Harvard University Museum of Comparative Zoology (MCZ) 1352 is a partial maxillary toothplate of a basal reptilian from the Lower Permian of Baylor County, north-central Texas. The specimen displays the straight rows of teeth characteristic of the subfamily Moradisaurinae (family: Captorhinidae) and is nearly identical in shape to the maxilla of Labidosaurikos meachami. Larger, more mesial individual teeth conform to the dental pattern previously determined for adults of the genus. Adults of L. meachami are known to possess six maxillary tooth rows, whereas MCZ 1352 has only five. Although only a partial specimen, it appears MCZ 1352 is most likely a juvenile specimen of L. meachmi. If correct, the comparative sizes suggest isometric growth of this element. The orientation of the lingual-most row of teeth, and the five as opposed to six maxillary tooth rows, suggest either new tooth rows may move labially during development or bone growth and remodeling occur lingually, resulting in the development of a margin of maxillary bone between the fifth row and the lingual edge.

Cyclooxygenase-2 (COX-2) catalyzes the rate-limiting step in the synthesis of prostaglandins. Its overexpression induces numerous tumor-promoting phenotypes and is associated with cancer metastasis and poor clinical outcome. Although COX-2 inhibitors are promising chemotherapeutic and chemopreventative agents for cancer, the risk of significant cardiovascular and gastrointestinal complications currently outweighs their potential benefits. Systemic complications of COX-2 inhibition could be avoided by specifically decreasing COX-2 expression in epithelial cells. To that end, we have investigated the signal transduction pathway regulating the COX-2 expression in response to DNA damage in breast epithelial cells. In variant human mammary epithelial cells that have silenced p16 (vHMEC), double-strand DNA damage or telomere malfunction results in a p53- and activin A-dependent induction of COX-2 and continued proliferation. In contrast, telomere malfunction in HMEC with an intact p16/Rb pathway induces cell cycle arrest. Importantly, in ductal carcinoma in situ lesions, high COX-2 expression is associated with high gammaH2AX, TRF2, activin A, and telomere malfunction. These data show that DNA damage and telomere malfunction can have both cell-autonomous and cell-nonautonomous consequences and can provide a novel mechanism for the propagation of tumorigenesis.