Top Tweets for #mapk
In this paper, the authors show that #MAPK inhibitors improved clinical outcomes and MRI findings in many children with neurodegenerative Langerhans cell histiocytosis, with manageable safety findings. Learn more: https://t.co/cXN3K8IMju
@CancerCytopath They should all have a #MAPK pathway driver, usually RET. It can be detected by mutational, transcriptional, or microtranscriptional profiling. We offer our clinicians the choice of all via commercial reference laboratories. #cytochat
#AACR26 #SanDiego @AACR | April 20: Data supports single agent anti-tumor activity with continuous pathway inhibition in #RAS/#MAPK mutant #solidtumors & emerging best-in-class in #NRAS- & #BRAF Class II/III-mutant #melanoma | @MoffittNews
https://t.co/RmNswKwfF4
❓Tech Q&A | #Fungal #MAPK pathways (e.g. #Hog1, #Cek1) are key regulators of pathogenesis, immune recognition, and cellular adaptation.
They influence:
🔸Cell cycle control
🔸Metabolic regulation: controlling #lipid homeostasis and respiratory metabolism
🔸Morphogenesis: regulating fungal dimorphism and structural transitions
🔸Host interaction: modulating cell-wall mannose exposure to affect immune recognition
📑PMID: 17715363; 27191378; 28111572; 33321998; 19202089; 40333127
#CellCycle #Microbiology #Homeostasis
#ASCO #GI26 #PDAC #SBRT #FAK #MAPK
•NCT07126158
Stereotactic Body Radiotherapy SBRT Plus FAK and RAF/MEK Inhibition in Advanced Pancreatic Adenocarcinoma (BRPC/LAPC post-induction chemo)
The new trial (NCT07126158, phase II, not yet recruiting as of January 2026, commencing in Spring 2026) is a direct evolution/advanced version of the original SBRT + defactinib trial, building on its promising early data by adding avutometinib (a RAF/MEK inhibitor) for enhanced MAPK pathway targeting.
How It's Advanced/Evolved
Treatment:
•
-Original:
SBRT + defactinib (experimental) vs. SBRT alone.
•
-New:
SBRT + defactinib + avutometinib (experimental, 5:1 randomization) vs. SBRT alone (small control).
-Rationale:
Adds avutometinib for dual vertical inhibition (RAF/MEK + FAK), aiming to overcome resistance, deepen responses, and further improve PFS/OS/local control based on the original's biologic signals (e.g., immune activation, reduced fibrosis).
-Endpoints:
Primary focus on PFS (experimental arm); secondary includes toxicity, local control, distant metastasis-free survival, OS.
An advanced iteration of the regimen to potentially boost efficacy in this challenging consolidative setting.
https://t.co/euIVzIaT08
Kicking things off is our Opening Keynote speaker, Prof Sabrina Spencer of @CUBolder. Her talk title is “Causes and Consequences of Escape From Quiescence Under MAPK Inhibition.”
Join the discussion in the comments 👇
#ICSB2025 #SystemsBiology #ComputationalModelling #MAPK
🚨"Mechanisms of Dupilumab" Paper:
- IL-4Rα Q576R variant pathway reprograms Tregs into Th17-like Tregs via #GRB2->#MAPK->#IL6/#STAT3 destabilising Tregs
Conclusion:
R576 variant results in mixed #Th2/#Th17 inflammation + more severe disease
https://t.co/rGaJrOIuDf
IL-4Rα Q576R polymorphism surprisingly common⤵️
Results in increased severity of atopic dermatitis (AD) in a dominant manner (one R allele), leads to increased #GRB2 binding, more #STAT6-independent pathways.
R Allele Global Frequency ~30-35%, carriers %:
Caucasians, 10-20%
Asians, 16-24%
Hispanics, 40%
Blacks, 65-70%
Drugs Blocking #PI3K + #MAPK Pathways So #ZFP36 Still Post-Transcriptionally Regulates #Th2 Inflammation⤵️
Yes Blocks
$SNY $REGN #Dupilumab IL4R
$ABBV #Upadacitinib JAK1i
$LLY #Lebrikizumab IL13 (partial)
#Nemolizumab IL31 (only keratinocytes)
$CRVS #Soquelitinib ITKi
#Amlitelimab OX40L
No Doesn't Block
$NKTR #Rezpeg Treg promoter
$KYMR KT-621 STAT6
Zinc finger protein 36 #ZFP36, #tristetraprolin (TTP), is an RNA-binding protein and negative regulator of mRNA stability for inflammatory cytokines by binding to AU-rich elements #ARE, leading to mRNA decay and reduced protein expression.
In #Th2 cells, ZFP36 regulates pro-inflammatory cytokines including IL4, IL5, IL13
https://t.co/4Ac0nN7Bco
Pathway Explanation⤵️
1. IL-4 binds to IL-4Rα activating it
2. #JAK1 recruited within cell, phosphorylating receptor
3. IRS1/2 and #GRB2 bind via SH2 domain to JAK1 phosphorylated tyrosine activating the #PI3K and #MAPK pathway respectively
4. PI3K and MAPK kinases phosphorylate serines on ZFP36 family protein negative regulators
5. ZFP36-P stabilised and negatively charged does not bind to ARE and/or associate w/ other proteins to decay mRNA. Thus, protein expression for pro-inflammatory cytokines can stay on longer resulting in higher production IL4, IL5, IL13
Plays role in exacerbated inflammation in asthma, psoriasis, and atopic dermatitis
In Th2 inflammation, #STAT6 drives #IgE class switching via germline transcription, but alternatives like #MAPK (via CD40 or IL-18) can compensate. In heterogeneous groups, this causes variability: STAT6-dominant individuals may see reductions, others not, leading to scattered results independent of dosing.
No dose response fits KT-621 STAT6 degradation (>90% at >1.5 mg, complete ≥50 mg), offering no further benefit at higher doses if non-STAT6 paths persist (e.g., driving Th2 activity or slow-turnover plasma cells). Short 14-day trial amplifies this, as IgE drops typically need longer periods, varying by kinetics. (Dupilumab can see IgE levels drop for up to 2.5 years)
Conversely, #Dupilumab prevents ligand binding of IL-4/13, shutting down all branches (STAT6, PI3K/Akt, MAPK) for uniform Th2 suppression (cytokines like IL-4/IL-5/IL-13, IgE switching). Dupilumab yields consistent IgE reductions in patients (minimal in healthy, like KT-621), but STAT6 targeting gaps coverage in severe cases (e.g., Q576R polymorphism with MAPK hyperactivation). KT-621 excels on biomarkers like Eotaxin-3 (up to 63% reduction), but IgE data could be suggestive that full blockade is key for reliable control in #Th2 diseases.
The authors identified that CHNQD-02792, a marine-derived #yaequinolone derivative, exhibits #antitumor activity, and investigated the mechanisms in HT-29 cells.
🔓Full-text: https://t.co/HXMqq7YIcD
#colorectalcancer #apoptosis #MAPK
ClinGen #RASopathy VCEP updates ACMG/AMP variant guidelines, enhancing classification for dominant and recessive RASopathies with broader applications to rare disease genomics https://t.co/leSBX2RJrF #GIMO #VariantInterpretation #MAPK #Noonan #ACMG #AMP #GeneticDiagnosis #ClinGen
💫Calling for Papers💫
📚Targeting MAPK in Human Diseases
👩🔬Guest Editor: Dr. Elisabetta Rovida
⏰Submission Deadline: 30 September 2025
🔗Find out more: https://t.co/UJHp7P0FTk
#MAPK #targetedtherapy #cellsignaling #kinase
🛡️Understanding #plant-#pathogen interactions will help us protect crucial #food #crops
🌾Shu et al. characterize a #MAPK signaling cascade that contributes to #wheat stripe rust resistance, providing new insights into crop immunity and the #pathogenicity of an obligate biotrophic #fungus.
https://t.co/wG0FWI4uZh @wileyplantsci #PlantSci #JIPB
Article✍️Reversing #metabolic #reprogramming by #CPT1 inhibition with #etomoxir promotes #cardiomyocyte proliferation & heart #regeneration via #DUSP1 ADP-#ribosylation-mediated #p38 #MAPK phosphorylation. From Dr. Zeng @theThirdMilitaryMedicalUniversity;
https://t.co/U35I2gYFvG.
Great talk by Dr. Wilson about MEK1 (MAP2K1) mutant NSCLC.
🛑 MAPK deactivation 👉🏻 🙅🏻♀️Resistance to Combination strategies of MEKi with KRASi, EGFRi
💊 Novel RAF/MEK clamp, molecular glue might hold the key 🔑 to solve this dilemma #TTLC25 #MEK1 #MAPK #TargetedTherapy 🎯
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