Laura Jelliffe-Pawlowski

Faculty

Jelliffe-Pawlowski Headsot

Laura Jelliffe-Pawlowski

MS PhD

1 212 998 9020

433 First Ave
New York, NY 10010
United States

Laura Jelliffe-Pawlowski, PhD, MS, is a Professor. Prof. Jelliffe-Pawlowski’s research interests focus on understanding and addressing the drivers and consequences of adverse pregnancy outcomes with a special emphasis on preterm birth and associated racial/ethnic and socioeconomic inequities. Her work is highly transdisciplinary and looks at the interplay of biomolecular, social, and policy factors in observed patterns and outcomes. Her teaching and mentorship activities reflect this transdisciplinary approach with an emphasis on motivating the translation of research findings into action.

 

Prof. Jelliffe-Pawlowski leads a number of statewide, national, and international research efforts funded by the National Institutes of Health, the Bill and Melinda Gates Foundation, the March of Dimes, the State of California, and other entities. These includes, notably, the “Healthy Outcomes of Pregnancy for Everyone (HOPE)” consortium and study which focuses on understanding the experience of pregnant people and their infants pre- and post-COVID 19 pandemic. HOPE examines how biomolecular, social, and community factors affect the well-being and outcomes of mothers and infants and includes enrollment during pregnancy with outcome follow-up to 18-months after birth. Other ongoing projects include, for example, the NIH funded “Prediction Of Maturity, Morbidity, and Mortality in PreTerm Infants (PROMPT)”, study which focuses on examining the metabolic profiles of newborns with early preterm birth and associated outcomes, the “Transforming Health and Reducing PerInatal Anxiety through Virtual Engagement (THRIVE)”, randomized control trial (RCT), funded by the State of California which examines whether digital cognitive behavior therapy delivered by mobile app can assist in reducing anxiety symptoms in pregnant people and also examines participant acceptability of the application. Ongoing efforts also include leading the “California Prediction of Poor Outcomes of Pregnancy (CPPOP)” cohort study which focuses on investigating multi-omic drivers of preterm birth. The study interrogates biomolecular signals associated with preterm birth and includes full genome sequencing and mid-pregnancy biomolecular signaling related to metabolic, immune, stress, and placental function in hundreds of pregnancies with and without preterm birth. 

 

Prior to her joining NYU Meyers, Prof. Jelliffe-Pawlowski was a Professor of Epidemiology & Biostatistics, Chief of the Division of Lifecourse Epidemiology, a Professor in the Institute of Global Health Sciences, and Director of Discovery and Precision Health for the UCSF California Preterm Birth Initiative in the University of California San Francisco (UCSF) School of Medicine. She has a lifetime appointment as an Emeritus Professor of Epidemiology & Biostatistics in the UCSF School of Medicine and continues to work closely with the new Center for Birth Equity at UCSF. Prior to her appointment at UCSF, she was a leader at the Genetic Disease Screening Program within the California Department of Public Health. 

 

Prof. Jelliffe-Pawlowski efforts have been highlighted in numerous academic and lay articles including in the New York Times, in WIRED Magazine, in the Atlantic, on CNN, and on MSNBC. In 2023, she was recognized by Forbes Magazine as one of the top 50 over 50 Innovators in the United States. She is also a Phase I and Phase II Bill and Melinda Gates Foundation Grand Challenges awardee for her work in the United States and Uganda which focused on the development and validation of newborn metabolic profile as a novel measure of gestational age in infants.

BA, Psychology, University of California Los Angeles
MS, Child Development, University of California Davis
PhD, Human Development, University of California Davis

Preterm Birth

Forbes 50 over 50 awardee in Innovation (2023)
Delegate, African Academy of Sciences (2016)
Governor Brown Appointee for the California Department of Public Health, Interagency Coordinating Council on Early Intervention
Awardee, Bill and Melinda Bates Foundation, Gates Grand Challenges Phase I and II

Risk of selected structural abnormalities in infants after increased nuchal translucency measurement

Baer, R. J., Norton, M. E., Shaw, G. M., Flessel, M. C., Goldman, S., Currier, R. J., & Jelliffe-Pawlowski, L. L. (2014). American Journal of Obstetrics and Gynecology, 211(6), 675.e1-675.e19. 10.1016/j.ajog.2014.06.025
Abstract
Abstract
OBJECTIVE: We sought to examine the association between increased first-trimester fetal nuchal translucency (NT) measurement and major noncardiac structural birth defects in euploid infants. STUDY DESIGN: Included were 75,899 singleton infants without aneuploidy or critical congenital heart defects born in California in 2009 through 2010 with NT measured between 11-14 weeks of gestation. Logistic binomial regression was employed to estimate relative risks (RRs) and 95% confidence intervals (CIs) for occurrence of birth defects in infants with an increased NT measurement (by percentile at crown-rump length [CRL] and by ≥3.5 mm compared to those with measurements <90th percentile for CRL). RESULTS: When considered by CRL adjusted percentile and by measurement ≥3.5 mm, infants with a NT ≥95th percentile were at risk of having ≥1 major structural birth defects (any defect, RR, 1.6; 95% CI, 1.3-1.9; multiple defects, RR, 2.1; 95% CI, 1.3-3.4). Infants with a NT measurement ≥95th percentile were at particularly high risk for pulmonary, gastrointestinal, genitourinary, and musculoskeletal anomalies (RR, 1.6-2.7; 95% CI, 1.1-5.4). CONCLUSION: Our findings demonstrate that risks of major pulmonary, gastrointestinal, genitourinary, and musculoskeletal structural birth defects exist for NT measurements ≥95th percentile. The ≥3-fold risks were observed for congenital hydrocephalus; agenesis, hypoplasia, and dysplasia of the lung; atresia and stenosis of the small intestine; osteodystrophies; and diaphragm anomalies.

Association of early-preterm birth with abnormal levels of routinely collected first- and second-trimester biomarkers

Jelliffe-Pawlowski, L. L., Shaw, G. M., Currier, R. J., Stevenson, D. K., Baer, R. J., O’Brodovich, H. M., & Gould, J. B. (2013). American Journal of Obstetrics and Gynecology, 208(6), 492.e1-492.e11. 10.1016/j.ajog.2013.02.012
Abstract
Abstract
Objective: The purpose of this study was to examine the relationship between typically measured prenatal screening biomarkers and early-preterm birth in euploid pregnancies. Study Design: The study included 345 early-preterm cases (<30 weeks of gestation) and 1725 control subjects who were drawn from a population-based sample of California pregnancies who had both first- and second-trimester screening results. Logistic regression analyses were used to compare patterns of biomarkers in cases and control subjects and to develop predictive models. Replicability of the biomarker early-preterm relationships that was revealed by the models was evaluated by examination of the frequency and associated adjusted relative risks (RRs) for early-preterm birth and for preterm birth in general (<37 weeks of gestation) in pregnancies with identified abnormal markers compared with pregnancies without these markers in a subsequent independent California cohort of screened pregnancies (n = 76,588). Results: The final model for early-preterm birth included first-trimester pregnancy-associated plasma protein A in the ≤5th percentile, second-trimester alpha-fetoprotein in the ≥95th percentile, and second-trimester inhibin in the ≥95th percentile (odds ratios, 2.3-3.6). In general, pregnancies in the subsequent cohort with a biomarker pattern that were found to be associated with early-preterm delivery in the first sample were at an increased risk for early-preterm birth and preterm birth in general (<37 weeks of gestation; adjusted RR, 1.6-27.4). Pregnancies with ≥2 biomarker abnormalities were at particularly increased risk (adjusted RR, 3.6-27.4). Conclusion: When considered across cohorts and in combination, abnormalities in routinely collected biomarkers reveal predictable risks for early-preterm birth.

A genome-wide association study (GWAS) for bronchopulmonary dysplasia

Wang, H., Julien, K. R., Stevenson, D. K., Hoffmann, T. J., Witte, J. S., Lazzeroni, L. C., Krasnow, M. A., Quaintance, C. C., Oehlert, J. W., Jelliffe-Pawlowski, L. L., Gould, J. B., Shaw, G. M., & O’Brodovich, H. M. (2013). Pediatrics, 132(2), 290-297. 10.1542/peds.2013-0533
Abstract
Abstract
OBJECTIVE: Twin studies suggest that heritability of moderate-severe bronchopulmonary dysplasia (BPD) is 53% to 79%, we conducted a genome-wide association study (GWAS) to identify genetic variants associated with the risk for BPD. METHODS: The discovery GWAS was completed on 1726 very low birth weight infants (gestational age = 250-296/7 weeks) who had a minimum of 3 days of intermittent positive pressure ventilation and were in the hospital at 36 weeks' postmenstrual age. At 36 weeks' postmenstrual age, moderate-severe BPD cases (n = 899) were defined as requiring continuous supplemental oxygen, whereas controls (n = 827) inhaled room air. An additional 795 comparable infants (371 cases, 424 controls) were a replication population. Genomic DNA from case and control newborn screening bloodspots was used for the GWAS. The replication study interrogated single-nucleotide polymorphisms (SNPs) identified in the discovery GWAS and those within the HumanExome beadchip. RESULTS: Genotyping using genomic DNA was successful. We did not identify SNPs associated with BPD at the genome-wide significance level (5 3 1028) and no SNP identified in previous studies reached statistical significance (Bonferroni-corrected P value threshold .0018). Pathway analyses were not informative. CONCLUSIONS: We did not identify genomic loci or pathways that account for the previously described heritability for BPD. Potential explanations include causal mutations that are genetic variants and were not assayed or are mapped to many distributed loci, inadequate sample size, race ethnicity of our study population, or case-control differences investigated are not attributable to underlying common genetic variation. Pediatrics 2013;132:290-297

High Quality Genome-Wide Genotyping from Archived Dried Blood Spots without DNA Amplification

St. Julien, K. R., Jelliffe-Pawlowski, L. L., Shaw, G. M., Stevenson, D. K., O’Brodovich, H. M., & Krasnow, M. A. (2013). PloS One, 8(5). 10.1371/journal.pone.0064710
Abstract
Abstract
Spots of blood are routinely collected from newborn babies onto filter paper called Guthrie cards and used to screen for metabolic and genetic disorders. The archived dried blood spots are an important and precious resource for genomic research. Whole genome amplification of dried blood spot DNA has been used to provide DNA for genome-wide SNP genotyping. Here we describe a 96 well format procedure to extract DNA from a portion of a dried blood spot that provides sufficient unamplified genomic DNA for genome-wide single nucleotide polymorphism (SNP) genotyping. We show that SNP genotyping of the unamplified DNA is more robust than genotyping amplified dried blood spot DNA, is comparable in cost, and can be done with thousands of samples. This procedure can be used for genome-wide association studies and other large-scale genomic analyses that require robust, high-accuracy genotyping of dried blood spot DNA.

Risk of bronchopulmonary dysplasia by second-trimester maternal serum levels of α-fetoprotein, human chorionic gonadotropin, and unconjugated estriol

Jelliffe-Pawlowski, L. L., Shaw, G. M., Stevenson, D. K., Oehlert, J. W., Quaintance, C., Santos, A. J., Baer, R. J., Currier, R. J., O’Brodovich, H. M., & Gould, J. B. (2012). Pediatric Research, 71(4), 399-406. 10.1038/pr.2011.73
Abstract
Abstract
INTRODUCTION: Although maternal serum α-fetoprotein (AFP), human chorionic gonandotropin (hCG), and estriol play important roles in immunomodulation and immunoregulation during pregnancy, their relationship with the development of bronchopulmonary dysplasia (BPD) in young infants is unknown despite BPD being associated with pre-and postnatal inflammatory factors. RESULTS: We found that these serum biomarkers were associated with an increased risk of BPD. Risks were especially high when AFP and/or hCG levels were above the 95th percentile and/or when unconjugated estriol (uE3) levels were below the 5th percentile (relative risks (RRs) 3.1-6.7). Risks increased substantially when two or more biomarker risks were present (RRs 9.9-75.9). DISCUSSION: Data suggested that pregnancies that had a biomarker risk and yielded an offspring with BPD were more likely to have other factors present that suggested early intrauterine fetal adaptation to stress, including maternal hypertension and asymmetric growth restriction. METHODS: The objective of this population-based study was to examine whether second-trimester levels of AFP, hCG, and uE3 were associated with an increased risk of BPD.

Second trimester serum predictors of congenital heart defects in pregnancies without chromosomal or neural tube defects

Jelliffe-Pawlowski, L., Baer, R., Moon-Grady, A. J., & Currier, R. J. (2011). Prenatal Diagnosis, 31(5), 466-472. 10.1002/pd.2720
Abstract
Abstract
Objective: To compare euploid pregnancies with congenital heart defects (CHDs) to similar pregnancies without CHDs on typically collected second trimester biomarker measurements. Method: Second trimester serum levels of alpha-fetoprotein (AFP), human chorionic gonadotrophin (hCG), and unconjugated estriol were compared for 306 CHD cases and 1224 no-CHD controls drawn from a sample of singleton pregnancies without chromosomal or neural tube defects (NTDs). Logistic regression models were built comparing biomarkers for cases and controls. Results: Regardless of the severity of defect, CHD cases were more likely to have unusually high AFP and/or hCG levels and/or unusually low hCG and/or uE3 levels [odds ratio (OR) 1.8-2.4, 95% confidence intervals (CIs) 1.2-4.0]. Cases with critical CHDs were more than twice as likely to have an AFP multiple of the median (MoM) ≥ the 95th percentile and/or an hCG and/uE3 MoM ≤ the 5th percentile (OR 2.1-3.9, 95% CIs 1.1-7.8). Conclusion: Abnormal levels of specific second trimester maternal serum biomarkers indicated an increased risk for CHDs among this sample of low risk pregnancies. Our data suggest that future efforts aimed at improving CHD detection in low risk pregnancies may benefit from considering serum biomarkers.

Second trimester serum predictors of preterm birth in a population-based sample of low-risk pregnancies

Jelliffe-Pawlowski, L. L., Baer, R. J., & Currier, R. J. (2010). Prenatal Diagnosis, 30(8), 727-733. 10.1002/pd.2489
Abstract
Abstract
Objective: To examine the relationship between typically collected second trimester maternal serum biomarkers and preterm birth among pregnancies without intrauterine-growth-retardation or other specific risk factors. Methods: Included were 102 861 singleton pregnancies without specific risks that resulted in the live birth of an infant of normal birth weight for gestational age without aneuploidy or a neural tube defect. Logistic binomial regression analyses were used to estimate the relative risk (RR) of giving birth preterm among pregnancies with an abnormal level of alpha-fetoprotein (AFP), human chorionic gonatotropin (hCG), and/or unconjugated estriol (uE3) compared to pregnancies with normal biomarker levels. Results: When compared to pregnancies with normal levels of AFP, hCG, and uE3, pregnancies with elevated levels of any biomarker [multiple of the median (MoM) ≥2.0] were at an increased risk for preterm birth regardless of preterm grouping (RRs 1.3-5.4). Risks for preterm birth tended to increase substantially when at least two biomarkers were elevated (RRs 2.2-18.7). Conclusion: The results suggest that second trimester maternal serum biomarkers may help identify pregnancies at increased risk for preterm birth when no other identified risks are present. Data indicates that biomarkers may be particularly predictive of early preterm birth.

Identification of second trimester screen positive pregnancies at increased risk for congenital heart defects

Jelliffe-Pawlowski, L. L., Walton-Haynes, L., & Currier, R. J. (2009). Prenatal Diagnosis, 29(6), 570-577. 10.1002/pd.2239
Abstract
Abstract
Objective: To examine whether second trimester biomarkers could be used to identify screen positive pregnancies at increased risk for congenital heart defects (CHDs) and measure the effect of using different biomarker cut points on the detection of CHDs and on the performance of predictive models. Methods: Included were 19,402 pregnancies without chromosomal defects, which were screen positive for Down syndrome or other birth defects based on maternal serum measurements of alpha-fetoprotein (AFP), human chorionic gonadotrophin (hCG), and unconjugated estriol (uE3). Logistic regression models were built that compared biomarkers for CHD cases compared to controls. Results: CHD cases were more likely to be screen positive for trisomy-18, to have a nuchal fold (NF) ≥5 mm, and/or to have an hCG multiple of the median (MoM) ≥95th percentile in models that considered screen positive grouping. In models that did not consider screen positive grouping, cases were more likely to have a NF ≥5 mm, an AFP MoM ≤10th percentile, an hCG MoM ≤25th percentile, and/or an hCG MoM ≥75th percentile. Conclusion: Along with NF, second trimester maternal serum biomarkers may be useful indicators for fetal and newborn evaluation for CHDs in screen positive pregnancies without identified chromosomal defects.

Triple-marker prenatal screening program for chromosomal defects

Kazerouni, N. N., Cunier, B., Malm, L., Riggle, S., Hodgkinson, C., Smith, S., Tempelis, C., Lorey, F., Davis, A., Jelliffe-Pawlowski, L., Walton-Haynes, L., & Roberson, M. (2009). Obstetrics and Gynecology, 114(1), 50-58. 10.1097/AOG.0b013e3181a9479e
Abstract
Abstract
OBJECTIVE: To examine screening performance of California's triple-marker screening program, using data from a statewide registry for chromosomal defects. METHODS: This study included 752,686 women who received a screening risk and had an expected date of delivery between July 2005 and the end of June 2007. Follow-up diagnostic services for screen-positive women were performed at state-approved centers. Data on diagnostic outcomes from these visits were entered into the California Chromosomal Defect Registry (CCDR). Other CCDR sources include mandatory reporting by all cytogenetic laboratories and hospitals and outcome data forms submitted by prenatal care providers. RESULTS: The observed detection rate for Down syndrome (N = 1,217) was 77.4%. It varied significantly by gestational dating method and maternal age. The rates for women aged younger than 35 years and 35 years and older were 62.4% and 94.0%, respectively. The detection rates were 81.3% for ultrasound-dated pregnancies and 67.5% for last menstrual period-dated pregnancies. For Turner syndrome, trisomy 18, triploidy, and trisomy 13, the detection rates were 79.4%, 82.5%, 98.1%, and 36.0%, respectively. The positive rate for Down syndrome was 5.4%. Of women with a Down syndrome fetus who were screen positive, only 49.5% opted for amniocentesis. Of women who obtained results from amniocentesis indicating a Down syndrome fetus, 61.4% had an elective termination, 26.2% had a live birth, 4.5% had a death or miscarriage, and 7.9% had an unknown outcome. CONCLUSION: The observed performance of this large triple-marker screening program exceeds generally predicted detection rates for Down syndrome. This study methodology will be used to measure the performance of subsequent screening enhancements.

Using second trimester ultrasound and maternal serum biomarker data to help detect congenital heart defects in pregnancies with positive triple-marker screening results

Jelliffe-Pawlowski, L. L., Walton-Haynes, L., & Currier, R. J. (2008). American Journal of Medical Genetics, Part A, 146(19), 2455-2467. 10.1002/ajmg.a.32513
Abstract
Abstract
Congenital heart defects (CHDs) are the most common of all birth defects. For many newborns with a CHD, prenatal versus postnatal detection is associated with substantially decreased morbidity and mortality risks. Although technological advances in fetal echocardiography have led to an increased capacity to detect CHDs prenatally, pregnancies without an identified risk factor are not routinely screened. With the aim of identifying pregnancies at increased risk for CHDs, this study examined the relationship between CHDs and typically collected second trimester biomarker data collected on a large population-based sample of singleton pregnancies with one or more second trimester screen positive result for Down syndrome, trisomy 18 (T-18), Smith-Lemli-Opitz syndrome (SLOS), or a neural tube defect (NTD). Where possible, logistic models for cases and controls were built and potential referral models were tested among study subsamples with information on the presence or absence of CHDs reported pre- and perinatally. When considered in combination, screen positive for T-18, screen positive for SLOS, nuchal fold measurement ≥ 5 mm, and/or having an adjusted hCG multiple of the median ≥ the 95th centile detected 42.7% of all pregnancies with a CHD in the combined subsample (where co-occurrence with chromosomal defects was not considered) and detected 29.7% of all pregnancies with a CHD in the no-chromosomal defect subsample. A nuchal fold measurement ≥ 5 mm detected 18.2% of those with a CHD in the Down syndrome subsample and an adjusted hCG multiple of the median (MoM) ≤ 5th centile detected 92.9% of those with a CHD in the T-18 subsample.