Is There an Increasing Interest in Facial Feminization Surgery? A Search Trends Analysis.

Facial feminization surgery (FFS) has increased in prevalence and recent studies show that transgender women are just as likely to want facial feminization surgery compared to genital affirmation surgery. While previous research has demonstrated an increase in individuals seeking gender affirmation surgery, little is known on the prevalence of facial feminization surgery. Categorizing the number of facial feminization surgeries performed is difficult given lack of reimbursement rates and paucity of centers of excellence which publish data on their case numbers.

Craniofacial Microsomia.

Craniofacial microsomia (CFM) encompasses a broad spectrum of phenotypes. It is thought to result from defective development of the first and second pharyngeal arch structures, and generally presents with anomalies of the mandible and other facial bones, ears, and overlying soft tissues. The cause of CFM is thought to involve both extrinsic and genetic risk factors.

Antibodies directed against integration host factor mediate biofilm clearance from Nasopore.

Objectives/hypothesis: Intranasal resorbable packing, such as Nasopore, is commonly used during sinus surgery despite a paucity of evidence that demonstrates clinical benefit. We theorized that Nasopore supports bacterial growth and biofilm formation. The DNABII family of bacterial nucleic acid binding proteins stabilizes the extracellular polymeric substance of the biofilm, thus protecting bacteria from host defenses and traditional antibiotics.

Integrative genomic and proteomic analyses identify targets for Lkb1-deficient metastatic lung tumors.

In mice, Lkb1 deletion and activation of Kras(G12D) results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and metastatic de novo lung cancers with integrated genomic and proteomic profiles, and have identified gene and phosphoprotein signatures associated with Lkb1 loss and progression to invasive and metastatic lung tumors. These studies revealed that SRC is activated in Lkb1-deficient primary and metastatic lung tumors, and that the combined inhibition of SRC, PI3K, and MEK1/2 resulted in synergistic tumor regression.

HIF2alpha cooperates with RAS to promote lung tumorigenesis in mice.

Members of the hypoxia-inducible factor (HIF) family of transcription factors regulate the cellular response to hypoxia. In non-small cell lung cancer (NSCLC), high HIF2alpha levels correlate with decreased overall survival, and inhibition of either the protein encoded by the canonical HIF target gene VEGF or VEGFR2 improves clinical outcomes. However, whether HIF2alpha is causal in imparting this poor prognosis is unknown.

Sunitinib prolongs survival in genetically engineered mouse models of multistep lung carcinogenesis.

Non-small cell lung cancer (NSCLC) has a poor prognosis, with substantial mortality rates even among patients diagnosed with early-stage disease. There are few effective measures to block the development or progression of NSCLC. Antiangiogenic drugs represent a new class of agents targeting multiple aspects of tumor progression, including cell proliferation, invasion, migration, and outgrowth of metastatic deposits.

HER2YVMA drives rapid development of adenosquamous lung tumors in mice that are sensitive to BIBW2992 and rapamycin combination therapy.

Mutations in the HER2 kinase domain have been identified in human clinical lung cancer specimens. Here we demonstrate that inducible expression of the most common HER2 mutant (HER2(YVMA)) in mouse lung epithelium causes invasive adenosquamous carcinomas restricted to proximal and distal bronchioles. Continuous expression of HER2(YVMA) is essential for tumor maintenance, suggesting a key role for HER2 in lung adenosquamous tumorigenesis.