LDN bei Krebs (für den Onkologen) (Forum)

thaddaeus @, Montag, 07. Januar 2008, 18:06 (vor 3998 Tagen)

kopiert von der yahoogruppe

Re: info for my doc on LDN

Hello L.,

In my opinion, if you can provide the proven clinical trials where
low dose naltrexone have successfully helped cancer, then it may help
your doctor in feeling more comfortable trying something 'cutting

The below published medical studies can be located on the National
Institutes of Health / National Library of Medicine / PubMed
Since the below are only excerpts, you will probably want to go to
the PUBMED website, pull up the Article (using the ID number that's
included below) and print each of the abstracts (that way it will
reflect the NIH/NLM/PUBMED originating website).

The first two studies are from Dr. Berkson's work actually
treating cancer patients and the other two articles are from Dr.
Zagon and others researchers at the Hershey Medical School. Dr.
Zagon has been one of the researching pioneers (and experts) in the
area of low dose naltrexone and opioid growth factor.

Also, you may want to print out a couple of links from the Hershey
Medical School about Dr. Zagon's and his work in the area of opioid


(*note: this article lists some of the cancers helped as part of Dr.
Zagon's research - including colon, pancreatic, head/neck, etc.)

The above and below may be helpful to your doctor to see that a
well respected Medical School is conducting the research in this
area, as well as a very respected doctor (BM Burkson) is actually
using LDN to help different patients with different cancers.

God bless you in your journey of healing!


Integr Cancer Ther. 2007 Sep;6(3):293-6.

Reversal of signs and symptoms of a B-cell lymphoma in a patient
using only low-dose naltrexone.

Berkson BM, Rubin DM, Berkson AJ.
Integrative Medical Center of New Mexico, Las Cruces, USA.

PMID: 17761642 [PubMed - indexed for MEDLINE]


Integr Cancer Ther. 2006 Mar;5(1):83-9.

The long-term survival of a patient with pancreatic cancer with
metastases to the liver after treatment with the intravenous alpha-
lipoic acid/low-dose naltrexone protocol.

Berkson BM, Rubin DM, Berkson AJ.
Integrative Medical Center of New Mexico and New Mexico State
University, Las Cruces.

The authors describe the long-term survival of a patient with
pancreatic cancer without any toxic adverse effects. The treatment
regimen includes the intravenous alpha-lipoic acid and low-dose
naltrexone (ALA-N) protocol and a healthy lifestyle program. The
patient was told by a reputable university oncology center in October
2002 that there was little hope for his survival. Today, January
2006, however, he is back at work, free from symptoms, and without
appreciable progression of his malignancy. The integrative protocol
described in this article may have the possibility of extending the
life of a patient who would be customarily considered to be terminal.
The authors believe that life scientists will one day develop a cure
for metastatic pancreatic cancer, perhaps via gene therapy or another
biological platform. But until such protocols come to market, the ALA-
N protocol should be studied and considered, given its lack of
toxicity at levels reported. Several other patients are on this
treatment protocol and appear to be doing well at this time.

PMID: 16484716 [PubMed - indexed for MEDLINE]


Neuropeptides. 2007 Dec;41(6):441-52. Epub 2007 Oct 1.

Opioids and migration, chemotaxis, invasion, and adhesion of human
cancer cells.

Zagon IS, Rahn KA, McLaughlin PJ.
Department of Neural and Behavioral Sciences, The Pennsylvania State
University, College of Medicine, Hershey, PA 17033, United States.

This study was designed to examine the role of opioids on cell
migration, chemotaxis, invasion, and adhesion, with an emphasis on
whether the opioid growth factor (OGF, [Met(5)]-enkephalin) or the
opioid antagonist naltrexone (NTX) impacts any or all of these
processes. Drug concentrations of OGF and NTX known to depress or
stimulate, respectively, cell proliferation and growth were analyzed.
Three different human cancers (pancreatic, colon, and squamous cell
carcinoma of the head and neck), represented by seven different
cancer cell lines (PANC-1, MIA PaCa-2, BxPC-3, CAL-27, SCC-1, HCT-
116, and HT-29), were evaluated. In addition, the influence of a
variety of other natural and synthetic opioids on cell motility,
invasion, and adhesion was assessed. Positive and negative controls
were included for comparison. OGF and NTX at concentrations of 10(-4)
to 10(-6)M, and dynorphin A1-8, beta-endorphin, endomorphin-1,
endomorphin-2, leucine enkephalin, [D-Pen(2,5)]-enkephalin (DPDPE),
[D-Ala(2), MePhe(4), Glycol(5)]-enkephalin (DAMGO), morphine, and
U69,593 at concentrations of 10(-6)M, did not alter cell migration,
chemotaxis, or invasion of any cancer cell line. OGF and NTX at a
concentration of 10(-6)M, and incubation for 24 or 72h, did not
change adhesion of these cancer cells to collagen I, collagen IV,
fibronectin, laminin, or vitronectin. Moreover, all other opioids
tested at 10(-6)M concentrations and for 24h had no effect on
adhesion. These results indicate that the inhibitory or stimulatory
actions of OGF and NTX, respectively, on cell replication and growth
are independent of cell migration, chemotaxis, invasion, and adhesive
properties. Moreover, a variety of other exogenous and endogenous
opioids, many specific for the mu, delta, or kappa opioid receptors,
also did not alter these biological processes, consonant with
previous observations of a lack of effects of these compounds and
their receptors on the biology of cancer cells.

PMID: 17910895 [PubMed - in process]


Cancer Res. 2007 Nov 1;67(21):10511-8.

The opioid growth factor (OGF)-OGF receptor axis uses the p16 pathway
to inhibit head and neck cancer.

Cheng F, Zagon IS, Verderame MF, McLaughlin PJ.
Department of Neural and Behavioral Sciences, The Pennsylvania State
University College of Medicine, Hershey, PA 17033, USA.

Head and neck squamous cell carcinoma (HNSCC) represents 5.5% of
malignancies worldwide, with approximately 30,000 new cases and
approximately 11,000 deaths reported in the United States annually.
The opioid growth factor (OGF; [Met(5)]-enkephalin) and the OGF
receptor (OGFr) form an endogenous growth regulating system; the OGF-
OGFr axis influences the G(0)-G(1) phase of the cell cycle in HNSCC.
Cells treated with small interfering RNA (siRNA) for OGFr no longer
responded to the growth inhibitory effects of OGF or the growth
stimulatory effects of naltrexone, indicating that these activities
are entirely mediated by OGFr. In this investigation, we examined the
precise target of OGF in the cell cycle. Using SCC-1 cells, OGF
decreased the phosphorylation of retinoblastoma protein. This change
was correlated with reduced Cdk4, but not Cdk2, kinase activity. OGF
treatment increased cyclin-dependent kinase inhibitor p16 protein
expression. Importantly, p16 complexed with Cdk4 was increased by OGF
treatment at all time points, consistent with the hypothesis that OGF
mediated growth inhibition through p16. Blockade of OGF-OGFr
interactions with naloxone abolished the increased expression of p16
protein by OGF. Inhibition of p16 (INK4a) activation by p16-specific
siRNA blocked OGF's repressive action on proliferation of SCC-1, CAL-
27, and SCC-4 HNSCC cells. These data are the first to reveal that
the target of cell proliferative inhibitory action of OGF in human
HNSCC is a cyclin-dependent kinase inhibitory pathway, and this may
be useful in the diagnosis and treatment of HNSCC.

PMID: 17974995 [PubMed - indexed for MEDLINE]

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