We suggest that this series of events results in a stoppage of the (retinoblastoma) cell cycle progression at the G1–>S phase transition thereby leading to a G0/G1 arrest and subsequent apoptotic cell death.
The good news for retinoblastoma (Rb) survivors and their caregivers is that “In the developed world, Rb has one of the best cure rates of all childhood cancers (95-98%), with more than nine out of every ten sufferers surviving into adulthood.”
As a survivor of an incurable cancer
I can tell you that the ongoing challenge for cancer survivors is the fear of relapse. As you can see from the link below, retinoblastoma can relapse in the other eye.
I take resveratrol and have for years now. It reduces the risk of my cancer, multiple myeloma, relapsing.
is non-toxic and has been shown to reduce the risk of other cancers as well. Have you been diagnosed with retinoblastoma? Please scroll down the page, post a question or comment and I will reply to you ASAP.
- Cancer Survivor
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- Director PeopleBeatingCancer
Rb is a rapidly developing cancer that develops in the cells of retina, the light-detecting tissue of the eye. In the developed world, Rb has one of the best cure rates of all childhood cancers (95-98%), with more than nine out of every ten sufferers surviving into adulthood…
“Retinoblastoma Relapse Cause-
In hereditary retinoblastoma, patients often have the genetic mutation that causes Rb in the RB1 gene in all cells of the body. Besides the egg and sperm cells, all cells of the body ordinarily have two RB1 genes. In patients with the genetic mutation, any change in the remaining RB1 gene in any body cell can cause a retinoblastoma tumor to develop in that cell. Patients with non-hereditary retinoblastoma are not as susceptible to relapse…”
“Resveratrol (trans-3,4′,5-trihydroxystilbene), a polyphenolic phytoalexin found in grapes, nuts, many other fruits, and red wine, is a potent antioxidant with anti-inflammatory and cancer-preventive properties.
The mechanism(s) by which resveratrol imparts cancer chemopreventive effects has not been clearly defined. Earlier, we have shown that resveratrol treatment results in an induction of the cyclin kinase inhibitor WAF1/CIP1/p21 which, by inhibiting cyclin (E, D1, and D2) and cyclin-dependent kinases (cdk2, cdk4, and cdk6), results in a G0/G1-phase arrest followed by apoptosis of A431 human epidermoid carcinoma cells (Ahmad et al., Clin. Cancer Res. 7, 1466-1473, 2001).
Rb and the E2F family of transcription factors are important proteins, which regulate the progression of the cell cycle at and near the G1–>S phase transition.
Here we provide evidence for the involvement of the pRb-E2F/DP pathway as an important contributor of resveratrol-mediated cell cycle arrest and apoptosis. Immunoblot analysis demonstrated that resveratrol treatment of A431 cells results in a dose- as well as time-dependent decrease in the hyperphosphorylated form of pRb with a relative increase in hypophosphorylated pRb.
This response was accompanied by downregulation of protein expression of all five E2F ( 1 – 5 ) family members of transcription factors studied and their heterodimeric partners DP1 and DP2. This suggests that resveratrol causes a downregulation of hyperphosphorylated pRb protein with a relative increase in hypophosphorylated pRb that, in turn, compromises with the availability of free E2F. We suggest that this series of events results in a stoppage of the cell cycle progression at the G1–>S phase transition thereby leading to a G0/G1 arrest and subsequent apoptotic cell death. To our knowledge, this is the first study showing the involvement of the pRb-E2F/DP pathway as a mechanism of the cancer-chemopreventive effects of resveratrol.”