Publications by authors named "K Burger"

Background: Early-life food exposures may influence food preferences and receptivity, thereby impacting long-term diet quality. Infant exposure to discretionary foods may be more detrimental for infants with high food approach traits; conversely, early exposure to fruits and vegetables may be more important for those with high food avoidance traits. This study investigated associations of infant food exposures with early childhood diet quality and whether these associations are modified by infant appetitive traits.

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Lymphoma is one of the leading causes of cancer and cancer deaths and yet has not been amenable to population screening. The role of methylated DNA markers (MDMs) in the detection of lymphoma has not been extensively studied. We aimed to discover, validate, and test tissue-derived MDMs of lymphoma in archival plasma specimens.

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Article Synopsis
  • A multicenter study aimed to evaluate the effectiveness of methylated DNA markers (MDMs) found in pancreatic juice (PJ) for detecting pancreatic ductal adenocarcinoma (PDAC) when used alone and in combination with a blood test, CA 19-9.
  • The analysis included DNA samples from 88 confirmed PDAC cases and 134 control cases, utilizing logistic regression to summarize accuracy through the area under the receiver-operating characteristic curve (AUROC).
  • Results showed that the combination model of PJ-MDMs and CA 19-9 achieved a higher accuracy (AUROC of 0.95) compared to using PJ-MDMs (0.87) or CA 19-9 alone (0
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Understanding the genetic ancestry of populations is central to numerous scientific and societal fields. It contributes to a better understanding of human evolutionary history, advances personalized medicine, aids in forensic identification, and allows individuals to connect to their genealogical roots. Existing methods, such as ADMIXTURE, have significantly improved our ability to infer ancestries.

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Long noncoding (lnc)RNAs emerge as regulators of genome stability. The nuclear-enriched abundant transcript 1 (NEAT1) is overexpressed in many tumors and is responsive to genotoxic stress. However, the mechanism that links NEAT1 to DNA damage response (DDR) is unclear.

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