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A lack of environmental education has been shown to lead to lower levels of environmental awareness and consequently fewer climate change prevention measures (Toksoz et al., 2011). Researchers who study this issue focus on identifying the populations most vulnerable to a lack of environmental awareness based on demographic factors like household income and education level (Ajuang et al., 2016; Philippsen et al., 2017; Sun et al., 2020). This research is essential in guiding future climate-related education efforts, but there is limited data on the topic. In order to fill in this research gap, this project focuses on the relationship between demographic factors and the environmental awareness of high school students in the Washington, D.C., metropolitan area. One hundred twenty-five high school students were surveyed, and data were collected relating to students' annual household income, parental/guardian education, age, gender, race, household recycling and gardening practices, and environmental awareness. It was found that, in general, students with higher household income levels, parental/guardian education levels, or age had higher levels of environmental awareness. However, students with the lowest parental education levels also showed increased environmental awareness compared to other lower levels. Male students tended to be slightly more environmentally aware than female students, and students whose families recycled or gardened regularly had higher levels of environmental awareness than those who did not. This information can help to guide future environmental education campaigns to improve environmental awareness levels and environmental relationships, which is needed to effectively address the risks posed by climate change.

EGFR is frequently mutated and amplified in lung adenocarcinomas sensitive to EGFR inhibitors gefitinib and erlotinib. A secondary mutation, T790M, has been associated with acquired resistance but has not been shown to be sufficient to render EGFR mutant/amplified lung cancers resistant to EGFR inhibitors. We created a model for studying acquired resistance to gefitinib by prolonged exposure of a gefitinib-sensitive lung carcinoma cell line (H3255; EGFR mutated and amplified) to gefitinib in vitro. The resulting resistant cell line acquired a T790M mutation in a small fraction of the amplified alleles that was undetected by direct sequencing and identified only by a highly sensitive HPLC-based technique. In gefitinib-sensitive lung cancer cells with EGFR mutations and amplifications, exogenous introduction of EGFR T790M effectively conferred resistance to gefitinib and continued ErbB-3/PI3K/Akt signaling when in cis to an activating mutation. Moreover, continued activation of PI3K signaling by the PIK3CA oncogenic mutant, p110alpha E545K, was sufficient to abrogate gefitinib-induced apoptosis. These findings suggest that allelic dilution of biologically significant resistance mutations may go undetected by direct sequencing in cancers with amplified oncogenes and that restoration of PI3K activation via either a T790M mutation or other mechanisms can provide resistance to gefitinib.

Somatic mutations in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) have recently been described in patients with non–small-cell lung cancer (NSCLC) who achieve radiographic regressions to the EGFR inhibitor gefitinib. One of these mutations, L858R (Leu→Arg), is also found in NSCLC cell line H3255, which is very sensitive to gefitinib treatment. We characterized nine NSCLC cell lines (three isolated from patients with bronchioloalveolar carcinoma and six isolated from patients with adenocarcinoma) for their in vitro sensitivity to gefitinib. Of these, only H3255 (EGFRL858R) and H1666 (EGFRWT) are sensitive to gefitinib with IC50 values of 40 nmol/L and 2 μmol/L, respectively. We examined the effects of gefitinib on H3255 and cell lines containing wild-type EGFR that are either sensitive (H1666) or resistant (A549 and H441) to gefitinib exposure in vitro. Gefitinib treatment (1 μmol/L) leads to significant apoptosis accompanied by increased poly(ADP-ribose) polymerase cleavage only in the H3255 cell line, leads to G1-S arrest in H1666, and has no effects in the A549 and H441 cell lines. Although EGFR and AKT are constitutively phosphorylated in H3255, H1666, and H441 cell lines, AKT is completely inhibited by gefitinib treatment only in the H3255 cell line. These findings further characterize a mechanism by which gefitinib treatment of NSCLC harboring EGFRL858R leads to a dramatic response to gefitinib.

Receptor tyrosine kinase genes were sequenced in non–small cell lung cancer (NSCLC) and matched normal tissue. Somatic mutations of the epidermal growth factor receptor geneEGFRwere found in 15of 58 unselected tumors from Japan and 1 of 61 from the United States. Treatment with the EGFR kinase inhibitor gefitinib (Iressa) causes tumor regression in some patients with NSCLC, more frequently in Japan.EGFRmutations were found in additional lung cancer samples from U.S. patients who responded to gefitinib therapy and in a lung adenocarcinoma cell line that was hypersensitive to growth inhibition by gefitinib, but not in gefitinib-insensitive tumors or cell lines. These results suggest thatEGFRmutations may predict sensitivity to gefitinib.