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hours per week. This association was<br />

observed among participants without<br />

a CRC family history and was more<br />

pronounced for rectal cancer. Overweight<br />

or obese participants were pronounced<br />

to be more susceptible. Researchers<br />

suggest further studies to be conducted<br />

to elucidate the underlying biological<br />

mechanism that may explain this<br />

phenomenon.<br />

Biomarkers open new gateways<br />

towards precision medicine for pain<br />

Niculescu et al open door towards<br />

precision medicine for pain,<br />

with the objective to determine<br />

the severity of a patient’s suffering.<br />

The study tracked hundreds of<br />

participants to identify biomarkers<br />

that can help determine the severity<br />

of a patient’s pain. The researchers<br />

were able to find a handful of genes<br />

that correlated to pain state and of<br />

future emergency department (ED)<br />

visits for pain. The genes which the<br />

scientists were able to correlate with<br />

pain were MFAP3, GNG7, CNTN1,<br />

LY9, CCDC144B, and GBP1. Using<br />

bioinformatic drug repurposing<br />

analyses, they were able to find<br />

novel drug compounds that would<br />

selectively target these genes and<br />

could be used to not only measure<br />

pain level but also inform the drug<br />

discovery process to use these<br />

genetic biomarkers to create more<br />

personalized treatments for pain.<br />

MFAP3, which had no prior evidence<br />

in the literature for involvement<br />

in pain, showed the most robust<br />

empirical evidence acting as a strong<br />

predictor for pain in the independent<br />

cohorts. The breakthrough research<br />

could help overcome the massive<br />

negative impact of untreated pain<br />

on quality of life, helping determine<br />

the appropriateness of treatment,<br />

and the severe addiction gateway<br />

potential of existing opioid-based<br />

pain medications.<br />

Source:MolecularPsychiatry(<strong>2019</strong>) https://<br />

www.nature.com/articles/s41380-018-0345-<br />

5#Sec23<br />

Source: JNCI Cancer Spectrum, Volume 2, Issue 4,<br />

1 November 2018, pky073,https://doi.org/10.1093/<br />

jncics/pky073<br />

Transplanted β cells<br />

rapidly restore glucose<br />

tolerance in mice<br />

Leonardo Velazco-Cruz et al<br />

demonstrated a breakthrough study<br />

by converting human pluripotent stem<br />

cells (hPSCs) into stem cell-derived<br />

β cells (SC-β cells) as a promising<br />

alternative source for diabetes cell<br />

replacement therapy. The researchers<br />

developed functioning healthy SC-β<br />

cells in vitro using an enriched serumfree<br />

media. On transplanting them into<br />

mice, the cells began to produce insulin<br />

and respond to blood sugar within<br />

days. Researchers introduced a new<br />

differentiation strategy which focused<br />

on modulating transforming growth<br />

factor β (TGF-β) signaling. This helps<br />

in controlling cellular cluster size, and<br />

express β cell markers and undergo GSIS<br />

(glucose stimulated-insulin secretion).<br />

The capacity of these cells to undergo<br />

GSIS with dynamic insulin release makes<br />

them a promising cell source for diabetes<br />

cellular therapy. This study provides<br />

insights into the role of TGF-β signaling<br />

in functional maturation where TGF-β<br />

inhibition has been shown to promote<br />

the replication of the cells. This helped<br />

protect against stress-induced loss of the<br />

phenotype and reduced apoptosis in a<br />

mouse model, which give hope<br />

for developing a potential cure for<br />

treating type 1 diabetes in the near<br />

future.<br />

Source: Stem Cell Reports | VOLUME 12, ISSUE<br />

2, P351-365, FEBRUARY 12, <strong>2019</strong> DOI: 10.1016/j.<br />

stemcr.2018.12.012<br />

—Compiled by Divya Choyikutty<br />

58 / FUTURE MEDICINE / <strong>March</strong> <strong>2019</strong>

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