Fandom

VroniPlag Wiki

Ww/Fragment 013 12

< Ww

31.366Seiten in
diesem Wiki
Seite hinzufügen
Diskussion0 Teilen

Störung durch Adblocker erkannt!


Wikia ist eine gebührenfreie Seite, die sich durch Werbung finanziert. Benutzer, die Adblocker einsetzen, haben eine modifizierte Ansicht der Seite.

Wikia ist nicht verfügbar, wenn du weitere Modifikationen in dem Adblocker-Programm gemacht hast. Wenn du sie entfernst, dann wird die Seite ohne Probleme geladen.


Typus
Verschleierung
Bearbeiter
SleepyHollow02
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 13, Zeilen: 12-29
Quelle: Stevenson 2004
Seite(n): 1773, Zeilen: 1773: r.col: 19ff
The translocation of the Philadelphia chromosome (Ph) generates a fusion gene called BCR-ABL. The translation product of this gene creates a constitutively active protein tyrosine kinase that induces and maintains leukemic transformation in chronic myelogenous leukemia and Ph-positive acute lymphoblastic leukemia. The siRNAs specific for the BCR-ABL transcript have been shown to silence the oncogenic fusion transcripts without affecting expression levels of normal c-ABL and c-BCR transcripts (Scherr et al, 2003; Wohlbold et al, 2003).

Pancreatic and colon carcinomas, in which RAS genes are often mutated, provide another example for potential RNAi applications. In many cases, the RAS oncogenes contain point mutations that differ by a single-base mutation from their normal counterparts. The use of retroviral vectors to introduce interfering RNAs specific for an oncogenic variant of KRAS (called K-RASV12) reduced the level of K-RASV12 transcripts and resulted in a loss of anchorage-independent growth and tumorigenicity (Brummelkamp et al, 2002). Studies of this kind provided proof-of-concept data for RNAi-based strategies aiming to reverse tumorigenesis.

1.2.2.2 Infectious diseases

The translocation of the Philadelphia chromosome (Ph) generates a fusion gene called BCR-ABL. The translation product of this gene creates a constitutively active protein tyrosine kinase that induces and maintains leukemic transformation in chronic myelogenous leukemia and Ph-positive acute lymphoblastic leukemia. The siRNAs specific for the BCR-ABL transcript have been shown to silence the oncogenic fusion transcripts without affecting expression levels of normal c-ABL and c-BCR transcripts.20,21

Pancreatic and colon carcinomas, in which RAS

[Seite 1775]

genes are often mutated, provide another example. In many cases, the RAS oncogenes contain point mutations that differ by a single-base mutation from their normal counterparts. The use of retroviral vectors to introduce interfering RNAs specific for an oncogenic variant of K-RAS (called K-RASV12) reduces the level of K-RASV12 transcripts and effects a loss of anchorage-independent growth and tumorigenicity.22,23 Studies of this kind provide proof-of-concept for RNAi-based strategies aimed at reversing tumorigenesis. [...]

[...]

Infectious Diseases


20. Scherr M, Battmer K, Winkler T, Heidenreich O, Ganser A, Eder M. Specific inhibition of bcr-abl gene expression by small interfering RNA. Blood 2003;101: 1566-9.

21. Wohlbold L, van der Kuip H, Miething C, et al. Inhibition of bcr-abl gene expression by small interfering RNA sensitizes for imatinib mesylate (STI571). Blood 2003; 102:2236-9.

22. Brummelkamp TR, Bernards R, Agami R. Stable suppression of tumorigenicity by virus-mediated RNA interference. Cancer Cell 2002;2:243-7.

23. Wilda M, Fuchs U, Wossmann W, Borkhardt A. Killing of leukemic cells with a BCR/ABL fusion gene by RNA interference (RNAi). Oncogene 2002;21:5716-24.

Anmerkungen

Kein Hinweis auf die Quelle.

Sichter
(SleepyHollow02), Hindemith

Auch bei Fandom

Zufälliges Wiki