11 april 2011: Ik ben kanker-actueel aan het herzien en heb onderaan het artikel uit 2004 enkele studies gedaan met dit zogeheten adenovirus toegevoegd.

4 juni 2004: bron DOW en Yahoonews

Onderzoekers van Cancer Research UK aan de universiteit van Londen maken melding van een succesvolle trial met het inbrengen van een genbewerkt virus in kankercellen. Het zogenoemde adenovirus is dusdanig bewerkt dat het zich razendsnel verspreid in de kankercellen zelf maar de gezonde cellen ongemoeid laat omdat deze tijdig het virus herkennen en onschadelijk maken. Kankercellen lukt het echter niet dit virus onschadelijk te maken en het virus zorgt ervoor dat de kankercellen als het ware 'exploderen' zoals de onderzoekers dat omschrijven. Hier twee persberichten over dit toch wel opzienbarende nieuws.

Genetically-modified virus explodes cancer cells
By Shaoni Bhattacharya

A genetically-modified virus that exploits the selfish behaviour of cancer cells may offer a powerful and selective way of killing tumours.

Deleting a key gene from the virus enabled it to infect and burst cancer cells while leaving normal tissues unharmed, reveals a study by researchers at Cancer Research UK and Queen Mary's School of Medicine and Dentistry, University of London.

Viruses spread by infiltrating the cells of their host. Normally, the detection of an intruder by a cell triggers a process called apoptosis, which causes the cell to commit suicide and prevents the virus spreading further. However, viruses can carry genes that allow them to slip past this cell death process in normal cells, causing infection.

The UK researchers deleted one such gene in an adenovirus. This meant that the virus was immediately detected by normal cells and was unable to spread. But in cancer cells, which grow uncontrollably and ignore the cell death process, the virus was able to thrive and spread rapidly. It then multiplied so vigorously that it killed the cancer cells by making them explode.

"The great thing about this strategy is that the cancer cell does all the hard work," says Nick Lemoine, director of the Cancer Research UK Clinical Centre at Bart's Medical School, who led the team. "It makes more and more virus to infect its neighbouring cancer cells. But if a normal cell is infected, it commits suicide before it can make new virus and spread of the virus is contained."

Unexpected benefit

The gene the team deleted from the adenovirus is called E1B-19kD. But, as well as removing the cloak the viruses normally use to evade detection by cells, it had another "unexpected" effect, says Lemoine.

This was enabling the viruses to replicate much faster than normal, which in turn helped burst the cancer cells. Previous GM viruses have not shown this effect.

The team examined the effects of the GM virus on pancreatic, lung, ovarian, liver and colorectal cancers in the test tube, as well as on live tumour-bearing mice. The team plans to test the GM virus in clinical trials in people in 2005.

"In tests so far it has proven both potent and selective, although only clinical trials will tell us whether the approach can be an effective treatment in people, "comments Robert Souhami, Cancer Research UK's director of clinical and external affairs.

Lemoine adds that the GM virus could also be armed with additional anti-cancer weapons, in the form of genes producing toxic compounds. "The fact that we have taken a gene out of the viral backbone means we could arm the virus with something that deliberately kills cancer," he told New Scientist .

Journal reference: Molecular Therapy (DOI: 10.1016/j.ymthe.2004.03.017)

Ook het DOW journaal maakt melding van deze studiepublicaties:

-- =WSJ.COM/The Daily Scan: Genetically Altered Viruses --


By Mark Ingebretsen
Of THE WALL STREET JOURNAL ONLINE

NEW YORK (Dow Jones)--Researchers in the U.K. may have found one of the
closest things yet to a magic bullet in the battle against cancer.
By removing a genetic component from a virus, the scientists prompted "it to
infect and burst cancer cells while leaving normal tissues unharmed," according
to the New Scientist.
The modified virus is able to destroy cancer cells by taking advantage of
their so-called "selfish behavior." As a news release from the group, Cancer
Research UK, explained, the body's normal cells will self-destruct if infected
with a virus, and this suicidal behavior helps to prevent the virus from
spreading. Cancer cells, by contrast, "refuse to stop for anything - allowing
the virus to thrive." Thus, the selfish behavior on the part of the cancer cells
- that is their abject refusal to self-destruct on cue - allows "the
(genetically modified) virus to replicate and spread through tumor tissue," the
release said.
The news from Britain follows a Dow Jones Newswires story that reported: "New
cancer drugs that target tumors and leave healthy cells alone are changing the
face of cancer treatment."
"Unlike traditional chemotherapy, which often debilitates patients with severe
nausea, diarrhea or opportunistic infections, these targeted drugs attack tumor
cells directly and with fewer side effects."

 

Referenties van studies met BCL2 - adenovirus E1B 19kD

References

  1. BNIPL-2, a novel homologue of BNIP-2, interacts with Bcl-2 and Cdc42GAP in apoptosis. Qin, W., Hu, J., Guo, M., Xu, J., Li, J., Yao, G., Zhou, X., Jiang, H., Zhang, P., Shen, L., Wan, D., Gu, J. Biochem. Biophys. Res. Commun. (2003)
  2. BNIPL-2 promotes the invasion and metastasis of human hepatocellular carcinoma cells. Xie, L., Qin, W., Li, J., He, X., Zhang, H., Yao, G., Shu, H., Yao, M., Wan, D., Gu, J. Oncol. Rep. (2007)
  3. The BNIP-2 and Cdc42GAP homology/Sec14p-like domain of BNIP-Salpha is a novel apoptosis-inducing sequence. Zhou, Y.T., Soh, U.J., Shang, X., Guy, G.R., Low, B.C. J. Biol. Chem. (2002)
  4. The apoptosis-associated protein BNIPL interacts with two cell proliferation-related proteins, MIF and GFER. Shen, L., Hu, J., Lu, H., Wu, M., Qin, W., Wan, D., Li, Y.Y., Gu, J. FEBS Lett. (2003)
  5. Differential gene expression in human hepatocellular carcinoma Hep3B cells induced by apoptosis-related gene BNIPL-2. Xie, L., Qin, W.X., He, X.H., Shu, H.Q., Yao, G.F., Wan, D.F., Gu, J.R. World J. Gastroenterol. (2004)
  6. cDNA expression array analysis of gene expression in human hepatocarcinoma Hep3B cells induced by BNIPL-1. Xie, L., Qin, W.X., Li, J.J., He, X.H., Shu, H.Q., Yao, G.F., Wan, D.F., Gu, J.R. Acta Biochim. Biophys. Sin. (Shanghai) (2005)

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