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Ahh, beklager. De har ingen analyse, Nordea i motsetning til et par andre.
Hadde vært så deilig om vi la oss over 45 til slutt i dag… Mandag blir like god👍
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Slike nettsider(inkludert clinicaltrials.gov) oppdateres ikke i sanntid, sannsynligvis er de i gang for lengst.
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Jaja… Eller 46😂
Noen som har sett denne før?
http://www.koreabiomed.com/news/articleView.html?idxno=8254
The researchers also confirmed in an animal study that when using an AXL inhibitor developed by Bergen Bio, a Norwegian biopharmaceutical company, it inhibited the metastasis and tumor formation of gastric cancer cells.
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Eg blir overasket om det ikkje blir et fredagsrally, det er kjipt å sitte ute til og med over natta 
eg tør ihvertfall ikkje selge 
snakkes på 50 something på mandag 
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Q1 tirsdag, klart det fortsetter.
Hva er sannsynligheten for Covid-19 stikkkere, 99’9% ish 
Next Algeta, x2/4
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Tror jeg skal henge opp et viltkamera utenfor kontoret til Bergen Bio i helgen.
Big Pharma kommer dunkende på døren.
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Godt mulig det, bare stusset litt over det, fra web archive kan en se at det stod “open to recruitment” 12.mai, nå står det “in setup”, så at det ikke er oppdatert ville være noe merkelig men godt mulig det bare er noe formelt ifb at de la til den 5.medisinen med blodfortynnende greier i studien at det er det “setup” referer til å tilrettelegge for den medisinen, ikke vet jeg, men tydelig at noen vet noe idag som de ikke visste igår, som de ikke vil dele med resten av klassen, og det er lov det, jeg får bare undres, og håper dere har rett for verdens skyld 
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But you also have to consider that bemcentinib is only the first of 6 being trialled. So potentially they are in set up until all 6 are actively recruiting. I don’t know. But i am working off the assumption and what RG said on the call and that was that it could be in patients by the end of the week. 6 hospitals, a tonne of patients and politcal/societal/economic pressures to get treatment, i am betting we are fully recruited in the not too distant future.
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@larsmkn har delt studien før, men artikkel er jo ny. Kanskje det sparkes i gang noe i Sør Korea da?
Gastric cancer is the most common cancer among Koreans, but there is a limit to the efficacy of existing anticancer chemotherapy treatments. Targeted therapeutics, which has recently been in the spotlight, is not frequently administered, either, increasing demand for the development of new drugs.
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Den britiske regjeringen har laget en omfattende plan for hvordan de skal få landet på fote igjen.
Funded by the Department of Health and Social Care and UKRI, the collaborative programme ACCORD (Accelerating COVID-19 Research & Development platform) will accelerate the development of new drugs for patients hospitalised with COVID-19, reducing the time taken to set up clinical studies for new therapies from months to weeks. The first of the new and existing medicines to be tested through the ACCORD platform is Bemcentinib.
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Ordre på ca 3mill som kommer og går, forsøk på å dra kursen ned?
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Forsøk på å få seg et godt påfyll, uten å presse kursen ytterligere.
Må høyt opp for å få 70+k
Noen med nivå 2 på ordedybde?
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Pre-klinisk studie fra Kina/ Hong Kong/ USA med bemcentinib i leverkreftceller skal presenteres på AACR av forskere som ikke er assosiert med BerGenBio:
Pharmacological inhibition of AXL with BGB324 sensitizes HCC cells to sorafenib treatment and promotes an immunostimulatory microenvironment
Presenter/Authors
Man Tong , Cheuk Yin Lin , Kwan Ho Tang , Lei Zhou , Kwan Man , Kin Wah Lee , Stephanie Ma . University of Hong Kong Faculty of Medicine, China, New York University, NY, University of Hong Kong Faculty of Medicine, China, The Hong Kong Polytechnic University, China
Disclosures
M. Tong: None. C. Lin: None. K. Tang: None. L. Zhou: None. K. Man: None. K. Lee: None. S. Ma: None.
Abstract
Sorafenib has been used as a first-line targeted therapy for patients of advanced hepatocellular carcinoma (HCC) for more than a decade. However, the benefits of sorafenib remain modest due to limited response rate and acquired drug resistance. To better understand the underlying mechanism of sorafenib resistance in HCC, RNA sequencing was performed to compare the altered transcriptome profiles between sorafenib resistant and sensitive HCC cells. Subsequent pathway enrichment analysis identified a significantly deregulated Hippo/YAP/AXL signaling cascade in sorafenib resistant HCC, with findings confirmed in an expanded cohort of sorafenib resistant HCC cells and HCC patient derived xenografts. AXL is a receptor tyrosine kinase whose cytoplasmic expression has previously been reported to be up-regulated in multiple cancers including HCC. Consistently, secretory AXL expression levels in HCC patient serum samples were also found elevated when compared with normal and healthy individuals. Pharmacological inhibition of AXL with BGB324/Bemcentinib sensitized sorafenib resistant HCC cells to sorafenib treatment and resulted in enhanced apoptosis. Combination treatment of sorafenib and BGB324 suppressed tumor growth in a syngeneic HCC mouse model. Immunophenotyping by flow cytometry was then performed to examine the immunological effect of the combination treatment of sorafenib and BGB324 on HCC suppression. Combination treatment enhanced CD4+ T cell proliferation and reduced PD-1 immune checkpoint expression in the tumors of the syngeneic HCC mouse model, suggesting the treatment to promote a more immunostimulatory microenvironment. Tumor cells derived lactate has been suggested to be an immunosuppressive metabolite which enhances immune evasion of tumor cells. We found sorafenib resistant HCC cells to secrete high levels of lactate, while blockade of AXL with BGB324 reduced lactate secretion. Investigation on the detailed mechanism of how AXL regulates lactate secretion and hence the immune microenvironment is currently underway. Taken together, our current data suggests sorafenib resistant HCC cells to regulate the immune microenvironment via AXL and lactate modulation. Combination treatment of sorafenib and BGB324 may represent a novel therapeutic approach to combat HCC
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Tross alt fredda😎
Tar vi helg over eller under 45,- i dag?
- Over 45.-
- Under 45.-
0 stemmegivere
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En til studie fra AACR. Denne fra forskere i Taiwan og Singapor. De sier i teksten at BGB324 aka R428 er godkjent i AML, men det er den jo ikke… enda… så se vekk fra akkurat det.
Role of receptor tyrosine kinase AXL in mediating DNA damage response
Presenter/Authors
Xun Hui Yeo , Wai Leong Tam , Ruby Yun-Ju Huang . Cancer Science Institute, Singapore, Singapore, Genome Institute of Singapore, Singapore, Singapore, National Taiwan University, Taipei, Taiwan
Disclosures
X.H. Yeo: None. W.L. Tam: None. R.Y. Huang: None.
Abstract
AXL is a receptor tyrosine kinase that is often overexpressed in many cancers. It contributes to tumor progression, metastasis and drug resistance through activating downstream signaling cascades, making it an emerging therapeutic target. Moreover, the first-in-class AXL inhibitor R428 (BGB321) was lately approved by the FDA for the treatment of relapsed or refractory acute myeloid leukemia. Previously, R428 (BGB321) was also reported to show selective sensitivity towards ovarian cancers with a Mesenchymal molecular subtype. Recently, a novel role of AXL in the regulation of DNA damage responses has been brought to light. Here, we further explored AXL’s role in mediating DNA damage responses by using ovarian cancer as a disease model. AXL inhibition using R428 resulted in the increase DNA damage foci in ovarian cancer cells SKOV3 and HeyA8. This occurred concurrently with the upregulation of classic DNA damage response signaling molecules such as γH2Ax, ATM and ATR. RNA sequencing results further validated this observation, that R428-treated cells showed downregulation of genes involved in cell cycle control and DNA replication, suggesting the decrease in proliferation. Through SILAC co-immunoprecipitation mass spectrometry, we uncovered a novel binding partner of AXL that could potentially regulate the DNA damage repair upon the inhibition of AXL, giving us insights to how AXL inhibition might contribute to DNA damage. Furthermore, our results showed that AXL inhibition rendered cells more sensitive to the inhibition of ATR, a crucial mediator for replication stress, paving ways to the rationale for potential combinatory use of AXL and DNA damage repair inhibitors.
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