Allelic loss is a hallmark of tumor suppressor gene (TSG) inactivation. We have allelotyped 29 paired lymphoblastoid and lung cancer cell lines derived from 11 patients with small cell (SCLC) and 18 patients with non‐small cell lung carcinomas (NSCLC). Statistical analysis indicated that a threshold of 30% separated non‐random allelic loss from the random genetic deletions of malignancy. We have identified non‐random allelic loss at 42 of 54 (78%) specific chromosomal regions examined, with 22 regions (52%) common between the two major lung cancer histologic types. There were 3 regions (7%) with allelic loss specific for SCLC and 17 regions (41%) specific for NSCLC. Furthermore, there were significant differences in loss of heterozygosity (LOH) frequencies between NSCLC and SCLC at 13 regions on eight chromosome arms (3p, 5q, 6q, 9p, 10q, 11p, 13q, and 19p). Eight homozygous deletions were present in seven cell lines at four regions, 3p12, 3p14.2, 9p21, and 10q23–25. We have also identified novel sites of chromosomal deletions. In particular, there was frequent loss at 11p13 in SCLC and loss at 6p21.3 and 13q12.3 in NSCLC. In this study, we demonstrate that a) non‐random allelic losses in lung cancer involve multiple regions; b) some losses are common to both NSCLC and SCLC subtypes, whereas others are subtype specific; c) there are genetic deletions at novel chromosomal regions; and d) several homozygous deletions have been noted. Our studies demonstrate the usefulness of continuous cell lines for detailed allelotyping, for comparing genetic abnormalities between SCLC and NSCLC, and for identifying homozygous deletions. Genes Chromosomes Cancer 21:308–319, 1998. © 1998 Wiley‐Liss, Inc.

The main short-term neonatal consequence of chorioamnionitis is infection. Short-term neurologic morbidity in infants is related to labor complications and not chorioamnionitis per se.

Our results suggest a link between clinical chorioamnionitis and several indices of neonatal morbidity in the very low birth weight infant. Chorioamnionitis appears to make the very low birth weight infant particularly vulnerable to neurologic damage.

Objective: To determine the effects of clinical chorioamnionitis on neonatal morbidity and mortality in very low birth weight infants.Methods: This was an observational cohort analysis of all singleton live-born infants weighing 500 -1500 g at 24 weeks' or greater gestational age and born between 1988 and 1996 at Parkland Memorial Hospital, Dallas, Texas. Chorioamnionitis was diagnosed on the basis of maternal fever of 38C with supporting clinical evidence, which included fetal tachycardia, uterine tenderness, and/or malodorous infant, and the absence of another source of infection. Multiple logistic regression analysis was used to adjust for outcomes of interest.Results: Ninety-five of 1367 very low birth weight infants (7%) were exposed to chorioamnionitis. Neonatal sepsis, respiratory distress syndrome, seizure in the first 24 hours of life, intraventricular hemorrhage (grade 3 or 4), and periventricular leukomalacia were all significantly increased with chorioamnionitis, after adjusting for preterm ruptured membranes, pregnancy-associated hypertension, cesarean birth, gestational age, and birth weight. The odds ratios for intraventricular hemorrhage, periventricular leukomalacia, and seizures in the first 24 hours were 2.8 (95% confidence interval [CI] 1.6, 4.8), 3.4 (95% CI 1.6, 7.3), and 2.9 (95% CI 1.2, 6.8), respectively. Conclusion: Our results suggest a link between clinical chorioamnionitis and several indices of neonatal morbidity in the very low birth weight infant. Chorioamnionitis appears to make the very low birth weight infant particularly vulnerable to neurologic damage. (Obstet Gynecol 1998;91: 725-9. © 1998 by The American College of Obstetricians and Gynecologists.)Recently, Eschenbach 1 observed that chorioamnionitis, long considered primarily a maternal infection, instead may be primarily an infection that involves the fetus. Polymorphonuclear leukocytes in infected amniotic fluid of mothers carrying a male fetus have been shown by means of X and Y chromosome staining to be fetal in origin. 2 Moreover, recent reports suggest that there are heretofore unrecognized long-term consequences of fetal infection, which manifest as cerebral palsy, possibly explained by maternal mediators of infection that cross the placenta. 3 For example, inflammatory cytokines, such as tumor necrosis factor and interleukin-6, released during intrauterine infection, have been implicated in the genesis of the white matter lesions (periventricular leukomalacia) leading to cerebral palsy. 4 -6

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