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Tobiloba Oni
8.6K posts

Tobiloba Oni
@CancerHacker
Hacking pancreatic cancer and anti-tumor immunity @WhiteheadInst. Valhalla Fellow. @Arsenal FC fanatic.
Cambridge, MA Katılım Mayıs 2009
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@NCICancerBio @BenStanger01 @rkalluriMDPhD @RonDePinho Beyond immunotherapies, it’s exciting to see a surge of preclinical work focused on maximizing the clinical potential of KRAS inhibitors. #PCAMChat24
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@NCICancerBio @BenStanger01 @rkalluriMDPhD @RonDePinho the key questions now are: which immunotherapies synergize best with KRAS inhibitors while minimizing toxicity, and how do different KRAS inhibitors compare in promoting this synergy?
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#PCAMChat24 A3: From a clinical/translational standpoint, we finally have drugs that can target KRAS in #PancreaticCancer. This gene is abnormal in >90% of cases, and it has taken four decades since the original discovery tofinally have a slew of drugs in the pipeline that can block aberrant KRAS function in patients. However, we also know that these drugs in and of themselves will not be effective and so a lot of preclinical (a.k.a. laboratory based, in experimental models) studies are ongoing looking at effective combinations that can sustain responses longer in patients, while ameliorating toxicities.
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@NCICancerBio A2: Major breakthroughs in #PancreaticCancer are impossible without fundamental research. We must understand the biological principles that make this disease so aggressive & resistant to most therapies. We can then turn this knowledge into predictive power & effective therapies
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@NCICancerBio @ednacukierman @DelgiornoKathy @CJHPhD @AshleyKiemen @Aiims1742 @KenOliveLab @MaraShermanLab @NinaSteele17 Hi everyone, I'm Tobiloba Oni from @WhiteheadInst. My lab’s mission is to unravel the cellular interaction circuits that drive aggressive biology and immune resistance in #PancreaticCancer. We also develop biologics to target these interactions for effective therapies
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Our latest work from lab member jimmy Ly! This fundamentally changed the way we see mitosis. Massive rewiring of translational control. There is something for everyone and an amazing mechanism. Check it out.
Whitehead Institute@WhiteheadInst
Cells make variants of thousands of proteins. These variants are not produced indiscriminately, but rather through precise regulatory mechanisms that can meet rapidly changing needs of the cell. New work from @iaincheeseman's lab in @Nature: wi.mit.edu/news/elegant-s… @MITBiology
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“There are not, and will never be, KRAS inhibitors” 👀
@Pasca_Lab presents a memorable reviewer comment from her 1st unfunded NIH grant at #AACRPan24.
The lesson is that you should not let deflating reviewer comments define the value of your science. Also, persistence!

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The company ran a 240 patient (!) randomized phase 2 trial of Simtuzumab in #PancreaticCancer that showed no therapeutic benefit.
academic.oup.com/oncolo/article…
As an angiogenesis inhibitor (versus the stated inhibition of LOXL2 catalytic activity) this was essentially a rerun of Gem plus Bev trial which had already failed years prior. Really infuriating.
Naftali Kaminski@KaminskiMed
Ever wondered why @gilead's Simtuzumab (Anti-LOXL2 antibody) failed in IPF? Prof Jones & @UHSFT team provide the answer - it does NOT inhibit LOXL2!! Really cool paper & model - and important lesson for #CurPF4All community! #MustRead #WhyDrugsFail doi.org/10.1016/j.xcrm…
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@ItaiYanai Well, both camps are right-- and wrong. Life isn’t about isolated parts but about the processes that animate those parts (ie. how those parts dynamically interact). The real debate is actually ancient: Form vs Process (Plato vs. Heraclitus)
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Glyco enthusiasts from MIT (including Chemistry Professors Laura Kiessling, Barbara Imperiali, and Matt Shoulders) and beyond recently gathered in Bartos Theatre to enjoy presentations of the latest advancements in glycobiology research.
chemistry.mit.edu/chemistry-news…

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@EmilyAshkin @NIH @theNCI @LabWinslow @JswLab @WhiteheadInst Congrats again Emily! Very well deserved! It’s truly an honor to be part of your incredible journey. Looking forward to the important discoveries we’ll make together
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I ask for your help to support this Turkey Earthquake Fund gofundme.com/f/xh8d5t-turke… that will directly help affected families in the region. Thanks everyone who reached out during these difficult times, truly appreciate and will never forget your support ❤️ Please share this 🙏
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@ChrisHeery I think the question was clear enough. I was responding to your comment that “uncontrolled cell division leads to the other aberrations of cancer”. This is not true.
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@CancerHacker I don’t think your question was clear then. Are you asking what “drives” cancer or what “defines” it? Because the drivers are different for different cancers, but the unifying defining characteristic is uncontrolled cell growth (IMO).
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@ChrisHeery The “it” in my response refers to “uncontrolled cell division”, not “cancer”
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@ChrisHeery Excuse my ambiguity. I meant proliferation is one of the consequences of cancer, not the driving force
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@ChrisHeery I don’t think uncontrolled cell division is the causal agent and defining factor of cancer. Rather, it’s a consequence of malignant transformation and, unfortunately, the predominant focus of research and clinical efforts. We need to rethink cancer.
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@CancerHacker But uncontrolled cell division leads to those aberrant (and abhorrent) behaviors. It’s just randomness of evolutionary biology after cell division goes unchecked.
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@anideshpandelab @CancerHacker Agreed. I’ve always thought that cancer is when cellular fitness becomes dominant over organismal fitness.
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