human breast cancer cells. II. Impact of the tumor pH gradient
David J Adams
Department of Medicine, Duke University Medical Center, 2638 Research Drive, Durham, NC 27710, USA
Cancer Chemother Pharmacol 57:145-54
..While several substitutions at the 7 and 10 positions enhance potency, 7-halomethyl and 10-amino CPT analogs show selective activity at the acidic pH common to the microenvironment of most solid tumors...
12. Angiostatin's molecular mechanism: aspects of specificity and regulation elucidated
Miriam L Wahl
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
J Cell Biochem 96:242-61
....
13. Ectopic localization of mitochondrial ATP synthase: a target for anti-angiogenesis intervention?
Daniel J Kenan
Department of Pathology, DUMC 3712, Duke University Medical Center, Durham, North Carolina 27710, USA
J Bioenerg Biomembr 37:461-5
..In order to explore the mechanism of action of angiostatin and its mimetics, further work needs to be done to evaluate clinical applicability, specificity, and contraindications for this class of therapeutics...
14. Angiostatin-like activity of a monoclonal antibody to the catalytic subunit of F1F0 ATP synthase
Sulene L Chi
Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
Cancer Res 67:4716-24
..Thus, MAb3D5AB1 shows angiostatin-like properties superior to angiostatin and may be exploited in cancer chemotherapy...

Aquí lo que hay es mucha mente estrecha, mucho lavado de cerebro y las habichuelas de por medio.

Mitrofán 2 · 31 Dic 2010

Lo que yo entiendo en el articulo es que hay unos señores que despues de muchos años en la investigacion delm cancer,ven que no se llega a ningun resultado y piensan que seria bueno abrir otras vias de investigacion(con su puyita a las farmaceuticas)

Tambien veo al triplemente galardonado con el nobel de medicina,quimica y punto de cruz,Sr. Minsy moment rebatiendo inteligentemente esa postura:
"Yo solo digo que lo que se afirma ahí arriba,son patrañas sin fundamento. "

Y al vago de turno en su linea:
"Este "señor" no es más que un timador profesional engañabobos. La credibilidad de su publicación es, aproximadamente, la de los horóscopos."

Esa publicacion se limita a publicar una carta abierta que posiblemente sea censurada en los medios afines al sistema.

melesigeni · 31 Dic 2010

Muchas revistas de salud publican publicidad de las empresas responsables de los productos comentados en sus artículos, es una lacra de la que empezamos a desembarazarnos. En DSalud se publicitan también -además de los productos- las personas, remedios y técnicas (nada barato todo ello, por cierto) que aparecen en sus artículos, tan faltos ellos de estadíticas significativas, muy "científico" todo ello: el negocio de la alternativa sin base contra el negocio de la oficial sin freno, pues vamos arreglados

Harold Alexander · 31 Dic 2010

"Se limita a publicar" una carta que vende como una crítica a la malvada "ciencia oficial" a la que constantemente desacredita en pro de los absurdos productos y terapias que aparecen en su revista, carente del mínimo rigor científico; leyendo la carta, se ve que es una disputa acerca de la metodología de investigación, diagnosis y tratamiento del cáncer, no una crítica la "medicina oficial".

Por usar un símil, es como si unos defensores del diésel publican una carta contra el uso de gasolina, y yo la uso como argumento a mi favor en una revista anti-coches.

annamaria · 31 Dic 2010

¿Esos curriculos tan extensos, esas publicaciones les dejará tiempo para investigar y trabajar?
Por ahí leo que únicamente dos o tres tipos de cancer son curados, germina, linfoma y otro más.

Los grandes descubrimientos son casi anónimos y siempre hay jefe supremo que se lo come en su beneficio.

Solo conozco de cerca un tipo de cancer, el germinal, de fácil curación si se alcanza a tiempo. Si no, es mortal de necesidad lo que me lleva a pensar que a los posibles pacientes salvables en un primer estadio no se les informa y no sé las razones.

El cancer de mama y sus cuantiosas campañas ha reducido su mortalidad....
Creo que las farmaceuticas son las que hacen subir y bajar. Las que por intereses propios pagan o no hasta esas cartas abiertas.
No sé a qué se refiere la carta cuando dice que los tratamientos quimio no dan resultado.
Hoy por hoy cada paciente obtendrá una determinada medicación ajustada a su situación. Y son los oncólogos de a pie los que se curran la curación y la fin también. Desde el laboratorio no sé yo.
He presenciado luchas entre médicos de un mismo servicio, unos tirando pedruscos a otro que sí había logrado sacar al paciente de una fin a plazo corto, si entre ellos ya se manifiestan esos ' desencuentros' mucho nos queda por ver en las revistas especializadas.
El cancer, además de enfermedad incurable en muchas ocasiones, es un gran negocio y veremos peleas entre unos y otros para obtener la mayor porción del pastel.

Un tratamiento de quimio de 6 días está valorado en 6000€/día. Si añadimos el resto de gasto hospitalario o los enfermos acuden a esos sacta sanctorum que tanta fama tienen curando lo mismo que cura un hospital normal; el negocio prima sobre la salud. Como información: los protocolos que maneja Houston es idéntico al protocolo usado en el hospital Valle Hebron.

Gran Shurmano · 31 Dic 2010

annamaria;3692883 Solo conozco de cerca un tipo de cancer dijo:
Me lo explique.

Para un profesional y un Hospital es mucho menos gravoso , no solo en dinero, sino en tiempo, personal, recursos, esfuerzos... un paciente diagnosticado y tratado en las fases iniciales de la enfermedad que uno con un cáncer avanzado. Pensar lo contrario me demuestra su catadura jovenlandesal.

El problema del cáncer germinal ( SEMINOMA ) es que cuando un tío nota un bulto en el testículo no solemos ser muy propensos a acudir al médico a que nos toqueteen la bolsa escrotal, o nos creemos que tenemos una hernia, un varicocele o un hidrocele. Y cuando acudimos ya se encuentra diseminado a los ganglios retroperitoneales o con metástasis pulmonares.
Por eso el diagnóstico se realiza mucho más tardíamente que por ejemplo en el cáncer de mama, del que las mujeres están mucho más concienciadas.

Asi que va a ser que la culpa no es del médico...

Gran Shurmano · 31 Dic 2010

De todas formas, habeis caido como pardillos con los firmantes de esta carta.
Lo que proponen en esta carta es que el pastel de los tratamientos anticáncer se reparta con las compañias farmacéuticas para las que eloos trabajan. Y que mejor manera que desprestigiar a tratamientos ya instaurados y demostradamente eficaces en muchas ocasiones:

Salvador Harguindey :
Director del Institute for Clinical Biology and Metabolism
Senior Research Associate, Biotechnology Institute “I mas D” :
Salvador Harguindey: Curriculum Vitae (abridged) Salvador Harguindey MD., Ph D.

Mimi Wahl :
trabaja como consultora para Cytorex y colabora en el
Institute for Clinical Biology and Metabolism
Mimi Wahl - LinkedIn

Stefano Fais :
Director de la Sección de Medicamentos Antitumorales del Departamento de Investigación Terapéutica y Evaluación de Medicinas del Instituto Nacional de la Salud de Roma (Italia)
Y seguramente no tendrá financiación de Farmacéuticas, no...
Está desarrollando un nuevo fármaco antiacido para el tratamiento de determinados tumores.

De todas dformas, si se entra en el articulo original de la fundacion del ISPDC , encontramos esto:

"The main goals of this International Symposium were:
a) To lead towards a unified and integrated understanding of the main role of H+ dynamics in modern cancer research;
b) To discuss the more recent scientific data of intra and extracellular pH abnormalities in the onset of cancer as well as in its local and metastatic progression, focusing mainly on the molecular mechanisms driving the alterations of pH in various tumor types and tissues;
c) To shed light on new potential targets for inducing selective apoptosis and other therapeutic interventions in malignant tumors and leukemias resistant to traditional treatments.

Proton dynamics in cancer

O sea, lo que proponen es coordinar a los grupos de estudio a nivel mundial de nuevos tratamientos anticancerosos para los tumores que son resistentes a los tratamientos tradicionales.
No se donde está aqui el cisma en la Oncología.

Porque no se si sabeis que se investiga y mucho sobre el cáncer, siguiendo líneas muy diferentes a la quimioterapia y la radioterapia. Se investiga sobre inmunoterapia, hormonoterapia, inibidores de los VGEF, etc... Y eso no significa que haya un cisma.

inmi_soy · 31 Dic 2010

pilinguinReReloaded dijo:
Así a primera vista el Dr. Stefano Fais no parece ningún magufo:

Istituto Superiore di Sanità: Stefano Fais*

ya sé que los expañoles lo valéis y tal... :bla: ... pero siempre a remolque del extranjero.

Pubblicazioni

1. Huber V, Fais S, Iero M, Lugini L, Canese P, Squarcina P, Zaccheddu A, Colone M, Arancia G, Gentile M, Seregni E, Valenti R, Ballabio G, Belli F, Leo E, Parmiani G, Rivoltini L. Human colorectal cancer cells induce T-cell death through release of proapoptotic microvesicles: role in immune escape. Gastroenterology 2005;128(7):1796-1804.
2. Fais S, De Milito A, Lozupone F. The role of FAS to ezrin association in FAS-mediated apoptosis. Apoptosis: an international journal on programmed cell death 2005;10(5):941 - 947.
3. Luciani F, Spada M, De Milito A, Molinari A, Rivoltini L, Montinaro A, Marra M, Lugini L, Logozzi M, Lozupone F, Federici C, Iessi E, Parmiani G, Arancia G, Belardelli F, Fais S. Effect of proton pump inhibitor pretreatment on resistance of solid tumors to cytotoxic drugs. Journal of the National cancer institute 2004;96(22):1702-1713.
4. Luciani F, Matarrese P, Giammarioli AM, Lugini L, Lozupone F, Federici C, Iessi E, Malorni V, Fais S. CD95/phosphorylated ezrin association underlies HIV-1 GP120/IL-2 induced susceptibility to CD95(APO-1/Fas)-mediated apoptosis of human resting CD4+T-lymphocytes. Cell death and differentiation 2004;11(5):574-582.
5. Lozupone F, Pende D, Burgio VL, Castelli C, Spada M, Venditti M, Luciani F, Lugini L, Federici C, Ramoni C, Rivoltini L, Parmiani G, Belardelli F, Rivera P, Marcenaro S, Moretta L, Fais S. Effect of human natural killer and gammadelta T cells on the growth of human autologous melanoma xenografts in SCID mice. Cancer research 2004;64(1):378-385.
6. Lozupone F, Lugini L, Matarrese P, Luciani F, Federici C, Iessi E, Margutti P, Stassi G, Malorni V, Fais S. Identification and relevance of the CD95-binding domain in the N-terminal region of Ezrin. Journal of biological chemistry 2004;279(10):9199-9207.
7. Migliaccio G, Testa U, Cometa MF, Fais S, Chistolini P, Bignami M, Agrimi U, Proietti E, Coccia EM. Linee guida sui prodotti per terapia cellulare. Notiziario dell'Istituto Superiore di Sanità 2004;17(07-08):9-14.
8. Lozupone F, Rivoltini L, Luciani F, Venditti M, Lugini L, Cova A, Squarcina P, Parmiani G, Belardelli F, Fais S. Adoptive transfer of an anti-mart1 27-35-specific CD8+ T cell clone leads to immunoselection of human melanoma antigen-loss variants in SCID mice. European journal of immunology 2003;33(2):556-566.
9. Lugini L, Lozupone F, Matarrese P, Funaro C, Luciani F, Malorni V, Rivoltini L, Castelli C, Tinari A, Piris A, Parmiani G, Fais S. Potent phagocytic activity discriminates metastatic and primary human malignant melanomas: a key role of Ezrin. Laboratory investigation 2003;83(11):1555-1567.
10. Fais S, Malorni V. Leukocyte uropod formation and membrane/cytoskeleton linkage in immune interactions. Journal of leukocyte biology 2003;73:556-563.
11. Andreola G, Rivoltini L, Castelli C, Huber V, Perego P, Deho P, Squarcina P, Accornero P, Lozupone F, Lugini L, Stringaro A, Molinari A, Arancia G, Gentile M, Parmiani G, Fais S. Induction of lymphocyte apoptosis by tumor cell secretion of FasL-bearing microvesicles. Journal of experimental medicine 2002;195(10):1303-1316.
12. Luciani F, Molinari A, Lozupone F, Calcabrini A, Lugini L, Stringaro A, Puddu P, Arancia G, Cianfriglia M, Fais S. P-glycoprotein-actin association through ERM family proteins: a role in P-glycoprotein ******** in human cells of lymphoid origin. Blood 2002;99(2):641-648.
13. Rivoltini L, Carrabba M, Huber V, Castelli C, Novellino L, Dalerba P, Mortarini R, Arancia G, Anichini A, Fais S, Parmiani G. Immunity to cancer: attack and escape in T lymphocyte-tumor cell interaction. Immunological reviews 2002;188(1):97-113.
14. Ramoni C, Luciani F, Spadaro F, Lugini L, Lozupone F, Fais S. Differential expression and distribution of ezrin, radixin and moesin in human natural killer cells. European journal of immunology 2002;32(11):3059-3065.
15. Fabbri A, Falzano L, Travaglione S, Stringaro A, Malorni V, Fais S, Fiorentini C. Rho-activating Escherichia coli cytotoxic necrotizing factor 1: macropinocytosis of apoptotic bodies in human epithelial cells. International journal of medical microbiology 2002;291(6-7):551-554.
16. Travaglione S, Falzano L, Fabbri A, Stringaro A, Fais S, Fiorentini C. Epithelial cells and expression of the phagocytic marker CD68: scavenging of apoptotic bodies amowing Rho activation. Toxicology in vitro 2002;16(4):405-411.
17. Santini SM, Lapenta C, Logozzi M, Parlato S, Spada M, Di Pucchio T, Fais S, Belardelli F. Chimeric models of SCID mice transplanted with human cells: the Hu-PBL-SCID mouse and its use in AIDS research. In: Cossarizza A, Kaplan D, ed. Cellular aspects of HIV infection New York: John Wiley & Sons Inc; 2002. p. 385-398.
18. Parlato S, Santini SM, Lapenta C, Di Pucchio T, Logozzi M, Spada M, Giammarioli AM, Malorni V, Fais S, Belardelli F. Expression of CCR-7, MIP-3beta, and Th-1 chemokines in type I IFN-induced monocyte-derived dendritic cells: importance for the rapid acquisition of potent migratory and ********al activities. Blood 2001;98(10):3022-3029.
19. Fiorentini C, Falzano L, Fabbri A, Stringaro A, Logozzi M, Travaglione S, Contamin S, Arancia G, Malorni V, Fais S. Activation of Rho GTPases by cytotoxic necrotizing factor 1 induces macropinocytosis and scavenging activity in epithelial cells. Molecular biology of the cell 2001;12(7):2061-2073.
20. Giammarioli AM, Garofalo T, Sorice M, Misasi R, Gambardella L, Gradini R, Fais S, Pavan A, Malorni V. GD3 glycosphingolipid contributes to Fas-mediated apoptosis via association with ezrin cytoskeletal protein. FEBS letters 2001;506:45-50.
21. Rizza P, Fais S, Pini C, Proietti E, Belardelli F. First international workshop on human/SCID mouse models. Journal of biological regulators and homeostatic agents 2001;15:170-174.
22. Arancia G, Molinari A, Calcabrini A, Stringaro A, Luciani F, Lozupone F, Luigini L, Puddu P, Cianfriglia M, Fais S. P-glycoprotein/actin association through erm family proteins: implication for development of multidrug resistance. In: 5. Multinational Congress on Electron Microscopy. Proceedings; September 20-25, 2001; Lecce. 2001. p. 157-158.
23. Rizza P, Fais S, Pini C, Proietti E, Belardelli F. L'impiego dei modelli animali in campo biomedico: i modelli chimerici uomo-topo. Notiziario dell'Istituto Superiore di Sanità 2001;14(10):11-15.
24. Parlato S, Giammarioli AM, Logozzi M, Lozupone F, Matarrese P, Luciani F, Falchi M, Malorni V, Fais S. CD95 (APO-1/Fas) linkage to the actin cytoskeleton through ezrin in human T lymphocytes: a novel regulatory mechanism of the CD95 apoptotic pathway. EMBO journal 2000;19(19):5123-5134.
25. Parlato S, Santini SM, Lapenta C, Spada M, Logozzi M, Rizza P, Proietti E, Belardelli F, Fais S. Primary HIV-1 infection of human CD4+ T cells passaged into SCID mice leads to selection of chronically infected cells through a massive Fas-mediated autocrine suicide of uninfected cells. Cell death and differentiation 2000;7:37-47.
26. Lozupone F, Luciani F, Venditti M, Rivoltini L, Pupa S, Parmiani G, Belardelli F, Fais S. Murine granulocytes control human tumor growth in scid mice. International journal of cancer 2000;87:569-573.
27. Fais S, Luciani F, Logozzi M, Parlato S, Lozupone F. Linkage between cell membrane proteins and actin-based cytoskeleton: the cytoskeletal-driven cellular ********s. Histology and Histopathology 2000;15:539-549.
28. Fais S. Tecniche immunocitochimiche PAP-APAAP per la identificazione di pathways differenziativi cellulari. In: Molinari A, Arancia G, ed. Le tecniche microscopiche nello studio delle caratteristiche strutturali e funzionali delle cellule in coltura Roma: Centro Stampa De Vittoria; 2000. p. 43-45.
29. Proietti E, Fais S, Belardelli F, ed. 1. International workshop. Human/scid mouse models. Abstract book. Roma: Istituto Superiore di Sanità; 2000. (ISTISAN Congressi ,00/70).
30. Fais S, Lapenta C, Santini SM, Spada M, Parlato S, Logozzi M, Rizza P, Belardelli F. Human immunodeficiency bichito type 1 strains R5 and X4 induce different pathogenic effects in hu-PBL-SCID mice, depending on the state of activation/differentiation of human target cells at the time of primary infection. Journal of virology 1999;73(8):6453-6459.
31. Lapenta C, Boirivant M, Marini L, Santini SM, Logozzi M, Viora M, Belardelli F, Fais S. Human intestinal lamina propria lymphocytes are naturally permissive to HIV-1 infection. European journal of immunology 1999;29:1202-1208 .
32. Lapenta C, Santini SM, Parlato S, Logozzi M, Spada M, Rizza P, Fais S, Proietti E, Belardelli F. The "added value" of using hu-scid mouse models for studies on the pathogenesis, therapy and prophylaxis of HIV-1 infection". In: Centro di coordinamento, organizzazione e verifica dei progetti per la lotta all'AIDS, ed. Second national research program on AIDS. Progress report. Istituto Superiore di Sanità. Rome, July 12-16,1999. Roma: Istituto Superiore di Sanità; 1999. (Rapporti ISTISAN 99/11). p.349.
33. Lapenta C, Santini SM, Proietti E, Rizza P, Logozzi M, Spada M, Parlato S, Fais S, Pitha PM, Belardelli F. Type 1 interferon is a powerful inhibitor of in vivo HIV-1 infection and preserves human CD4+ T cells from bichito-induced depletion in SCID mice transplanted with human cells. Virology 1999;263:78-88.
34. Monini P, Colombini S, Stürzl M, Goletti D, Cafaro A, Sgadari C, Buttò S, Franco M, Leone P, Fais S, Leone P, Melucci-Vigo G, Chiozzini C, Carlini F, Ascherl G, Cornali E, Zietz C, Ramazzotti E, Ensoli F, Andreoni M, Pezzotti P, Rezza G, Yarchoan R, Gallo RC, Ensoli B. Reactivation and persistence of human herpesvirus-8 infection in B cells and monocytes by Th-1 cytokines increased in Kaposi's sarcoma. Blood 1999;93(12):4044-4058.
35. Monini P, Stürzl M, Goletti D, Cafaro A, Sgadari C, Buttò S, Franco M, Leone P, Fais S, Leone P, Melucci-Vigo G, Chiozzini C, Carlini F, Andreoni M, Pezzotti P, Rezza G, Ensoli B. Reactivation and persistence of human herpesvirus-8 infection in B cells and monocytes by TH-1 cytokines increased in Kaposi's sarcoma. In: Centro di coordinamento, organizzazione e verifica dei progetti per la lotta all'AIDS, ed. Second national research program on AIDS. Progress report. Istituto Superiore di Sanità. Rome, July 12-16,1999. Roma: Istituto Superiore di Sanità; 1999. (Rapporti ISTISAN 99/11). p.326.
36. Puddu P, Fais S, Luciani F, Gherardi G, Dupuis ML, Romagnoli G, Ramoni C, Cianfriglia M, Gessani S. Interferon-gamma up-regulates expression and activity of P-glycoprotein in human peripheral blood monocyte-derived macrophages. Laboratory investigation 1999;79(10):1299-1309.
37. Rozera C, Mecchia M, Gresser I, Bandu MT, Proietti E, Venditti M, Sestili P, Santini SM, Fais S, Belardelli F, Ferrantini M. Murine interferon-alfa1 gene transduced ESb tumor cells are rejected by host-metiated mechanisms despite the resistance of the parental tumor to interferon-alfa/beta therapy. Cancer gene therapy 1999;6(3):246-253.
38. Rozera C, Mecchia M, Gresser I, Bandu MT, Proietti E, Venditti M, Sestili P, Santini SM, Fais S, Belardelli F, Ferrantini M. Murine interferon-alpha1 gene-transduced ESb tumor cells are rejected by host-mediated mechanisms despite resistance of the parental tumor to interferon-alpha/beta therapy. Cancer gene therapy 1999;6(3):246-253.
39. Lapenta C, Parlato S, Spada M, Santini SM, Rizza P, Logozzi M, Proietti E, Belardelli F, Fais S. Human lymphoblastoid CD4(+) T cells become permissive to macrophage-tropic strains of human immunodeficiency bichito type 1 after passage into severe combined immunodeficient mice through in vivo upregulation of CCR5: in vivo dynamics of CD4(+) T-cell differentiation in pathogenesis of AIDS. Journal of virology 1998;72(12):10323-10327.
40. Lapenta C, Parlato S, Spada M, Santini SM, Rizza P, Logozzi M, Proietti E, Belardelli F, Fais S. Human lymphoblastoid CD4(+) T cells become permissive to macrophage-tropic strains of human immunodeficiency bichito type 1 after passage into severe combined immunodeficient mice through in vivo upregulation of CCR5: in vivo dynamics of CD4(+) T-cell differentiation in pathogenesis of AIDS. Journal of virology 1998;72(12):10323-10327.
41. Lapenta C, Parlato S, Spada M, Santini SM, Rizza P, Logozzi M, Proietti E, Belardelli F, Fais S. Human lymphoblastoid CD4(+) T cells become permissive to macrophage-tropic strains of human immunodeficiency bichito type 1 after passage into severe combined immunodeficient mice through in vivo upregulation of CCR5: in vivo dynamics of CD4(+) T-cell differentiation in pathogenesis of AIDS. Journal of virology 1998;72(12):10323-10327.
42. Malorni V, Fais S, Fiorentini C. Morphological aspects of apoptosis. In: Boraschi D, Bossù P, Cossarizza A, ed. Apoptosis. A laboratory manual of experimental methods L'Aquila: Graphic Press; 1998. .
43. Santini SM, Spada M, Parlato S, Logozzi M, Lapenta C, Proietti E, Belardelli F, Fais S. Treatment of severe combined immunodeficiency mice with anti-murine granulocyte monoclonal antibody improves human leukocyte xenotransplantation. Transplantation 1998;65(3):416-420.
44. Fais S, Burgio VL, Capobianchi MR, Gessani S, Pallone F, Belardelli F. The biological relevance of polykaryons in the immune response. Immunology today (Reference ed.) 1997;18(11):522-527.
45. Lapenta C, Fais S, Rizza P, Spada M, Logozzi M, Parlato S, Santini SM, Pirillo MF, Belardelli F, Proietti E. U937-SCID mouse xenografts: a new model for acute in vivo HIV-1 infection suitable to test antiviral strategies. Anticancer research 1997;36(2):81-90.
46. Monini P, Goletti D, Cafaro A, Sgadari C, Stürzl M, Buttò S, Franco M, Leone P, Fais S, Leone P, Ensoli F, Fiorelli V, Sirianni MC, Ensoli B. In vivo presence and in vitro transmission of human herpesvirus-8 (HHV-8) infection B cells, T cells, and monocytes-macrophages: viral activation by inflammatory cytokines (IC). Roma: Istituto Superiore di Sanità; 1997. (Rapporti ISTISAN ,97/30). p.27.
47. Fais S, Borghi P, Gherardi G, Logozzi M, Belardelli F, Gessani S. Human immunodeficiency bichito type 1 induces cellular polarization, intercellular adhesion molecule-1 redistribution, and multinucleated giant cell generation in human primary monocytes but not in monocyte-derived macrophages. Laboratory investigation 1996;75(6):783-790.
48. Rizza P, Santini SM, Logozzi M, Lapenta C, Sestili P, Gherardi G, Lande R, Spada M, Parlato S, Belardelli F, Fais S. T-cell dys********s in hu-PBL-SCID mice infected with human immunodeficiency bichito (HIV) shortly after reconstitution: in vivo effects of HIV on highly activated human immune cells. Journal of virology 1996;70(11):7958-7964.
49. Fais S, Pallone F. Inability of normal human intestinal macrophages to form multinucleated giant cells in response to cytokines. Gut 1995;37(6):798-801.
50. Santini SM, Rizza P, Logozzi M, Sestili P, Gherardi G, Lande R, Lapenta C, Belardelli F, Fais S. The scid mouse reaction to human peripheral blood mononuclear leukocyte engraftment. Transplantation 1995;60(11):1306-1314.
51. Fais S, Maiuri L, Pallone F, De Vincenzi M, De Ritis G, Troncone R, Auricchio S. Gliadin induced changes in the expression of MHC-class II antigens by human small intestinal epithelium. Organ culture studies with coeliac disease mucosa. Gut 1992;33:472-475.

stiff upper lip dijo:
Pues la siguiente de la lista Miriam L. Wahl tampoco se queda corta:

No veo ningún artículo sobre la orgonita en sus publicaciones...

1. Abnormal acidification of melanoma cells induces tyrosinase retention in the early secretory pathway
Ruth Halaban
Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
J Biol Chem 277:14821-8
2. The H+-linked monocarboxylate transporter (MCT1/SLC16A1): a potential therapeutic target for high-risk neuroblastoma
Jun Fang
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
Mol Pharmacol 70:2108-15
3. Angiostatin and anti-angiogenic therapy in human disease
Miriam L Wahl
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
Recent Prog Horm Res 59:73-104
4. Intracellular acidification abrogates the heat shock response and compromises survival of human melanoma cells
Ronald A Coss
Department of Radiation Oncology, and the Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
Mol Cancer Ther 2:383-8
5. Tumor oxygenation and acidification are increased in melanoma xenografts after exposure to hyperglycemia and meta-iodo-benzylguanidine
Randy Burd
Department of Radiation Oncology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
Radiat Res 159:328-35
6. Regulation of intracellular pH in human melanoma: potential therapeutic implications
Miriam L Wahl
Department of Biochemistry and Molecular Pharmacology, Haverford College, Haverford, Pennsylvania 19041, USA
Mol Cancer Ther 1:617-28
7. Angiostatin induces intracellular acidosis and anoikis in endothelial cells at a tumor-like low pH
Miriam L Wahl
Department of Biochemistry and Molecular Pharmacology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
Endothelium 9:205-16
8. The mechanism of action of angiostatin: can you teach an old dog new tricks?
Tammy L Moser
Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
Thromb Haemost 87:394-401
9. Effects of microenvironmental extracellular pH and extracellular matrix proteins on angiostatin's activity and on intracellular pH
M L Wahl
Department of Biochemistry and Molecular Pharmacology, Thomas Jefferson University, 233 South, 10th Street, Room 226, Philadelphia, PA 19107, USA
Gen Pharmacol 35:277-85
10. An Inhibitor of the F1 subunit of ATP synthase (IF1) modulates the activity of angiostatin on the endothelial cell surface
Nick R Burwick
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
J Biol Chem 280:1740-5

Collaborators

* Somnath Mukhopadhyay
* Jun Fang
* Ulrich Rodeck
* John M Maris
* Qun Wang
* Randy Burd
* John E Biaglow
* R A Coss
* David Berd
* Ruth Halaban
* Mark W Dewhirst
* Mario Gonzalez-Gronow
* David J Adams
* Phyllis R Wachsberger
* Daniel J Kenan
* Salvatore V Pizzo
* Tammy L Moser
* Sulene L Chi
* Roderick A Capaldi
* Nick R Burwick
* Barbara D Lipes
* Yvonne M Mowery
* Susana C Hilderbrand
* Michael F Marusich
* Siqing Shan
* Carrie E Johnson
* Zhaoxi Zhong
* Bo Li
* M Sharon Stack

Detail Information
Publications14

1. Abnormal acidification of melanoma cells induces tyrosinase retention in the early secretory pathway
Ruth Halaban
Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
J Biol Chem 277:14821-8
....
2. The H+-linked monocarboxylate transporter (MCT1/SLC16A1): a potential therapeutic target for high-risk neuroblastoma
Jun Fang
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
Mol Pharmacol 70:2108-15
..Such treatment would have selectivity by virtue of the acidic milieu surrounding tumors, because MCT is increasingly active as extracellular pH decreases below 7.0 and lactic acid production increases...
3. Angiostatin and anti-angiogenic therapy in human disease
Miriam L Wahl
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
Recent Prog Horm Res 59:73-104
....
4. Intracellular acidification abrogates the heat shock response and compromises survival of human melanoma cells
Ronald A Coss
Department of Radiation Oncology, and the Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
Mol Cancer Ther 2:383-8
..This strategy could result in a therapeutic gain, because normal tissues, existing at a pHe above 7.0, would not be sensitized...
5. Tumor oxygenation and acidification are increased in melanoma xenografts after exposure to hyperglycemia and meta-iodo-benzylguanidine
Randy Burd
Department of Radiation Oncology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
Radiat Res 159:328-35
..Hyperglycemia plus MIBG has the potential to improve response to radiation therapy as well as to hyperthermia and some chemotherapies...
6. Regulation of intracellular pH in human melanoma: potential therapeutic implications
Miriam L Wahl
Department of Biochemistry and Molecular Pharmacology, Haverford College, Haverford, Pennsylvania 19041, USA
Mol Cancer Ther 1:617-28
..In most tissues, it is proposed that the NHE-1 could compensate for an inhibited MCT to prevent acidification, but in melanoma cells this did not occur. Therefore, MCT inhibitors may be particularly effective against malignant melanoma...
7. Angiostatin induces intracellular acidosis and anoikis in endothelial cells at a tumor-like low pH
Miriam L Wahl
Department of Biochemistry and Molecular Pharmacology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
Endothelium 9:205-16
..The results also implicate roles for both pH(e) and pH(i) regulation in the mechanism of angiostatin action...
8. The mechanism of action of angiostatin: can you teach an old dog new tricks?
Tammy L Moser
Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
Thromb Haemost 87:394-401
..This review will describe what is known about the mechanism of action of angiostatin from the current literature...
9. Effects of microenvironmental extracellular pH and extracellular matrix proteins on angiostatin's activity and on intracellular pH
M L Wahl
Department of Biochemistry and Molecular Pharmacology, Thomas Jefferson University, 233 South, 10th Street, Room 226, Philadelphia, PA 19107, USA
Gen Pharmacol 35:277-85
..These data indicate that substrate and pH(e) are critical parameters in the evaluation of this antiangiogenic substance, and probably for others as well...
10. An Inhibitor of the F1 subunit of ATP synthase (IF1) modulates the activity of angiostatin on the endothelial cell surface
Nick R Burwick
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
J Biol Chem 280:1740-5
..These data suggest that there is a relationship between the binding sites of IF1 and angiostatin on ATP synthase and that IF1 could be employed to modulate angiogenesis...
11. Camptothecin analogs with enhanced activity against human breast cancer cells. II. Impact of the tumor pH gradient
David J Adams
Department of Medicine, Duke University Medical Center, 2638 Research Drive, Durham, NC 27710, USA
Cancer Chemother Pharmacol 57:145-54
..While several substitutions at the 7 and 10 positions enhance potency, 7-halomethyl and 10-amino CPT analogs show selective activity at the acidic pH common to the microenvironment of most solid tumors...
12. Angiostatin's molecular mechanism: aspects of specificity and regulation elucidated
Miriam L Wahl
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
J Cell Biochem 96:242-61
....
13. Ectopic localization of mitochondrial ATP synthase: a target for anti-angiogenesis intervention?
Daniel J Kenan
Department of Pathology, DUMC 3712, Duke University Medical Center, Durham, North Carolina 27710, USA
J Bioenerg Biomembr 37:461-5
..In order to explore the mechanism of action of angiostatin and its mimetics, further work needs to be done to evaluate clinical applicability, specificity, and contraindications for this class of therapeutics...
14. Angiostatin-like activity of a monoclonal antibody to the catalytic subunit of F1F0 ATP synthase
Sulene L Chi
Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
Cancer Res 67:4716-24
..Thus, MAb3D5AB1 shows angiostatin-like properties superior to angiostatin and may be exploited in cancer chemotherapy...

Aquí lo que hay es mucha mente estrecha, mucho lavado de cerebro y las habichuelas de por medio.

¿ Estos son los "libros rellenitos" de Kasandra ?

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