BEGIN:VCALENDAR VERSION:2.0 METHOD:PUBLISH PRODID:-//Telerik Inc.//Sitefinity CMS 15.2//EN BEGIN:VTIMEZONE TZID:Eastern Standard Time BEGIN:STANDARD DTSTART:20251102T020000 RRULE:FREQ=YEARLY;BYDAY=1SU;BYHOUR=2;BYMINUTE=0;BYMONTH=11 TZNAME:Eastern Standard Time TZOFFSETFROM:-0400 TZOFFSETTO:-0500 END:STANDARD BEGIN:DAYLIGHT DTSTART:20250301T020000 RRULE:FREQ=YEARLY;BYDAY=2SU;BYHOUR=2;BYMINUTE=0;BYMONTH=3 TZNAME:Eastern Daylight Time TZOFFSETFROM:-0500 TZOFFSETTO:-0400 END:DAYLIGHT END:VTIMEZONE BEGIN:VEVENT DESCRIPTION:Jessie Guo\, PhDTargeting Cancer Metabolism to Treat KRAS-drive n Lunch CancerMetabolic reprogramming is a hallmark of KRAS-driven non-sma ll cell lung cancer (NSCLC)\, yet the metabolic dependencies imposed by di stinct co-occurring mutations remain incompletely understood. Using geneti cally engineered mouse models and integrated metabolomic approaches\, we d emonstrated that both tumor-intrinsic and host autophagy support tumor met abolism and promote the progression of KRAS-driven lung cancer. We further identified genotype-specific metabolic vulnerabilities that can be therap eutically exploited. In particular\, we found that glucose-6-phosphate deh ydrogenase (G6PD) is selectively required for maintaining redox homeostasi s and tumor growth in LKB1-deficient (KL)\, but not TP53-deficient (KP)\, KRAS-driven lung cancer\, revealing a novel therapeutic vulnerability. Fin ally\, our ongoing work has identified methionine synthase (MTR) and folat e one-carbon metabolism as critical metabolic dependencies in KP lung tumo rs. Together\, these studies demonstrate how distinct oncogenic genotypes shape metabolic vulnerabilities and provide new opportunities for precisio n metabolic therapies in KRAS-driven lung cancer. DTEND:20260924T170000Z DTSTAMP:20260920T140409Z DTSTART:20260924T160000Z LOCATION:Ohio\,United States\,Cincinnati\,3125 Eden Ave SEQUENCE:0 SUMMARY:Vontz Center Cancer Seminar Series UID:RFCALITEM639255098493915138 X-ALT-DESC;FMTTYPE=text/html:

Jessie Guo\, PhD
Ta rgeting Cancer Metabolism to Treat KRAS-driven Lunch Cancer

Met abolic reprogramming is a hallmark of KRAS-driven non-small cell lung canc er (NSCLC)\, yet the metabolic dependencies imposed by distinct co-occurri ng mutations remain incompletely understood. Using genetically engineered mouse models and integrated metabolomic approaches\, we demonstrated that both tumor-intrinsic and host autophagy support tumor metabolism and promo te the progression of KRAS-driven lung cancer. We further identified genot ype-specific metabolic vulnerabilities that can be therapeutically exploit ed. In particular\, we found that glucose-6-phosphate dehydrogenase (G6PD) is selectively required for maintaining redox homeostasis and tumor growt h in LKB1-deficient (KL)\, but not TP53-deficient (KP)\, KRAS-driven lung cancer\, revealing a novel therapeutic vulnerability. Finally\, our ongoin g work has identified methionine synthase (MTR) and folate one-carbon meta bolism as critical metabolic dependencies in KP lung tumors. Together\, th ese studies demonstrate how distinct oncogenic genotypes shape metabolic v ulnerabilities and provide new opportunities for precision metabolic thera pies in KRAS-driven lung cancer.

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