Correction to: Extreme Precipitation, Public Health Emergencies, and Safe Drinking Water in the USA.

Unfortunately, the original publication of this article contained mistakes. The publisher introduced an error after proofreading where the name of the co-author was mistakenly captured as "David P. E. Harvey". The correct name should be "David E. Harvey".

Extreme Precipitation, Public Health Emergencies, and Safe Drinking Water in the USA.

PURPOSE OF REVIEW: This review examines the effectiveness of drinking water regulations to inform public health during extreme precipitation events. This paper estimates the vulnerability of specific populations to flooding in their public water system, reviews the literature linking precipitation to waterborne outbreaks, examines the role that Safe Drinking Water Act and Public Notification (PN) Rule have in public health emergencies, and reviews the effectiveness of the PN Rule during the 2017 Hurricane Maria in Puerto Rico. RECENT FINDINGS: Public water systems in large metropolitan areas have substantial portions of their customer base at risk for a waterborne outbreak during a flooding event. The PN Rule are ambiguous for who is responsible for declaring a "waterborne emergency" following a natural disaster like Hurricane Maria. Revisions to the current PN Rule that mandate public notification and water quality sampling during extreme precipitation events are necessary to ensure the public is aware of their drinking water quality following these events.

Concurrent MEK2 mutation and BRAF amplification confer resistance to BRAF and MEK inhibitors in melanoma.

Although BRAF and MEK inhibitors have proven clinical benefits in melanoma, most patients develop resistance. We report a de novo MEK2-Q60P mutation and BRAF gain in a melanoma from a patient who progressed on the MEK inhibitor trametinib and did not respond to the BRAF inhibitor dabrafenib. We also identified the same MEK2-Q60P mutation along with BRAF amplification in a xenograft tumor derived from a second melanoma patient resistant to the combination of dabrafenib and trametinib. Melanoma cells chronically exposed to trametinib acquired concurrent MEK2-Q60P mutation and BRAF-V600E amplification, which conferred resistance to MEK and BRAF inhibitors. The resistant cells had sustained MAPK activation and persistent phosphorylation of S6K. A triple combination of dabrafenib, trametinib, and the PI3K/mTOR inhibitor GSK2126458 led to sustained tumor growth inhibition. Hence, concurrent genetic events that sustain MAPK signaling can underlie resistance to both BRAF and MEK inhibitors, requiring novel therapeutic strategies to overcome it.