Interesting MIT article on blocking tumor formation

LivinginNH

I just came across this MIT article and thought you might like to read about new advances in the fight against tumor formation.

http://web.mit.edu/newsoffice/2012/turning-on-key-enzyme-blocks-tumor-formation-0827.html


Take care,

Cyn

manwithnoname

Very interesting
They stopped the tumour growth in mice, how about this one from 1994; http://www.ncbi.nlm.nih.gov/pubmed/8040891

A non-toxic treatment that completely regressed tumours in all mice treated. 18 years ago.

pete43lost_at_sea

great article cynthia
i have put it on my blog, i think its cited in the latest conference i went to.
boosting pmk1 was discussed as a key goal of supplementation and diet at the conference.

hugs,
Pete

ps hey tony, ndv has a place in this as well, but i suspect they are not mutually exclusive. i will use both in my treatment if needed.

manwithnoname

pete43lost_at_sea said:

great article cynthia
i have put it on my blog, i think its cited in the latest conference i went to.
boosting pmk1 was discussed as a key goal of supplementation and diet at the conference.

hugs,
Pete

ps hey tony, ndv has a place in this as well, but i suspect they are not mutually exclusive. i will use both in my treatment if needed.

Hi Pete
I am becoming convinced that the only cancer treatments that become available will be those that can be patented, it is disgraceful but an economic fact.

PMK seems to have a relationship with thyroid which I am investigating now for a while, see here; http://musli.co.il/eng/method.html

pete43lost_at_sea

manwithnoname said:

Hi Pete
I am becoming convinced that the only cancer treatments that become available will be those that can be patented, it is disgraceful but an economic fact.

PMK seems to have a relationship with thyroid which I am investigating now for a while, see here; http://musli.co.il/eng/method.html

thanks mate
i just published on my blog my genetics profile test, it took 6 months to get the online results.

i agree about the disgraceful state of alt therapies, but guess what one day we will prevail.

to many lives lost, the alts will win in the end. trust me, i have faith in our biology. its all just time.

smile and be happy even in the turmoil.

musli, really interesting..... thanks again

hugs,
Pete

PatchAdams

Would this work?
Effects of daily oral administration of quercetin chalcone and modified citrus pectin on implanted colon-25 tumor growth in Balb-c mice.

The health benefits of fruits and vegetables have been the subject of numerous investigations over many years. Two natural substances, quercetin (a flavonoid) and citrus pectin (a polysaccharide found in the cell wall of plants) are of particular interest to cancer researchers. Two modified versions of these substances - quercetin chalcone (QC) and a pH-modified citrus pectin (MCP) - are the focus of this study. Previous research has confirmed that quercetin exhibits antitumor properties, likely due to immune stimulation, free radical scavenging, alteration of the mitotic cycle in tumor cells, gene expression modification, anti-angiogenesis activity, or apoptosis induction, or a combination of these effects. MCP has inhibited metastases in animal studies of prostate cancer and melanoma. To date, no study has demonstrated a reduction in solid tumor growth with MCP, and there is no research into the antitumor effect of QC. This study examines the effects of MCP and QC on the size and weight of colon-25 tumors implanted in balb-c mice. Fifty mice were orally administered either 1 ml distilled water (controls), low-dose QC (0.8 mg/ml), high-dose QC (1.6 mg/ml), low-dose MCP (0. 8 mg/ml) or high-dose MCP (1.6 mg/ml) on a daily basis, beginning the first day of tumor palpation (usually eight days post-implantation). A significant reduction in tumor size was noted at day 20 in all groups compared to controls. The groups given low-dose QC and MCP had a 29% (NS) and 38% (p<0.02) decrease in size, respectively. The high-dose groups had an even more impressive reduction in size; 65% in the QC group and 70% in the mice given MCP (both p<0.001). This is the first evidence that MCP can reduce the growth of solid primary tumors, and the first research showing QC has antitumor activity. Additional research on these substances and their effect on human cancers is warranted.
Altern Med Rev. 2000 Dec;5(6):546-52


Inhibitory effect of modified citrus pectin on liver metastases in a mouse colon cancer model.

AIM: To discuss the expression of glactin-3 in liver metastasis of colon cancer and its inhibition by modified citrus pectin (MCP) in mice. METHODS: Seventy-five Balb/c mice were randomly divided into negative control group (n = 15), positive control group (n = 15), low MCP concentration group (n = 15), middle MCP concentration group (n = 15) and high MCP concentration group (n = 15). CT26 colon cancer cells were injected into the subcapsule of mouse spleen in positive control group, low, middle and high MCP concentrations groups, except in negative control, to set up a colon cancer liver metastasis model. The concentration of MCP in drinking water was 0.0%, 0.0%, 1.0%, 2.5% and 5.0% (wt/vol), respectively. Liver metastasis of colon cancer was observed after 3 wk. Enzyme-linked immunosorbent assay (ELISA) was used to detect the concentration of galectin-3 in serum. Expression of galectin-3 in liver metastasis was detected by immunohistochemistry. RESULTS: Except for the negative group, the percentage of liver metastasis in the other 4 groups was 100%, 80%, 73.3% and 60%, respectively. The number of liver metastases in high MCP concentration group was significantly less than that in positive control group (P = 0.008). Except for the negative group, the median volume of implanted spleen tumor in the other 4 groups was 1.51 cm(3), 0.93 cm(3), 0.77 cm(3) and 0.70 cm(3), respectively. The volume of implanted tumor in middle and high MCP concentration groups was significantly smaller than that in positive control group (P = 0.019; P = 0.003). The concentration of serum galectin-3 in positive control and MCP treatment groups was significantly higher than that in the negative control group. However, there was no significant difference between them. Except for the negative control group, the expression of galectin-3 in liver metastases of the other 4 groups showed no significant difference. CONCLUSION: Expression of galetin-3 increases significantly in liver metastasis of colon cancer, which can be effectively inhibited by MCP.
World J Gastroenterol. 2008 Dec 28;14(48):7386-91


Expression of galectin-3 in liver metastasis of colon cancer and the inhibitory effect of modified citrus pectin.

OBJECTIVE: To observe the expression of galectin-3 in the liver metastasis of colon cancer in mice and the inhibitory effect of modified citrus pectin (MCP) on galectin-3 expression. METHODS: Seventy-five Balb/c mice were randomized into 5 groups, namely the negative control, positive control, low-concentration MCP, moderate-concentration MCP and high-concentration MCP groups. CT26 colon cancer cells were injected into the subcapsule of the mouse spleen to establish liver metastasis models of colon cancer, but the mice in the negative control group received no tumor cell injection. MCP was added into the drinking water of the mice at the concentrations of 0, 1.0%, 2.5% and 5.0% (m/V). The liver metastasis was observed 3 weeks after tumor cell inoculation. Enzyme-linked immunosorbent assay was performed to determine the serum galectin-3 level. A tissue microarray of the liver metastasis was prepared for immunohistochemical detection of galectin-3 expression in the liver metastasis. RESULTS: In the positive control, low-, moderate- and high-concentration MCP groups, the rates of liver metastasis were 100%, 80%, 73.3% and 60%, respectively. The number of liver metastases in high-concentration MCP group was significantly smaller than that in the positive control group (P<0.05). In the 4 groups with tumor cell inoculation, the median volume of the primary lesions in the spleen was 1.51, 0.93, 0.77 and 0.70 cm(3), respectively, which were significantly smaller in the moderate- and high-concentration MCP groups than in the positive control group (P<0.05). The serum galectin-3 level in the positive control group and MCP-treated groups were significantly higher than that in the negative control group (P<0.01), but similar between the positive control group and the MCP-treated groups (P>0.05). In the positive control and the MCP-treated groups, the expression of galectin-3 in the liver metastases showed no significant differences (P>0.05). CONCLUSION: The expression of galetin-3 is significantly increased in the liver metastasis of colon cancer, and MCP can effectively inhibit the liver metastasis.
Nan Fang Yi Ke Da Xue Xue Bao. 2008 Aug;28(8):1358-6