LDN Found to Suppress Ovarian Cancer and Enhance Chemo
RoseyR
Member Posts: 471 Member
It's just one article, but suggest all with ovarian cancer--and related uterine cancers--to take a look and consider adding LDN to an arsenal of maintenance maneuvers: good nutrition, exercise, and spirits.
Best,
Rosey
Low-dose naltrexone suppresses ovarian cancer and exhibits enhanced inhibition in combination with cisplatin
Renee N Donahue,
Patricia J McLaughlin and
Ian S Zagon
Department of Neural and Behavioral Sciences, The Pennsylvania State University College of Medicine, H109, The Milton S Hershey Medical Center, 500 University Drive, Room C3729, Hershey, PA 17033, USA
Corresponding author: Dr Ian S Zagon. Email: isz1{at}psu.edu
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Abstract
Ovarian cancer is the leading cause of death from gynecological malignancies. Although initial therapeutic modalities are successful, 65% of these women relapse with only palliative treatments available thereafter. Endogenous opioids repress the proliferation of human ovarian cancer cells in vitro, and do so in a receptor-mediated manner. The present study examined whether modulation of opioid systems by the opioid antagonist naltrexone (NTX), alone or in combination with standard of care therapies (taxol/paclitaxel, cisplatin), alters human ovarian cancer cell proliferation in tissue culture and tumor progression in mice. Administration of NTX for six hours every two days, but not continuously, reduced DNA synthesis and cell replication from vehicle-treated controls in tissue culture. Moreover, brief exposure to NTX in combination with taxol or cisplatin had an enhanced anticancer action. Mice with established ovarian tumors and treated with a low dosage of NTX (LDN), which invokes a short period of opioid receptor blockade, repressed tumor progression in a non-toxic fashion by reducing DNA synthesis and angiogenesis but not altering cell survival. The combination of LDN with cisplatin, but not taxol, resulted in an additive inhibitory effect on tumorigenesis with enhanced depression of DNA synthesis and angiogenesis. LDN combined with cisplatin alleviated the toxicity (e.g. weight loss) associated with cisplatin. LDN treatment upregulated the expression of the opioid growth factor (OGF, chemical term ([Met5]-enkephalin) and its receptor, OGFr. Previous tissue culture studies have reported that OGF is the only opioid peptide with antiproliferative activity on ovarian cancer cells, with OGF action mediated by OGFr. Thus, the common denominator of intermittent opioid receptor blockade by short-term NTX or LDN on ovarian cancer proliferation and tumorigenesis recorded herein appears to be related to the OGF–OGFr axis. These preclinical data may offer a non-toxic and efficacious pathway-related treatment that can benefit patients with ovarian cancer.
Best,
Rosey
Low-dose naltrexone suppresses ovarian cancer and exhibits enhanced inhibition in combination with cisplatin
Renee N Donahue,
Patricia J McLaughlin and
Ian S Zagon
Department of Neural and Behavioral Sciences, The Pennsylvania State University College of Medicine, H109, The Milton S Hershey Medical Center, 500 University Drive, Room C3729, Hershey, PA 17033, USA
Corresponding author: Dr Ian S Zagon. Email: isz1{at}psu.edu
Next Section
Abstract
Ovarian cancer is the leading cause of death from gynecological malignancies. Although initial therapeutic modalities are successful, 65% of these women relapse with only palliative treatments available thereafter. Endogenous opioids repress the proliferation of human ovarian cancer cells in vitro, and do so in a receptor-mediated manner. The present study examined whether modulation of opioid systems by the opioid antagonist naltrexone (NTX), alone or in combination with standard of care therapies (taxol/paclitaxel, cisplatin), alters human ovarian cancer cell proliferation in tissue culture and tumor progression in mice. Administration of NTX for six hours every two days, but not continuously, reduced DNA synthesis and cell replication from vehicle-treated controls in tissue culture. Moreover, brief exposure to NTX in combination with taxol or cisplatin had an enhanced anticancer action. Mice with established ovarian tumors and treated with a low dosage of NTX (LDN), which invokes a short period of opioid receptor blockade, repressed tumor progression in a non-toxic fashion by reducing DNA synthesis and angiogenesis but not altering cell survival. The combination of LDN with cisplatin, but not taxol, resulted in an additive inhibitory effect on tumorigenesis with enhanced depression of DNA synthesis and angiogenesis. LDN combined with cisplatin alleviated the toxicity (e.g. weight loss) associated with cisplatin. LDN treatment upregulated the expression of the opioid growth factor (OGF, chemical term ([Met5]-enkephalin) and its receptor, OGFr. Previous tissue culture studies have reported that OGF is the only opioid peptide with antiproliferative activity on ovarian cancer cells, with OGF action mediated by OGFr. Thus, the common denominator of intermittent opioid receptor blockade by short-term NTX or LDN on ovarian cancer proliferation and tumorigenesis recorded herein appears to be related to the OGF–OGFr axis. These preclinical data may offer a non-toxic and efficacious pathway-related treatment that can benefit patients with ovarian cancer.
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Comments
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LDN user
Thank you for posting this. I am an ovarian cancer survivor who went from stage III at the time of surgery to stage IV AFTER surgery before chemo. I've been on LDN for a few months. My last chemo was in March 2011.
I did the standard treatment starting about a year ago; couldn't tolerate Taxol & finished up on carboplatin but never got into remission. I've been using high dose ascorbic acid treatment along with an anti-cancer lifestyle and some anti-inflammatory herbs.
I've been on "chemo break" for the past 8 months and feel really well--no ascites or any problems. The PET/CT scan shows the neoplasms splattered in my upper abdominal area & in my liver--like peppercorns. If my CA-125 wasn't over 500, I would be inclined to continue my "wait & see" attitude. The research you posted possibly explains why I have been able to manage to slow the growth of the neoplasms. I'm sure the ascorbic acid IVs are keeping the ascites away...the longer I can stay off chemo, the better.
I'm gearing up to jump back on the chemo train for more chemo...very reluctantly. If I could afford the IPT low dose chemo treatments at a Tijuana clinic, I'd be there in a heartbeat. I've been taking Astragalus to protect my bone marrow and at least now I can feel confident continuing the LDN throughout the second lone chemo.0
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