Top Tweets for #Pi3K
What does #PI3Kδ inhibition reveal about the biology of #APDS? This pediatric approval highlights how insights into signaling pathways can translate into new research directions for rare genetic disorders.
#RareDisease #Immunology #PI3K #Leniolisib #DrugDiscovery #Research
🚨FDA Approval Update | A first treatment option for children with #APDS
The #FDA has approved #Joenja (leniolisib) as the first treatment for children aged 4-11 years with activated phosphoinositide 3-kinase delta syndrome (#APDS), a rare genetic disorder affecting the immune system.
🧬Joenja is an oral, selective #PI3Kδ inhibitor. The approval covers children who weigh at least 27 kg, with weight-based dosing of 40, 50, or 70 mg twice daily.
📊The approval was supported by a Phase 3 study showing improvements in key features of APDS, including reduced lymphadenopathy and increased naïve B cells.
🔬 Explore PI3Kδ and related research: https://t.co/VZosH6DgfK
#FDAApproval #RareDisease #Leniolisib #Immunology #PI3K #DrugDiscovery #Research
This review maps #PI3K/#AKT signalling and its molecular crosstalk across diverse #Cancers, examining how pathway dysregulation drives tumour progression and resistance while informing safer, more effective targeted therapies.
#STTT #OpenAccess: https://t.co/bcjjWKVhnn
#CancerSignaling #CancerBiology
What makes the gedatolisib triplet so exciting?
🎙️ Drs. @jhaveri_komal & @Neil_Iyengar
▶️ Watch on YouTube - https://t.co/8QwUQqmCGI
🎧 Listen on Spotify, Apple Podcasts, Amazon Music, CastBox, & iHeartRadio - https://t.co/hcwkG9RM5G
#CancerUnfiltered #Gedatolisib #PI3K
Epigenetics Update - Nuclear class 3 PI3K co-activates fasting-specific chromatin remodelling https://t.co/ffwolOtDS9
Nathaniel F. Henneman & Ganna Panasyuk (@unipariscite) in @NatureCellBio
#Epigenetics #Chromatin #PI3K
---
Gain deeper insights; https://t.co/WmSYDGXnzb
Nancy Lin, MD (@nlinmd), presents on ER+ Metastatic Breast Cancer: #SERDs, #CDK4/6, #PI3K, and novel endocrine agents at the #DanaFarberBreastCancerCourse.
#MBC #BreastCancer
💡The approval of #gedatolisib underscores the growing importance of the #PI3K/#AKT/#mTOR axis in breast cancer.
#BreastCancer #PI3K #Oncology #DrugDiscovery #CancerResearch
💊#FDAApproval Update | The FDA has approved #Revtorpyk (#gedatolisib) in combination with #fulvestrant, with/without #palbociclib, for adults with #HR-positive, #HER2-negative, #PIK3CA wild-type locally advanced or metastatic breast cancer following progression on endocrine therapy.
💡Gedatolisib is a pan-PI3K/mTOR inhibitor, simultaneously targeting all class I PI3K isoforms and both mTORC1/2 complexes to inhibit a key signaling pathway driving endocrine resistance.
📊VIKTORIA-1 trial:
🔹76% reduction in the risk of disease progression or death with gedatolisib + palbociclib + fulvestrant vs fulvestrant alone
🔹Median progression-free survival: 9.3 vs 2.0 months
🔹Significant benefit observed in patients with PIK3CA wild-type disease
#BreastCancer #HRPositive #HER2Negative #PI3K #Oncology #CancerResearch #DrugDiscovery #MedicinalChemistry
#dcvax $nwbo #gbm
Key Points are: 1) #HGGs including #DMG are dependent on the PI3K/mTOR pathway; 2) Brain-penetrant #PI3K/mTOR offers hope for precision-guided treatment; 3) #Clinicaltrials for children need to be aware of the limitations of PI3K/mTOR inhibition in pediatric brain tumors, as children are not adults"
Incorporating the key findings from Duchatel et al. (2025) into the context of the DCVax platform reveals a sophisticated strategy for treating High-Grade Gliomas (HGG) and Diffuse Midline Gliomas (DMG).
The synergy between these two technologies addresses the three critical points you raised by creating a "dual-engine" attack on the tumor's biology and its immune-evasion tactics.
1. Dependency on PI3K/mTOR: The Vulnerability
Key Point: HGGs and DMGs are genetically "addicted" to the PI3K/mTOR pathway for survival and growth.
Relevance to DCVax: While DCVax provides a broad-spectrum immune response, the PI3K/mTOR pathway is often what makes these tumors so aggressive and resistant to standard care.
The Synergy: By using a targeted inhibitor to shut down this primary growth driver, you essentially "stun" the tumor. A stunned tumor is less able to produce the immunosuppressive chemicals (like TGF-beta or IL-10) that usually create a "shield" against the immune system. This makes the DCVax-trained T-cells far more effective at infiltrating and destroying the tumor mass
2. Brain-Penetrant Inhibitors: Precision-Guided Entry
Key Point: New "brain-penetrant" PI3K/mTOR inhibitors (like paxalisib, discussed in the article) can finally cross the blood-brain barrier (BBB).
Relevance to DCVax: One of the historic failures of "precision medicine" in the brain was that the drugs simply couldn't get to the target.
The Synergy: Precision drugs can now act as a "pathfinder." By crossing the BBB and weakening the tumor's internal structure, they create a more favorable environment for the immune system. DCVax-L is autologous (personalized); when combined with a drug that hits the tumor's specific genetic weakness, you are attacking the cancer from the inside-out (the inhibitor) and the outside-in (the DCVax immune response)
3. Pediatric vs. Adult Considerations: Tailored Care
Key Point: Children are not adults. Their tumors have different genetic drivers, and their developing brains have different toxicological thresholds.
Relevance to DCVax: This is where the DCVax platform truly shines. Because DCVax is made from the patient's own tumor tissue, it is inherently "aware" of the differences between a child's DMG and an adult's GBM. It doesn't rely on a "standard" antigen; it learns from the specific pediatric mutations present in that individual child.
The Synergy: The article warns about the "limitations" and toxicities of PI3K inhibitors in children (like hyperglycemia or developmental impacts). By combining these drugs with DCVax, clinicians might be able to use lower, less-toxic doses of the PI3K inhibitor. The drug doesn't have to do 100% of the work; it only needs to weaken the tumor enough for the DCVax-primed immune system to take over.
Conclusion
The "hope for precision-guided treatment" Dr. Brem mentioned is found in this overlap. The PI3K/mTOR inhibitor provides the immediate, surgical strike against the tumor's engine, while DCVax provides the long-term, adaptive surveillance needed to prevent recurrence—a particularly vital combination for pediatric patients where long-term survival and quality of life are the ultimate goals - (Gemini AI Analysis)
🧵2/3 Recipient of the Medal of the Order of Australia, and numerous other honors, Matt Dun has made seminal contributions to our understanding and future treatment of #DIPG, #DMG, with novel approaches
https://t.co/UHvb0k2G1P
Key Points are: 1) #HGGs including #DMG are dependent on the PI3K/mTOR pathway; 2) Brain-penetrant #PI3K/mTOR offers hope for precision-guided treatment; 3) #Clinicaltrials for children need to be aware of the limitations of PI3K/mTOR inhibition in pediatric brain tumors, as children are not adults.
The #MutantSelective #PI3K inhibitor has a name! #zovegalisib + fulvestrant after CDK4/6i demonstrates efficacy including in pts w prior SERD or ESR1mut (IMO oral SERD would be better). mPFS 10.3 mo, 38.7% ORR, low grade TRAEs. Does response vary by PIK3CA mut type? #SABCS25
Dr. Shalinda Fernando @NeilVasan lab @nyulangone establishes #PIK3R1 mutations as actionable #PI3K pathway alterations in breast cancer. Opportunity for inclusion in trials including mutant selective PI3K inhibitors. And PIK3R1 should be included on liquid biopsy panels! #SABCS25
🔍 Explore updated findings from the PIKALO-1 trial, a phase1/2 study of a pan-mutant selective PI3Kα inhibitor in HR+,HER2- ABC.
#SABCS2025 | https://t.co/oKGK3TDdOO
#AdvancedBreastCancer #PI3K
Congrats to the newly minted Dr. Ge @Xiangyu_GigiG for defending her thesis today! A tour de force talk on her work unraveling signaling interactions between #PI3K and #KRAS. @yalepathology @YaleCancer @CancerYale. Check out her preprint: https://t.co/JghjDU6ApJ
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
First, IL-4 and IL-13 activate multiple parallel intracellular pathways beyond STAT6, including STAT6-independent arms such as the insulin receptor substrate (IRS)-1/2 pathway leading to phosphoinositide 3-kinase (#PI3K)/Akt activation, and the Ras/mitogen-activated protein kinase (#MAPK) pathway. These alternative routes contribute to key aspects of type 2 inflammation, such as cell proliferation, survival, and chemokine production, without relying on #STAT6 phosphorylation or nuclear translocation. For instance, IRS/PI3K signaling is essential for IL-4-induced proliferative responses in immune cells, while MAPK activation amplifies inflammatory gene expression and cytokine release. Inhibiting or degrading STAT6 would leave these pathways intact, potentially allowing residual type 2 immune responses to persist, whereas dupilumab's upstream blockade prevents activation of all branches, achieving more comprehensive pathway shutdown.
🔬 ℙ𝕒𝕥𝕙𝕨𝕒𝕪 𝕊𝕡𝕠𝕥𝕝𝕚𝕘𝕙𝕥 | 4️⃣ 𝑷𝑰3𝑲-𝑨𝒌𝒕 𝑺𝒊𝒈𝒏𝒂𝒍𝒊𝒏𝒈 𝑷𝒂𝒕𝒉𝒘𝒂𝒚
#Pathway #PI3K #Akt #CellBiology #CancerResearch #Solarbio #Biotech #ResearchTools
🔬 ℙ𝕒𝕥𝕙𝕨𝕒𝕪 𝕊𝕡𝕠𝕥𝕝𝕚𝕘𝕙𝕥 | 4️⃣ 𝑷𝑰3𝑲-𝑨𝒌𝒕 𝑺𝒊𝒈𝒏𝒂𝒍𝒊𝒏𝒈 𝑷𝒂𝒕𝒉𝒘𝒂𝒚
#Pathway #PI3K #Akt #CellBiology #CancerResearch #Solarbio #Biotech #ResearchTools
Way to go, @Xiangyu_GigiG, for a fantastic talk on how #PI3K governs resistance to #KRAS inhibition in #PancreaticCancer cells @FASEBorg Protein Phosphorylation! @yalepathology @YaleCancer @CancerYale @moitrayee_lab @JuraLab_UCSF. Check out her preprint: https://t.co/jIVfbH3fvw
✅If the #Notch, b-catenin, #Wnt, #PI3K, #Akt, and #mTORC signaling pathways control #tumor #proliferation and differentiation in #osteosarcoma, which process could be defined as a priority #therapeutic target: tumor #proliferation/differentiation or #angiogenesis?
✅If spike-shaped #ECs determine the early development of #metastases and express #adhesion #molecules such as #MCAM, #CXCR4, #ANGPT2, and #KDR, could these molecules be used as #biomarkers for the #early #detection of metastases?
@ATHjournal @CardiologyPlus @atvbahajournals @CircRes @CircHF @CytoskelJournal @gkolost @HaoYin20 @IEEEembs @J_Cell_Sci @JCI_insight @JPBY_official @physiolrev @APSPhysiology @JPhysiol @Ahmed43101178 @drshafikuchay @RCMjournal @TrackYourHeart @JCVPOnline @CNIC_CARDIO @LuisSobrevia2 @CMPLPUCCHILE @FacMedicinaUC @Cancer_Cell @NatureRevCancer @CRC_AACR @RockUPress @WashUCardiology @WashUDeptMed @rust_ruslan @isth @The_MCSociety @cancerwarriors_ @ContraCancerEs 👇🧵👇
Research into tip-like endothelial cells (ECs) within #osteosarcoma is extremely rare.
The authors found that tip-like ECs were abundant in the primary tumors and metastatic foci.
🔓 Find out more in @Nature_NPJ: https://t.co/7HL66aaM1B
1/🚨 New preprint out!🚨
We uncovered that #PI3K-driven wild-type RAS activation bypasses #KRAS inhibition in pancreatic adenocarcinoma (#PDAC) to drive #resistance.
🔑PI3K isn’t just a downstream RAS effector – it can be an upstream RAS regulator.
📄 https://t.co/JghjDU6ApJ
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