Journal
CANCER RESEARCH
Volume 66, Issue 14, Pages 6964-6971Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-06-0505
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Funding
- NCI NIH HHS [CA-21765] Funding Source: Medline
- NINDS NIH HHS [NS-37956] Funding Source: Medline
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The sonic hedgehog (SHH) receptor Patched 1 (Ptch1) is critical for embryonic development, and its loss is linked to tumorigenesis. Germ line inactivation of one copy of Ptch1 predisposes to basal cell carcinoma and medulloblastoma in mouse and man. In many cases, medulloblastoma arising from perturbations of Ptch1 function leads to a concomitant up-regulation of a highly similar gene, Patched2 (Ptch2). As increased expression of Ptch2 is associated with medulloblastoma and other tumors, we investigated the role of Ptch2 in tumor suppression by generating Ptch2-deficient mice. In striking contrast to Ptch1(-/-) mice, Ptch2(-/-) animals were born alive and showed no obvious defects and were not cancer prone. However, loss of Ptch2 markedly affected tumor formation in combination with Ptch1 haploinsufficiency. Ptch1(+/-)Ptch2(-/-) and Ptch(+/1)Ptch2(+/-) animals showed a higher incidence of tumors and a broader spectrum of tumor types compared with Ptch1(+/-) animals. Therefore, Ptch2 modulates tumorigenesis associated with Ptch1 haploinsufficiency.
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