For et selskap PCIB er. Og for noen skribenter! Takk!
Med resultater og siste oppdateringer og slik dere som kan biotek er det uforståelig at PCIB i dag ikke er i all time high og langt over 60kr?! Dere beskriver statistikken og det er gull!
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''Oh, wow. That’s going into a lot of scientific details, really. I can – I think I can mention that there was – there is a way of staging bile duct cancer into 4 different stages, which is not very relevant for the prognostic outcome of these patients. And one of the foremost clinics in treating bile duct cancer, the Mayo Clinic, has produced a different kind of scheme for this. They’ve looked at the number of different parameters and have managed to make up a kind of – or prepare a kind of staging scheme that fits better with prognostic values. And I think the most relevant to look at there is probably that because that really correlates very well with the survival of patients.
And looking into that, when we look at the extension study, half of the extension patients approximately, I think, are in the worst category in that specific study. That has been published a number of years ago, which was then retrospectively done on patients over a 10-year period, I think.
So there’s – looking into that staging system [where already] talked about prognostic between different patients, the extension group is much worse than the dose escalation group. The dose escalation group, most of the patients go into Stage III but half of them would be Stage IV in the extension I think. This hasn’t been done formally and properly. I just had a quick look to try to see how this fits, but it looks like that. I think that’s the best answer I can give on that.’’
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Overall Survival (OS) er pdd 17.5 mnd for samme N (13), med to som fortsatt lever. Vet at det er PFS som er endepunkt i den pivotale studien. Men vil det vurderes på OS eller MOS mtp overlevelse i pf2 ifm sekundærendepunkt?
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Ja, selvfølgelig 
OS er sekundærendepunkt.
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Da ser det jo veldig lovende ut. Lav N, men foreløpig 17.5 mnd OS med fortsatt to i live er bra. Og kun dobbel behandling på 5 av 13 personer. Dette er data uten person 6 som levde i 50mnd og fikk en dose lik den som blir gitt i PF2.
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Blir resultatene i release studien rangsjert etter tumorstørrelsen eller blir alt miksa sammen og gjennomsnittet servert som resultatet?
Blir det målt tumorstørrelse i starten av studien for å kontrollere om der er en maksimum storleik på tumoren som gir negative resultater?
Livskvalitet teller jo også med mht til om det blir medisin.
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Løfter denne tråden så vi kan pensle noe av diskusjonen inn hit.
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Nordnet øker belåningsgrad på PCIB. 
Fra 20% til 45%. Dette skal ha skjedd den 27.09.19 men ikkje hos meg, eg har forsatt 20%. Hva med dere?
20% her også
Lurer på om vi misforstår Nordnet litt: Altså at de mener OPP til 45% basert på hvor mye aksjen utgjør av porteføljen din.
Altså ikke at belåningsgraden går fra 20% til 45%.
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Mulig du har rett @Savepig. For eg ser at eg har ny belåning på ein av aksjen. Må prøve å finne ut av det.
Men litt rart da eg kun har ein aksje som er over 30% av portoføljen.
PCIB står for 38,3% av portoføljen og eg får belåningsgrad på 31% som jo er greit nok.
Edit:
Riktig det som Savepig skriv. Altså belåningsgraden varierer mellom 20% til 45%. (20% viss du har 50% eller meir av EK i PCIB)
Grunnen til at dette ikkje stemmer for meg er at eg har ein spesialavtale med Nordnet.
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Det er plutselig rikelig med #Cholangiocarcinoma fra ESMO.
https://twitter.com/hashtag/Cholangiocarcinoma?src=hashtag_click&f=live
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Førstnevnte studie:
“Median overall survival was10.8 months for patients treated with ivosidenib and 9.7 months for placebo.”
Skremmer vel ikke vannet av oss dette.
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Litt usikker på om dette er samme indikasjon også, er dette extrahepatic (utvendig) cholangiocarcinoma?
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Bør ikke dette bety at våre data står seg enda bedre? 185/2 pasienter med en MOS på 9,7 mnd. - og det etter at de fikk gå over på medisin når sykdommen utviklet seg. Ren placebo ga 6(!) mnd…
Results showed a favourable trend in overall survival with ivosidenib. Median overall survival was 10.8 months for ivosidenib and 9.7 months for placebo (HR 0.69, one-sided p=0.06). Adjusting the overall survival results to take account of 57% of placebo patients crossing over to ivosidenib gave an adjusted overall survival of 6 months for placebo, which was significantly shorter than with ivosidenib (HR 0.46, p=0.0008).
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Hva med den i midten da, Pemigatinib?
FGFR hemmere funker vel ikke på alle pasienter heller?
FGFR genetic aberrations (GAs) occur in an estimated 10% to 16% of intrahepatic cholangiocarcinomas (CCAs).
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En FGFR inhibitor som er relevant for iCCA, men ikke som jeg har sett eCCA.
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A phase III trial has begun for the investigational agent pemigatinib (INCB54828) in comparison with gemcitabine and cisplatin chemotherapy for the treatment of newly diagnosed patients with metastatic or surgically unresectable cholangiocarcinoma who have activating FGFR2 rearrangements. https://www.targetedonc.com/news/phase-iii-trial-begins-for-frontline-pemigatinib-in-fgfr2-cholangiocarcinoma
A molecular abnormality indicating rearrangement of the FGFR2 gene.
https://www.ncbi.nlm.nih.gov/medgen/1656455
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Purpose
FGFR genetic aberrations (GAs) occur in an estimated 10% to 16% of intrahepatic cholangiocarcinomas (CCAs). The natural history of CCA with FGFR GAs, the prognostic role of coexisting GAs, and the outcome with FGFR-targeted inhibitors are unknown.
Patients and Methods
Patients with CCA with FGFR GAs were identified using next-generation sequencing or fluorescence in situ hybridization from four tertiary cancer centers and compared with FGFR wild-type counterparts. Data reviewed included demographic, treatment, overall survival (OS), and GA data. Fisher’s exact test, Kaplan-Meier plots, and log-rank tests were used for statistical analysis.
Results
Three hundred seventy-seven patients with CCA were identified, and 95 had FGFR GAs. FGFR2 GA was most common (n = 74, with 63 fusions) and seen in intrahepatic CCA. In patients with CCA, FGFR GAs occurred more frequently in younger patients (≤ 40 years; 20%) compared with older patients (> 40 years; 6.7%; P < .001), presented at an earlier stage (TNM stage I/II v III/IV: 35.8% v 22%, respectively; P = .001), and were associated with a longer OS compared with patients without FGFR GAs (37 v 20 months, respectively; P < .001). This difference remained significant after excluding 36 patients treated with FGFR inhibitors. There was no OS difference ( P = .60) between CCA with FGFR2 fusions (n = 63) versus other FGFR GAs (n = 29). Patients with FGFR GAs had a better OS with FGFR-targeted therapy compared with standard treatment ( P = .01). BAP1 mutation was the most common coexisting mutation without prognostic impact, whereas TP53 ( P = .04) and CDKN2A/B ( P = .04) were correlated with a shorter OS.
Conclusion
CCA with FGFR GAs represents a unique subtype occurring in younger patients with an indolent disease course. FGFR-targeted therapy may have a positive impact on OS in this subgroup.
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