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Status |
Public on Feb 10, 2009 |
Title |
Mammary tumors from K14-cre; ApcCKO/+ mice vs control mammary glands |
Organism |
Mus musculus |
Experiment type |
Expression profiling by array
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Summary |
Many components of Wnt/β-catenin signaling pathway also play critical roles in mammary tumor development. To study the role of Apc in mammary tumorigensis, we introduced conditional Apc mutations specifically into two different mammary epithelial populations using K14-Cre (progenitor) and WAP-cre (lactaing luminal) transgenic mice. Only the K14-cre mediated Apc heterozygosity developed mammary adenocarcinomas demonstrating histological and molecular heterogeneity, suggesting the progenitor cell origin of these tumors. These tumors harbored truncation mutation in a very defined region in the remaining wild-type allele of Apc that would retain some down-regulating activity of β-catenin signaling. Our results suggest that not only the epithelial origin but also a certain Apc mutations are selected to achieve a specific level of β-catenin signaling optimal for mammary tumor development.
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Overall design |
We have compared 3 mammary tumors from K14-cre; ApcCKO/+ mice with 3 control mammary glands.
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Contributor(s) |
Kuraguchi M, Ohene-Baah NY, Sonkin D, Bronson RT, Kucherlapati R |
Citation(s) |
19197353 |
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Submission date |
Feb 09, 2009 |
Last update date |
Feb 11, 2019 |
Contact name |
Dmitriy Sonkin |
Organization name |
Novartis Institutes for BioMedical Research
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Street address |
250 Massachusetts Avenue
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City |
Cambridge |
State/province |
MA |
ZIP/Postal code |
02139 |
Country |
USA |
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Platforms (1) |
GPL1261 |
[Mouse430_2] Affymetrix Mouse Genome 430 2.0 Array |
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Samples (6)
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GSM368467 |
control mammary gland, biological replicate 1 |
GSM368468 |
control mammary gland, biological replicate 2 |
GSM368469 |
control mammary gland, biological replicate 3 |
GSM368470 |
mammary tumor, biological replicate 1 |
GSM368471 |
mammary tumor, biological replicate 2 |
GSM368472 |
mammary tumor, biological replicate 3 |
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Relations |
BioProject |
PRJNA112245 |