CANCER.

Information on current developments in both regular and alternative or complementary treatments for cancer types and resources at all stages. We have basically all articles and information put in alphabetical order, scroll in left column in alphabetical list.

Experiences of cancer patients with complementary approaches can be found by experience stories and there are also some videos of experiences of cancer patients to see. To click on video button top left . Or visit the website of the SNFK information where movies are shown on complementary approaches to cancer.

Gene therapy in cancer: Some gene and PRL-3 gene only cases that appear to be responsible for development of intestinal cancer and the metastasis process

Already on July 17, 2002 reported the University of Maastricht, the message that together with the Johns Hopkins Oncology Center in Baltimore (U.S.) a number of genes have mapped the cause could be linked to cancer and its recurrence. Particularly in this post is that it seems certain nutrients just a brake on the activation of these genes: "It is possible that the mechanism responsible for the inactivation of genes that inhibit, influenced by environmental factors such as nutrition. The researchers continued their investigation continued to add extra attention to the effect of certain foods. October 12, 2002 reported by researchers at Johns Hopkins and the same resulting from the Maastricht study where they devote themselves to the single gene called PRL-3 is responsible for the process of metastasis of cancer cells. An interesting development because it was through focusing on food patterns and the effect of nutrients on the activation of this gene appears to be a patient-friendly approach to cancer closer. Healthy nutrition for some supplementation to cancer seems to be working as evidenced by the experiences of several patients ( see your story ) who provide complementary or stand their incurable cancer with metastases - mostly in the liver - often coming to a halt and sometimes even reduced. But read these successive releases. First time in Maastricht, then from America on the PRL-3 gene in the abstract of the study.

July 17, 2002
UM researchers in Nature Genetics
Breakthrough research on cancer gene

Investigation of the Johns Hopkins Oncology Center in Baltimore (USA) in collaboration with Maastricht University (UM) has led to the discovery of genes that play a role in the development of colon cancer. In the study, published in the journal Nature Genetics, has developed a method to the gene expression of untreated cancer cells compared with the gene expression of cancer cells treated with agents that activate cancer-suppressing genes. The screening of 10,000 genes, 74 genes came forward to respond to treatment with these agents.

Cancer of the colon and rectum (colorectal cancer) is common in the Netherlands, and are increasing after middle age. Colorectal cancer usually arises from a benign tumor. The transition from benign tumor to carcinoma is characterized by an increasing number of changes in genes involved in the control of the division of intestinal cells. If the genes responsible for inhibiting cell division are disabled, intestinal cells start sharing and may develop a malignant tumor. In this study using a new method, the genes identified in colorectal cancer are disabled.

It is possible that the mechanism responsible for inactivating genes that inhibit, influenced by environmental factors such as nutrition. Wherefore, the Maastricht researchers and their U.S. colleagues are currently available or there are links between diet and gene changes in human cancer. Use is made of a large Dutch cohort study on diet and cancer in 1986 was set by Maastricht University and TNO Nutrition Zeist. This study was conducted among more than 120,000 Dutch. Of the 800 participants who developed colon cancer, several genetic changes related to the diet of these people.

The research was conducted under the direction of Prof.. Stephen Baylin in his laboratory in Baltimore. The Maastricht contribution consisted of the contribution of Dr. Manon of England (Research Institute GROW) and Dr. Matty Weijenberg (NUTRIM Research) and was co-financed by the Dutch Cancer Society Koningin Wilhelmina Fonds and the René Vogels Foundation.


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A genomic screen for genes upregulated by demethylation and histone deacetylase inhibition in human colorectal cancer

Hiromu Suzuki1, Edward Gabrielson1, 2, Wei Chen1, 3, Ramaswamy Anbazhagan1, 2, Manon Engeland1, 4, Matty P. Weijenberg5, James G. Herman1 & Stephen B. Baylin 1, 3, 6


Aberrant hypermethylation of gene promoters is a major mechanism associated with inactivation of tumor suppressor genes in cancer. Previously we showed this transcriptionalBoth silencing to be mediated by methylation and histone deacetylase activity, with methylation being dominant. Here, we have Used cDNA microarray analysis to screen for genes are epigenetically silenced That in human colorectal cancer. By screening over 10,000 genes, we show our approach can-identify "That a Substantial Number of genes with promoter hypermethylation in a Given cancer; These are distinct from genes with unmethylated promoters, for Increased expression Which is Produced by histone deacetylase inhibition alone. Many of the hypermethylated genes we have Identified high potential for roles in tumorigenesis by Virtue of Their predicted function and chromosome position.We Also Identified That a group of genes are preferentially hypermethylated in colorectal cancer and gastric cancer. One of These genes, SFRP1, Belongs to a gene family, we show That hypermethylation or four genes in this family very frequently occure in colorectal cancer, Providing for (i) a unique potential mechanism for loss of tumor suppressor gene function and (ii ) construction of a molecular marker panel could-That Virtually all colorectal cancer detection.

1. The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, 1650 Orleans Street, Baltimore, Maryland 21231, USA.
2. Department of Pathology, The Johns Hopkins University School of Medicine, 1650 Orleans Street, Baltimore, Maryland 21231, USA.
3. Predoctoral Training Program in Human Genetics, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
4. Department of Pathology, University Maastricht, The Netherlands.
5. Department of Epidemiology, Maastricht University, The Netherlands.
6. Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Correspondence Should Be Addressed to SB Baylin. E-mail: sbaylin@welchlink.welch.jhu.edu

October 12, 2001 - Researchers have discovered a gene to allow That Appears to colon tumors
Spread to Other Parts of the body, a process called metastasis. The gene codes for an Enzyme That May Be Central to the meta-static process, Suggesting That The Possibility Could the enzyme targeted by drugs to block the spread of colon cancers.
Metastasis is the primary cause of death from colon cancer.
In an article published online in the October 12, 2001, edition of Science, Howard Hughes Medical Institute investigator Bert Vogelstein and colleagues at the Johns Hopkins
University Oncology Center Reported Identifying the gene, called PRL-3.
The researchers Identified after PRL-3 Developing a profile of gene expression in cells They
That from microdissected cancers had metastasized to the liver. The genetic profile was Developed Using SAGE (serial analysis of gene expression), a technique invented by the
researchers to determining the level of expression of genes.
In SAGE, the enzyme reverse transcriptase is Used to produce complementary DNA from the messenger RNA (mRNA) derived from cells understudy. The DNA is then snipped at a defined position, creating a unique identifier "tag" that corresponds to a single gene. The researchers can-then analyze the number of unique tags present in Their sample and deduce how much mRNA exists For Each gene - a measure of gene activity.
Vogelstein said thats the group's initial analysis of gene expression in the meta-static tissue yielded confusing results. "When we initially fired meta static lesions from
patiënten, the purified RNA, and then Looked at Their gene expression profiles, we found many of the transcripts [gene] Were Clearly Derived from Non-Neoplastic cells, "he said." The Problem Is That tumors are composed of multiple cell types, not just the Neoplastic Cells. Liver metastases from colon cancers containerization a supporting stroma tissue, as well as inflammatory cells and normal liver cells, "he said.
The researchers devised a purification procedure to isolate themself That enabled only the meta-static cells. This technique Involved separate cells based on Their attraction to an antibody specific for colorectal epithelial cells in liver tissue, Which constitute the meta-static cancer cells. "Once we did this separation," Vogelstein said, "the
Became gene expression patterns much clearer and more reliable. "
SAGE analysis or synthesis isolated cells revealed 38 gene transcripts That appeared to be enriched in the meta-static cells, Indicating That They Were constantly switched on metastasis. Although all the genes elevated in some Were "This gene was overexpressed at very low
or undetectable levels in normal colon epithelium, "said HHMI investigator Bert
Vogelstein. "It was overexpressed at low levels in the early stages of colorectal neoplasia. And ItsClearly expression was much higher in meta static lesions from the liver. "
Importantly, the scientists Were Also Able to compare PRL-3 expression in normal epithelium, primary cancers and meta static lesions from the Same patient. Such comparison eliminates the differences Potentially deceit When tissues from patiënten differentiation are compared. "In Each of the six cases studied, PRL-3 expression was quite a bit higher in the metastases Than in the primary tumor," said Vogelstein.
The Scientist Also discovered thats the higher levels of PRL-3 expression They Measured Were associated in a few cases with a Process Known As gene amplification - in Which overexpression of a gene is caused by a large Increase in the number of copies of the gene. Gene amplification is a Characteristic Mechanism by Which the overexpression of growth-regulating genes in human cancers occure.
"The discovery That this gene was only overexpressed but not amplified Provided Also very strong evidence for causality of this gene in the meta-static process," said Vogelstein.
According To Vogelstein, the scientists willing now search for the biochemical and physiologic roles of PRL-3 in colon cancer metastasis. One of the goals of future studies to compromise
be to launch a search for molecules That function or inhibit the phosphatase PRL-3 and to discover whethere this inhibition thwartsmetastasis.