Innleggelser i UK forsetter akselerasjonen.
Sist kjente døgn (26 oktober) ble det lagt inn 1489.
Det er ca 15x mer enn for to mnd siden.
Myndighetene i UK skal ha kred for at de var raskt med å få igang Accord da de så hva som var i ferd med å skje.
Hver måned kårer jeg det jeg kaller Teksperter™ for noen av de mest populære investeringene våre 
Det er de 3 medlemmene som har fått flest likes på innleggene sine de siste 90 dagene. Teksperter™ får også en unikt merke på profilen sin og et trofé-ikon ved siden av navnet sitt. Du kan bli Tekspert™ i flere aksjer/investeringer, og troféet vil bare vises i tråder der du er Tekspert™.
Her er denne månedens Teksperter™ og det mest likte innlegget deres fra de siste 90 dagene:
Resten av topp 10:
@drdr (146 likes)
@alfred_e_neuman (124 likes)
@Shattering84 (107 likes)
@Flottesen (105 likes)
@Mykle (104 likes)
@Scrivener (96 likes)
@HeldigFyr (94 likes)
Gratulerer!
Jeg får ikke opp abstractene, bare forsiden på tidsskriftet hvor de publiseres. Får du de opp?
Takk til @Boykie for disse. Her kommer det noen meldinger i morgen, I guess. (har ikke lest enda)
Trodde abstraktene skulle komme først i midten av november. Bah.
Dette var vel en feil, kommer inne inn på abstraktene lenger.
Se tråden Biotekaksjer og en alternativ link av Boykie.
Fire treff på Bemcentinib:
bull
Results:
Between 2018 and 2020, 58 patients in 10 European centers were screened (MDS=27/AML=31) with a median age of 78 years (range, 62-86 years). 45 patients (MDS=21, AML=24) received at least one cycle of BEM and were eligible for safety and efficacy analysis after the first 4 months of treatment. Thirty six (80%) out of 45 patients were considered relapsed after a response to HMA, 8 (18%) had primary resistance and 1 patient (2%) had HMA intolerance. The median number of prior AZA or DAC cycles was 13. In addition, 18 patients (40%) (MDS=9/AML=9) were red blood cell transfusion-dependent.
Treatment with BEM was generally well tolerated with only low rates of grade 3-4 hematologic toxicities (n=7). Forty-seven serious adverse events (SAE) occurred in 22 patients (MDS=9/AML=13), mostly due to infectious complications (n=12), hematological toxicity (n=4) or gastrointestinal disturbance (n=6). Until the first 4 months of BEM treatment, the median number of BEM treatment cycles received was 1.5 (range, 0.5-4). During study, 9 patients (20%) died due to infection (MDS=1/AML=3), deterioration of general condition (MDS=1/AML=2) and progressive disease (MDS=0/AML=2). BEM treatment is currently ongoing in four patients (MDS=3/AML=1).
The primary endpoint was met in 9 of 45 patients (20.0%). Within the MDS cohort 33.3% achieved a response (n=7/21; CR=1, CRi= 3, SD=3), while 8.3% of patients (n=2/24) with AML achieved stable disease(SD). The 4 MDS patients achieving CR/CRi had a normal karyotype and a median baseline IPSS-R score of 4 (range 3-5). Among the MDS non-responders 4 patients had a complex karyotype, median IPSS-R score was 5 (range 3-5). Median baseline bone marrow blast count was 15% vs. 13% and median pretreatment hemoglobin-, platelet- and WBC levels were 9.2 g/dl (range 7.9-11.8 g/dl), 51 G/L(range 26-120 G/L) and 1.9x109/l (range 1.18-8.9 x109/l) vs. 9.6 g/dl (range 7.9-11.3 g/dl), 35 G/L (range 0-167 G/L) and 1.45x109/l (range 0.82-6.97 x109/l) comparing MDS responders (CR/CRi) vs MDS non-responders, respectively.
Preliminary data evaluating soluble AXL (sAXL) in blood plasma at baseline showed that 66.6 % (n=2/3) of MDS patients achieving CR/CRi displayed sAXL levels below a defined threshold, while this was only seen in 20% (n=2/10) of MDS non-responders.
Conclusion:
These results of the prospective phase II BERGAMO trial confirm, that single agent BEM is generally safe and well tolerated in this patient population with an unmet medical need. Importantly, BEM showed clinical efficacy in a subgroup of MDS patients. These encouraging clinical results are being further explored by an in depth translational research program aiming to identify additional molecular and biological prognostic factors associated with response
Ble trangt inn døra på slutten her 
Oral presentation her også! Sweet.
Vil du dele tankene dine eller evt @Boykie vedr resultatet som foreligger her?
På forhånd takk
Ser veldig bra ut dette for BergenBio! Dette må jo føre til kursøkning fremover. Et hav av triggere i vente!
Fantastisk.Kan bli mye brukt for mange myelodysplastisketilstander, akutt myeloid leukemi,polycytemianvera etc.Kan muligens bli brukt som bremsemedisin før stamcelle? Det vi trenger et en AXL expression marker så kan dette bli standard behandling.
First published: 05 November 2020
https://doi.org/10.1096/fj.201903105R
Vitreous has been reported to prevent tumor angiogenesis, but our previous findings indicate that vitreous activate the signaling pathway of phosphoinositide 3‐kinase (PI3K)/Akt, which plays a critical role in angiogenesis. The goal of this research is to determine which role of vitreous plays in angiogenesis‐related cellular responses in vitro. We found that in human retinal microvascular endothelial cells (HRECs) vitreous activates a number of receptor tyrosine kinases including Anexelekto (Axl), which plays an important role in angiogenesis. Subsequently, we discovered that depletion of Axl using CRISPR/Cas9 and an Axl‐specific inhibitor R428 suppress vitreous‐induced Akt activation and cell proliferation, migration, and tuber formation of HRECs. Therefore, this line of research not only demonstrate that vitreous promotes angiogenesis in vitro, but also reveal that Axl is one of receptor tyrosine kinases to mediate vitreous‐induced angiogenesis in vitro, thereby providing a molecular basis for removal of vitreous as cleanly as possible when vitrectomy is performed in treating patients with proliferative diabetic retinopathy.
(Diabetisk retinopati er en synsskade som følge av diabetes. Diabetes er en sykdom som ofte medfører komplikasjoner i øynene. Sykdommen er den hyppigste årsaken til blindhet blant mennesker i arbeidsfør alder i den industrialiserte del av verden. Skadene på synet skyldes hovedsakelig at det skjer endringer på øyets netthinne.)
Axl depletion suppressed vitreous‐stimulated Akt activation and angiogenesis in vitro (Figure [4]), suggesting that pharmacological inhibition of Axl could block vitreous‐induced Akt activation so that a potential pharmacological inhibitor could be used for treating retinal pathological angiogenesis. To this end, we found that 4 μM R428, a specific inhibitor of Axl, completely blocked vitreous‐induced Akt phosphorylation at S473 in HRECs, indicating that this drug at this concentration is able to abrogate vitreous‐stimulated Akt activation and cellular responses. As expected, R428 inhibited vitreous‐enhanced proliferation, migration, and tube formation of HRECs (Figure [5]), suggesting that Axl is a potential mediator of abnormal retinal angiogenesis.
Results showed a dramatic decrease in the number of preretinal tufts after treatment with R428 compared to vehicle (Figure [6A‐B]), and the tufts stand for pathological angiogenesis were outline in (Figure [6C‐D]). Taken together, these data show that inhibition of Axl prevents hypoxia‐induced pathological angiogenesis in a mouse model of OIR.
(Bemcentinib, also known as BGB324 or R428)
