El BIRM® en España


El Doctor Edwin Cevallos señala en la entrevista al periódico Ecuador Inmediato lo siguiente:


- Indica que viene hablándose de un premio noble en el area de medicina.

- Son 35 años de investigación para el BIRM® y que recientemente tuvo una reunión con el doctor y descubridor del VIH/SIDA y premio nobel Luc Montagnier en París, dónde fue analizado el efecto del BIRM sobre el virus.

- Son 12 años de pruebas en la Universidad Autónoma de Madrid probando el BIRM® en cáncer de colón, cancer de recto y leucemia y se hayó que cada 6 días el BIRM® mata 800.000 células tumorales.

- En el Congreso Mundial del SIDA en 1994 en Japón se presentan los resultados en pacientes con menos de un mes de vida provenientes de Estados Unidos por no tener casos de éste tipo en latinoamérica.

- Con patente en Estados Unidos como tratamiento o medicina para cáncer de próstata ya que en este país se realiza la patente enfermedad por enfermedad.

- El BIRM® gana cada ves más terreno como producto natural que cumpla las funciones de actuar sobre el sistema inmunológico modulandolo. Para personas con las defensas bajas de avanzada edad, o personas con alérgias, lupus y enfermedades autoinmunes.

- El  BIRM® se elabora en los laboratorios más sofisticados de los Estados Unidos con el fin de seguir generando patentes.

- ¿Por qué no se le vende a las transnacionales farmaceuticas?, el doctor argumenta que no es el dinero su motivación, y que recibió la residencia de los Estados Unidos gracias al BIRM®.
- Fue nominado en el Congreso Mundial de Medicina Natural de Madrid y al presentar las bondades del producto y por el asombro de los participantes hicieron la propuesta para ser merecedor del Premio Nobel.

Para ver la entrevista completa clic aquí.
 




Estudio probado en Estados Unidos para el BIRM®


BIRM, AN ANDEAN PLANT EXTRACT, DOWN REGULATES ANDROGEN RECEPTOR AND SHOWS ANTI-TUMOR ACTIVITY IN PROSTATE CANCER

Shinako Araki*, Dominic Lyn and Bal L. Lokeshwar
Department of Urology, University of Miami School of Medicine, Gautier Research Building, Suites 403-408, 1011 NW 15th St., Miami, FL 33136

INTRODUCTION: BIRM is a root extract of an Andean plant, Solanum dulcamara. We reported recently about the potent antiproliferative and anti- tumor activities of BIRM against prostate cancer (1). The glycosaminoglycan (GAG)-rich oligosaccharides make up the most active components of BIRM. It is orally bioavailable without systemic toxicity. The androgen receptor (AR) levels and activities are critical for prostate cancer (CaP) progression. Down- regulating AR may slow or halt CaP progression. We present evidence here to demonstrate potent-antiproliferative and anti-androgen receptor activity of BIRM in CaP cells that are androgen- sensitive or insensitive, synthesize normal or mutant AR. METHOD Anti-proliferative activity or BIRM on AR-positive, and AR-negative cell lines (LAPC-4, LNCaP, C4-2 and PC-3ML) was investigated by DNA synthesis activity by [3H]-thymidine (3H-TdR) incorporation assay and flow cytometry.
Activity of BIRM against AR was investigated by immunoblotting, co-immunoprecipitation and AR-promoter activity. BIRM activity against AR activity was probed by a PSA ELISA and PSA-promoter reporter assays.
RESULTS BIRM inhibited DNA synthesis activity in CaP cells (IC 50: 1.0 μl/ml). BIRM induced cell-cycle arrest in CaP cells, increases in G2M (80-112% increase) with a concomitant decrease in S-Phase (23-38%). More significantly, BIRM caused a dose and
time-dependent down regulation of normal and mutant- AR in androgen- sensitive LAPC-4 and LNCaP cells (Fig. 1) as well as androgen-insensitive C4-2 cells. AR degradation by BIRM preceded of DNA synthesis. AR down regulation was due to increased proteosome- mediated AR degradation and was independent of PI-3 kinase/Akt pathway, a novel mechanism. BIRM also suppressed PSA promoter activity by 70.2±3.4% and PSA production by 86±2.7%. Decrease of phospho-AR level was seen by BIRM treatment and it was associated with degradation of total AR. Inhibition of PSA promoter by BIRM occurred concurrent with AR degradation. Accelerated AR degradation by BIRM was independent of androgens, suggesting its potential activity in androgen-insensitive CaP. BIRM decreased tumor growth in both LNCaP and PC-3ML tumor xenografts by 71% and 72.2%. Starting the treatment immediately following tumor implantation was more effective in preventing tumor incidence (25% in treated versus 90% in un-treated) than starting after tumors are palpable (100% incidence in either cases), thus implicating potential chemopreventive potential of BIRM against prostate cancer. DISCUSSION: Total androgen deprivation is a common treatment option for patients with advanced prostate cancer (2). Although most patients initially respond to this therapy, the disease quickly progresses to an androgen-refractory state. Several studies have shown that androgen-ablation leads to the androgen refractory state which is attributed to AR overexpression, AR mutations or activation by its co- activators (2-3). Thus, ablation of AR would be a great therapeutic opportunity not only for localized androgen-dependent prostate cancer but also for the prostate cancer that is resistant to androgen ablation therapy. The plant extract BIRM, has significant anti-proliferative activity, contributed by its ability to induce cell-cycle arrest and AR down regulation. Studies with AR-positive LAPC-4, LNCaP, C4-2 as well as AR- negative PC-3 tumor models (reported earlier, 1) suggest a potential chemo- preventive function of BIRM on all forms of prostate cancer. ACKNOWLEDGMENT This work was supported by NIH Grant No. 2R01 CA 61038-13 (BLL) and Sylvester Comprehensive Cancer Center/University of Miami. REFERENCES
  1. Dandekar, D.S., Lokeshwar, V.B., Cevallos-Arellano, E., Soloway, M.S., Lokeshwar, B.L. (2003) Cancer Chemother Pharmacol. 52, 59-66.
  2. Chen, C.D., Welsbie, D.S., Tran, C., Baek, S.H., Chen, R., Vessella, R., Rosenfeld, M.G., Sawyers, C.L. (2004) Nat Med. 10, 33-39.
  3. Linja, M.M., Savinainen, K.J., Saramaki, O.R., Tammela, T.L., Vessella, R.L., Visakorpi, T. (2001) Cancer Res. 61, 3550-3555. 
cell cycle arrest and inhibition