Since the 1980's, prenatal care for pregnant women and their babies has improved maternal and neonatal health. However, despite prenatal care, the rate of some complications, such as major fetal anomalies, preterm labor, and low birth weight have not improved. Only 10.3% of Korean women of childbearing age take folic acid supplementation and approximately 14% still consume alcohol during pregnancy. Because in Korea about 50% of pregnancies are unintended, those women have higher exposure rates to alcohol, drugs, and ionizing radiation. Because most fetal anomalies occur between 5 to 10 gestational weeks, the initial prenatal care provided at 7 to 8 gestational weeks is too late to prevent fetal anomalies. Preconception care may identify and modify adverse health, behavioral, and social outcomes for women and their unborn babies. Recently, a number of preconception interventions have been reported to have evidence-based effectiveness in improving pregnancy outcomes. These include folic acid supplementation, avoiding alcohol intake, smoking cessation, counseling on potentially teratogenic drugs, infection control, immunizations, and control of chronic diseases such as diabetes, hypothyroidism, obesity. For the improvement of maternal and fetal health, guidelines for preconception care must be developed in Korea. All health care providers should understand the clinical importance of evidence-based preconception care.
Chronic Disease ; Counseling ; Female ; Folic Acid ; Health Personnel ; Humans ; Hypothyroidism ; Immunization ; Infant, Low Birth Weight ; Infant, Newborn ; Infection Control ; Korea ; Obesity ; Obstetric Labor, Premature ; Preconception Care ; Pregnancy ; Pregnancy Outcome ; Pregnant Women ; Prenatal Care ; Radiation, Ionizing ; Smoking Cessation ; Teratogens

Identification of the precise molecular pathways involved in oncogene-induced transformation may help us gain a better understanding of tumor initiation and promotion. Here, we demonstrate that SOX2 foregut epithelial cells are prone to oncogenic transformation upon mutagenic insults, such as Kras and p53 deletion. GFP-based lineage-tracing experiments indicate that SOX2 cells are the cells-of-origin of esophagus and stomach hyperplasia. Our observations indicate distinct roles for oncogenic KRAS mutation and P53 deletion. p53 homozygous deletion is required for the acquisition of an invasive potential, and Kras expression, but not p53 deletion, suffices for tumor formation. Global gene expression analysis reveals secreting factors upregulated in the hyperplasia induced by oncogenic KRAS and highlights a crucial role for the CXCR2 pathway in driving hyperplasia. Collectively, the array of genetic models presented here demonstrate that stratified epithelial cells are susceptible to oncogenic insults, which may lead to a better understanding of tumor initiation and aid in the design of new cancer therapeutics.