Understanding family dynamics of obesity: Do parents and children lose and gain weight together?

BACKGROUND: Obesity is prevalent among children and adults. Yet, understanding the relationship between parent and child weight trajectories is limited. OBJECTIVE: (1) Examine the association between parent/child undesirable body mass index (BMI) category change. (2) Assess whether parental BMI category predicts child modified BMI z-score (mBMIz) annual change. METHODS: We conducted a cross-sectional study of weight trajectories of 3821 parent-child dyads between March 2020 and December 2021 within the NYC Health + Hospitals system. Undesirability of child and parental BMI category change and the magnitude of mBMIz change by parental BMI are analysed. RESULTS: Of 3821 children (mean [SD] baseline age, 9.84 [3.51]), 1889 were female. Of the 3220 parents (mean [SD] baseline age, 39.9 [8.51]), 2988 were female. Most children (53.52%) and parents (81.94%) presented with overweight and obesity. Undesirable BMI change in children was associated with concordant change in parents (adjusted OR: 1.7, 95% CI [1.45, 2.01], adjusted p < 0.001). Children of parents with obesity (adjusted coef: 0.076, 95% CI [0.004, 0.147], p < 0.038) and severe obesity (adjusted coef: 0.1317, 95% CI [0.024, 0.239], adjusted p < 0.016) demonstrated greater change in mBMIz than those of parents with normal weight or underweight. CONCLUSION: Parents and children have concordant weight trajectories, and public health interventions targeting both populations are essential.

Genome-wide analysis of therapeutic response uncovers molecular pathways governing tamoxifen resistance in ER+ breast cancer.

BACKGROUND: Prioritization of breast cancer patients based on the risk of resistance to tamoxifen plays a significant role in personalized therapeutic planning and improving disease course and outcomes. METHODS: In this work, we demonstrate that a genome-wide pathway-centric computational framework elucidates molecular pathways as markers of tamoxifen resistance in ER+ breast cancer patients. In particular, we associated activity levels of molecular pathways with a wide spectrum of response to tamoxifen, which defined markers of tamoxifen resistance in patients with ER+ breast cancer. FINDINGS: We identified five biological pathways as markers of tamoxifen failure and demonstrated their ability to predict the risk of tamoxifen resistance in two independent patient cohorts (Test cohort1: log-rank p-value = 0.02, adjusted HR = 3.11; Test cohort2: log-rank p-value = 0.01, adjusted HR = 4.24). We have shown that these pathways are not markers of aggressiveness and outperform known markers of tamoxifen response. Furthermore, for adoption into clinic, we derived a list of pathway read-out genes and their associated scoring system, which assigns a risk of tamoxifen resistance for new incoming patients. INTERPRETATION: We propose that the identified pathways and their read-out genes can be utilized to prioritize patients who would benefit from tamoxifen treatment and patients at risk of tamoxifen resistance that should be offered alternative regimens. FUNDING: This work was supported by the Rutgers SHP Dean's research grant, Rutgers start-up funds, Libyan Ministry of Higher Education and Scientific Research, and Katrina Kehlet Graduate Award from The NJ Chapter of the Healthcare Information Management Systems Society.