Abstract | BACKGROUND: RESULTS: PDAC tumors were initiated in LSL-Kras G12D/+ ;Trp53 flox/flox ;Pdx-1-Cre (KP-/-C) mice harboring a conditional Pkm2 allele. Immunohistochemical analysis showed PKM2 expression in wild-type tumors and loss of PKM2 expression in tumors from Pkm2 conditional mice. PKM2 deletion had no effect on overall survival or tumor size. Loss of PKM2 resulted in pyruvate kinase M1 (PKM1) expression, but did not affect the number of proliferating cells. These findings are consistent with results in other cancer models. CONCLUSIONS: PKM2 is not required for initiation or growth of PDAC tumors arising in the KP-/-C pancreatic cancer model. These findings suggest that, in this mouse PDAC model, PKM2 expression is not required for pancreatic tumor formation or progression.
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Authors | Alissandra L Hillis, Allison N Lau, Camille X Devoe, Talya L Dayton, Laura V Danai, Dolores Di Vizio, Matthew G Vander Heiden |
Journal | Cancer & metabolism
(Cancer Metab)
Vol. 6
Pg. 17
( 2018)
ISSN: 2049-3002 [Print] England |
PMID | 30386596
(Publication Type: Journal Article)
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