Overvågning og styring af glukoseniveauer hos mennesker med kræft i bugspytkirtlen (PEGASUS)
10. september 2026 opdateret af: British Columbia Cancer Agency
Undersøgelse af glukosevurdering og regulering af bugspytkirtelkræft
Denne undersøgelse vil undersøge, om det er muligt at nøje overvåge og styre glukoseniveauer hos mennesker med bugspytkirtelkræft. Det vil også undersøge, hvilken indflydelse glukosestyring kan have på kræft i bugspytkirtlen.
Dette er et pilotstudie, der vil bruge kontinuerlige glukosemonitorer (CGM) til at overvåge glukoseniveauer hos cirka 50 deltagere med kræft i bugspytkirtlen. Deltagerne vil modtage standard kemoterapi med en kombination af op til fire lægemidler til behandling af deres bugspytkirtelkræft: oxaliplatin, irinotecan, 5-fluorouracil og leucovorin (FOLFIRINOX). For at behandle høje glukoseniveauer vil deltagerne blive tilfældigt inddelt i en af to grupper: Gruppe 1 vil modtage antihyperglykæmisk behandling som vejledt af en endokrinolog med det formål at opretholde glukoseniveauer mellem 4 og 10 mmol/L; Gruppe 2 vil modtage antihyperglykæmisk behandling, hvis deres glukoseniveauer er over 15 mmol/L, hvilket er standardbehandling. Deltagere i både gruppe 1 og 2 vil modtage standard antihyperglykæmiske behandlinger: metformin, insulin, glukagon-lignende peptid-1 (GLP-1) receptoragonister, natriumglucose co-transporter (SGLT2) hæmmere og dipeptidyl peptidase 4 (DPP- 4) hæmmere.
Efter 4 cyklusser med FOLFIRINOX vil CGM blive fjernet, men alle antihyperglykæmiske behandlinger vil fortsætte efter behov. Hvis deltagerne ophører med behandlingen med FOLFIRINOX, vil de fortsat blive fulgt med henblik på overlevelse og efterfølgende kræftbehandling og vil fortsætte opfølgningen for glukoserelaterede bekymringer efter deres endokrinologs og/eller medicinske onkologs skøn.
Studieoversigt
Status
Rekruttering
Intervention / Behandling
Undersøgelsestype
Interventionel
Tilmelding (Anslået)
50
Fase
- Ikke anvendelig
Kontakter og lokationer
Dette afsnit indeholder kontaktoplysninger for dem, der udfører undersøgelsen, og oplysninger om, hvor denne undersøgelse udføres.
Studiekontakt
- Navn: Daniel Renouf, MD, MPH
- Telefonnummer: 800-663-3333
- E-mail: drenouf@bccancer.bc.ca
Studiesteder
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British Columbia
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Vancouver, British Columbia, Canada, V5Z 4E6
- Rekruttering
- British Columbia Cancer
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Ledende efterforsker:
- Daniel Renouf, MD, MPH
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Kontakt:
- Daniel Renouf, MD, MPH
- Telefonnummer: 800-663-3333
- E-mail: drenouf@bccancer.bc.ca
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Ontario
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Toronto, Ontario, Canada, M5G 2M9
- Rekruttering
- Princess Margaret Cancer Centre
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Kontakt:
- Erica Tsang, MD, MPH
- Telefonnummer: 416-946-2000
- E-mail: erica.tsang@uhn.ca
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Kontakt:
- Robert Grant, MD
- Telefonnummer: 416-946-2000
- E-mail: robert.grant@uhn.ca
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Deltagelseskriterier
Forskere leder efter personer, der passer til en bestemt beskrivelse, kaldet berettigelseskriterier. Nogle eksempler på disse kriterier er en persons generelle helbredstilstand eller tidligere behandlinger.
Berettigelseskriterier
Aldre berettiget til at studere
18 år og ældre (Voksen, Ældre voksen)
Tager imod sunde frivillige
Ingen
Beskrivelse
Inklusionskriterier:
- Histologisk/cytologisk diagnose af pancreas duktalt adenokarcinom (PDAC).
- Planlagt at gennemgå førstelinjes systemisk behandling med FOLFIRINOX.
- Alder større end eller lig med 18 år.
- Eastern Cooperative Oncology Group (ECOG) præstationsstatus 0-1.
Tilstrækkelig knoglemarvs- og organfunktion som defineret af følgende laboratorieværdier:
- Absolut neutrofiltal (ANC) større end eller lig med 1,5 x 10^9/L.
- Blodpladeantal større end eller lig med 75 x 10^9/L.
- Hæmoglobin større end eller lig med 9,0 g/dL.
- Estimeret glomerulær filtrationshastighed (GFR) ved Cockroft-Gault-ligning ELLER 24 timers urinopsamling større end eller lig med 40 ml/min.
- Kreatininclearance større end eller lig med 40 ml/min ved brug af Cockcroft-Gault formel.
- Kalium inden for normale grænser, eller korrigeret med kosttilskud.
- International normaliseret ratio (INR) mindre end eller lig med 1,5.
- Total serumbilirubin mindre end eller lig med 2 x øvre normalgrænse (ULN) (enhver forhøjet bilirubin bør være asymptomatisk ved tilmelding) undtagen for deltagere med dokumenteret Gilberts syndrom, som kun må inkluderes, hvis den totale bilirubin er mindre end eller lig med 3 x ULN eller direkte bilirubin mindre end eller lig med 1,5 x ULN).
- Alaninaminotransferase (ALT) og aspartataminotransferase (AST) mindre end eller lig med 2,5 x ULN (eller mindre end eller lig med 5 x ULN, hvis levermetastaser er til stede).
- Kunne forstå og frivilligt underskrive den informerede samtykkeerklæring.
- I stand til at overholde studiebesøgsplanen og andre protokolkrav.
- I stand til at sluge oral medicin og har ingen kontraindikationer til subkutane insulininjektioner.
- Målbar eller evaluerbar sygdom ved responsevalueringskriterier i solide tumorer (RECIST) 1.1 ved baseline.
- Forventet levetid på mere end 90 dage som vurderet af undersøgelsens læge.
Ekskluderingskriterier:
- Fravær af fjern- eller lymfeknudemetastaser. Deltagere med borderline resektabel eller lokalt avanceret PDAC er ikke kvalificerede.
- Modtaget tidligere systemisk terapi (kemoterapi eller ethvert andet anti-cancermiddel) til behandling af metastatisk PDAC. Deltagere, der modtog adjuverende kemoterapi efter kirurgisk resektion af sygdom i tidligt stadie, er kvalificerede.
- Modtager i øjeblikket anti-cancerterapi (kemoterapi eller ethvert andet anti-cancermiddel).
- Ikke egnet til kombinationskemoterapi som vurderet af undersøgelseslægen.
- Tilstedeværelse af hjernemetastaser.
- Kendt diagnose af type I diabetes, hvor streng glukosekontrol og tæt endokrinologisk opfølgning allerede er indiceret.
- Kendt diagnose af type II diabetes og allerede efterfulgt af endokrinolog.
- Kvindelige deltagere med positiv graviditetstest.
- Deltagere, der ikke er sikre at inkludere i undersøgelsen som vurderet af undersøgelseslægen af en hvilken som helst medicinsk eller ikke-medicinsk årsag.
- Ude af stand til at overholde studievurderinger og opfølgning.
Studieplan
Dette afsnit indeholder detaljer om studieplanen, herunder hvordan undersøgelsen er designet, og hvad undersøgelsen måler.
Hvordan er undersøgelsen tilrettelagt?
Design detaljer
- Primært formål: Behandling
- Tildeling: N/A
- Interventionel model: Enkelt gruppeopgave
- Maskning: Ingen (Åben etiket)
Våben og indgreb
Deltagergruppe / Arm |
Intervention / Behandling |
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Eksperimentel: Glucose Measurements via Blood Draws
Participants will have glucose levels measured using blood drawn prior to each cycle of systemic therapy.
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Blood glucose levels will be measured using blood drawn prior to each cycle of systemic therapy.
Anti-cancer treatment can follow standard care protocols or be given within another clinical trial.
Anti-hyperglycemic treatment will be administered when indicated by and following standard care protocols.
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Hvad måler undersøgelsen?
Primære resultatmål
Resultatmål |
Foranstaltningsbeskrivelse |
Tidsramme |
|---|---|---|
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Proportion of participants who experience at least one episode of hyperglycemia
Tidsramme: From baseline (up to 2 weeks prior to first dose) until progression of disease, assessed up to 24 months.
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The proportion of participants who experience at least one episode of hyperglycemia.
Hyperglycemia is defined by standard non-fasting criteria: random plasma glucose greater than or equal to 11.1 mmol/L or hemoglobin A1c greater than or equal to 6.5%.
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From baseline (up to 2 weeks prior to first dose) until progression of disease, assessed up to 24 months.
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Percentage of glucose measurements above the target range
Tidsramme: From baseline (up to 2 weeks prior to first dose) until progression of disease, assessed up to 24 months.
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The percentage of random plasma glucose measurements that are greater than or equal to 11.1 mmol/L or hemoglobin A1c measurements that are greater than or equal to 6.5%.
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From baseline (up to 2 weeks prior to first dose) until progression of disease, assessed up to 24 months.
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Sekundære resultatmål
Resultatmål |
Foranstaltningsbeskrivelse |
Tidsramme |
|---|---|---|
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Overall response rate (ORR) of the cohort, as defined by RECIST 1.1
Tidsramme: From the date of the screening scan (within 28 days of first dose) until the date of confirmed progression, assessed up to 24 months.
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The proportion of participants who have a complete response (CR) or partial response (PR) to first-line systemic therapy, as defined by RECIST 1.1.
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From the date of the screening scan (within 28 days of first dose) until the date of confirmed progression, assessed up to 24 months.
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Progression-free survival (PFS) of the cohort from the initiation of first-line systemic therapy
Tidsramme: From the date of first dose of first-line systemic therapy until the date of confirmed progression, assessed up to 24 months.
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The length of time from the first dose of first-line systemic therapy until the date of progressive disease (PD), as defined by RECIST 1.1.
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From the date of first dose of first-line systemic therapy until the date of confirmed progression, assessed up to 24 months.
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Overall survival (OS) of the cohort from the initiation of first-line systemic therapy
Tidsramme: From the date of first dose of first-line systemic therapy until the date of death or end of study, assessed up to 24 months.
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The length of time from the initiation of first-line systemic therapy that participants survive.
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From the date of first dose of first-line systemic therapy until the date of death or end of study, assessed up to 24 months.
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Andre resultatmål
Resultatmål |
Foranstaltningsbeskrivelse |
Tidsramme |
|---|---|---|
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Overall response rate (ORR) of the cohort, as defined by RECIST 1.1 and stratified by prognostic and metabolic gene expression subtypes of PDAC
Tidsramme: From the date of the screening scan (within 28 days of first dose) until the date of confirmed progression, assessed up to 24 months.
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The proportion of participants stratified by prognostic and metabolic gene expression subtypes of PDAC who have a complete response (CR) or partial response (PR) to first-line systemic therapy, as defined by RECIST 1.1.
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From the date of the screening scan (within 28 days of first dose) until the date of confirmed progression, assessed up to 24 months.
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Progression-free survival (PFS) of the cohort stratified by prognostic and metabolic gene expression subtypes of PDAC from the initiation of first-line systemic therapy
Tidsramme: From the date of first dose of first-line systemic therapy until the date of confirmed progression, assessed up to 24 months.
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The length of time from the first dose of first-line systemic therapy until the date of progressive disease (PD), as defined by RECIST 1.1, for participants stratified by prognostic and metabolic gene expression subtypes of PDAC.
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From the date of first dose of first-line systemic therapy until the date of confirmed progression, assessed up to 24 months.
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Overall survival (OS) of the cohort stratified by prognostic and metabolic gene expression subtypes of PDAC from the initiation of first-line systemic therapy
Tidsramme: From the date of first dose of first-line systemic therapy until the date of death or end of study, assessed up to 24 months.
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The length of time from the initiation of first-line systemic therapy that participants survive stratified by prognostic and metabolic gene expression subtypes of PDAC.
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From the date of first dose of first-line systemic therapy until the date of death or end of study, assessed up to 24 months.
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Overall response rate (ORR) of the cohort, as defined by RECIST 1.1 and stratified by clinical features (i.e. type 2 diabetes), pathological profiles, and genomic profiles
Tidsramme: From the date of the screening scan (within 28 days of first dose) until the date of confirmed progression, assessed up to 24 months.
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The proportion of participants stratified by clinical features (i.e.
type 2 diabetes), pathological profiles, and genomic profiles who have a complete response (CR) or partial response (PR) to first-line systemic therapy, as defined by RECIST 1.1.
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From the date of the screening scan (within 28 days of first dose) until the date of confirmed progression, assessed up to 24 months.
|
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Progression-free survival (PFS) of the cohort, stratified by clinical features (i.e. type 2 diabetes), pathological profiles, and genomic profiles from the initiation of first-line systemic therapy
Tidsramme: From the date of first dose of first-line systemic therapy until the date of confirmed progression, assessed up to 24 months.
|
The length of time from the first dose of first-line systemic therapy until the date of progressive disease (PD), as defined by RECIST 1.1, for participants stratified by clinical features (i.e.
type 2 diabetes), pathological profiles, and genomic profiles.
|
From the date of first dose of first-line systemic therapy until the date of confirmed progression, assessed up to 24 months.
|
|
Overall survival (OS) of the cohort stratified by clinical features (i.e. type 2 diabetes), pathological profiles, and genomic profiles from the initiation of first-line systemic therapy
Tidsramme: From the date of first dose of first-line systemic therapy until the date of death or end of study, assessed up to 24 months.
|
The length of time from the initiation of first-line systemic therapy that participants survive stratified by clinical features (i.e.
type 2 diabetes), pathological profiles, and genomic profiles.
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From the date of first dose of first-line systemic therapy until the date of death or end of study, assessed up to 24 months.
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Amount of insulin, measured in molar, for participants from screening until the end of study visit
Tidsramme: From the date of screening blood sample collection until the date of the end of study blood sample collection (an average of 6 months).
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The quantity of insulin, measured in molar from immunoassays, from blood samples collected throughout the study.
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From the date of screening blood sample collection until the date of the end of study blood sample collection (an average of 6 months).
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Amount of proinsulin, measured in molar, for participants from screening until the end of study visit
Tidsramme: From the date of the screening blood sample collection until the date of the end of study blood sample collection (an average of 6 months).
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The quantity of proinsulin, measured in molar from immunoassays, from blood samples collected throughout the study.
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From the date of the screening blood sample collection until the date of the end of study blood sample collection (an average of 6 months).
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Amount of C-peptide, measured in molar, for participants from screening until the end of study visit
Tidsramme: From the date of the screening blood sample collection until the date of the end of study blood sample collection (an average of 6 months).
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The quantity of C-peptide, measured in molar from immunoassays, from blood samples collected throughout the study.
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From the date of the screening blood sample collection until the date of the end of study blood sample collection (an average of 6 months).
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Amount of circulating biomarkers, measured in molar, for participants from screening until the end of study visit
Tidsramme: From the date of the screening blood sample collection until the date of the end of study blood sample collection (an average of 6 months).
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The quantity of circulating biomarkers, measured in molar from immunoassays, from blood samples collected throughout the study.
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From the date of the screening blood sample collection until the date of the end of study blood sample collection (an average of 6 months).
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Samarbejdspartnere og efterforskere
Det er her, du vil finde personer og organisationer, der er involveret i denne undersøgelse.
Sponsor
Samarbejdspartnere
Efterforskere
- Ledende efterforsker: Daniel Renouf, MD, MPH, BC Cancer
Publikationer og nyttige links
Den person, der er ansvarlig for at indtaste oplysninger om undersøgelsen, leverer frivilligt disse publikationer. Disse kan handle om alt relateret til undersøgelsen.
Generelle publikationer
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- Harris D, Barts A, Connors J, Dahl M, Elliott T, Kong J, Keane T, Thompson D, Stafford S, Ur E, Sirrs S. Glucocorticoid-induced hyperglycemia is prevalent and unpredictable for patients undergoing cancer therapy: an observational cohort study. Curr Oncol. 2013 Dec;20(6):e532-8. doi: 10.3747/co.20.1499.
- Huxley R, Ansary-Moghaddam A, Berrington de Gonzalez A, Barzi F, Woodward M. Type-II diabetes and pancreatic cancer: a meta-analysis of 36 studies. Br J Cancer. 2005 Jun 6;92(11):2076-83. doi: 10.1038/sj.bjc.6602619.
- Pannala R, Leirness JB, Bamlet WR, Basu A, Petersen GM, Chari ST. Prevalence and clinical profile of pancreatic cancer-associated diabetes mellitus. Gastroenterology. 2008 Apr;134(4):981-7. doi: 10.1053/j.gastro.2008.01.039. Epub 2008 Jan 18.
- Becker S, Dossus L, Kaaks R. Obesity related hyperinsulinaemia and hyperglycaemia and cancer development. Arch Physiol Biochem. 2009 May;115(2):86-96. doi: 10.1080/13813450902878054.
- Dawson DW, Hertzer K, Moro A, Donald G, Chang HH, Go VL, Pandol SJ, Lugea A, Gukovskaya AS, Li G, Hines OJ, Rozengurt E, Eibl G. High-fat, high-calorie diet promotes early pancreatic neoplasia in the conditional KrasG12D mouse model. Cancer Prev Res (Phila). 2013 Oct;6(10):1064-73. doi: 10.1158/1940-6207.CAPR-13-0065. Epub 2013 Aug 13.
- Hart AR, Kennedy H, Harvey I. Pancreatic cancer: a review of the evidence on causation. Clin Gastroenterol Hepatol. 2008 Mar;6(3):275-82. doi: 10.1016/j.cgh.2007.12.041.
- Hassan MM, Bondy ML, Wolff RA, Abbruzzese JL, Vauthey JN, Pisters PW, Evans DB, Khan R, Chou TH, Lenzi R, Jiao L, Li D. Risk factors for pancreatic cancer: case-control study. Am J Gastroenterol. 2007 Dec;102(12):2696-707. doi: 10.1111/j.1572-0241.2007.01510.x. Epub 2007 Aug 31.
- Hjartaker A, Langseth H, Weiderpass E. Obesity and diabetes epidemics: cancer repercussions. Adv Exp Med Biol. 2008;630:72-93. doi: 10.1007/978-0-387-78818-0_6.
- Karasinska JM, Topham JT, Kalloger SE, Jang GH, Denroche RE, Culibrk L, Williamson LM, Wong HL, Lee MKC, O'Kane GM, Moore RA, Mungall AJ, Moore MJ, Warren C, Metcalfe A, Notta F, Knox JJ, Gallinger S, Laskin J, Marra MA, Jones SJM, Renouf DJ, Schaeffer DF. Altered Gene Expression along the Glycolysis-Cholesterol Synthesis Axis Is Associated with Outcome in Pancreatic Cancer. Clin Cancer Res. 2020 Jan 1;26(1):135-146. doi: 10.1158/1078-0432.CCR-19-1543. Epub 2019 Sep 3.
- Kawada K, Toda K, Sakai Y. Targeting metabolic reprogramming in KRAS-driven cancers. Int J Clin Oncol. 2017 Aug;22(4):651-659. doi: 10.1007/s10147-017-1156-4. Epub 2017 Jun 24.
- Kenner BJ, Chari ST, Maitra A, Srivastava S, Cleeter DF, Go VL, Rothschild LJ, Goldberg AE. Early Detection of Pancreatic Cancer-a Defined Future Using Lessons From Other Cancers: A White Paper. Pancreas. 2016 Sep;45(8):1073-9. doi: 10.1097/MPA.0000000000000701.
- Kleeff J, Costello E, Jackson R, Halloran C, Greenhalf W, Ghaneh P, Lamb RF, Lerch MM, Mayerle J, Palmer D, Cox T, Rawcliffe CL, Strobel O, Buchler MW, Neoptolemos JP. The impact of diabetes mellitus on survival following resection and adjuvant chemotherapy for pancreatic cancer. Br J Cancer. 2016 Sep 27;115(7):887-94. doi: 10.1038/bjc.2016.277. Epub 2016 Sep 1.
- Koorstra JB, Hustinx SR, Offerhaus GJ, Maitra A. Pancreatic carcinogenesis. Pancreatology. 2008;8(2):110-25. doi: 10.1159/000123838. Epub 2008 Apr 1.
- Kopp JL, von Figura G, Mayes E, Liu FF, Dubois CL, Morris JP 4th, Pan FC, Akiyama H, Wright CV, Jensen K, Hebrok M, Sander M. Identification of Sox9-dependent acinar-to-ductal reprogramming as the principal mechanism for initiation of pancreatic ductal adenocarcinoma. Cancer Cell. 2012 Dec 11;22(6):737-50. doi: 10.1016/j.ccr.2012.10.025. Epub 2012 Nov 29.
- Lauby-Secretan B, Scoccianti C, Loomis D, Grosse Y, Bianchini F, Straif K; International Agency for Research on Cancer Handbook Working Group. Body Fatness and Cancer--Viewpoint of the IARC Working Group. N Engl J Med. 2016 Aug 25;375(8):794-8. doi: 10.1056/NEJMsr1606602. No abstract available.
- Li D, Xie K, Wolff R, Abbruzzese JL. Pancreatic cancer. Lancet. 2004 Mar 27;363(9414):1049-57. doi: 10.1016/S0140-6736(04)15841-8.
- McCarty MF. Insulin secretion as a determinant of pancreatic cancer risk. Med Hypotheses. 2001 Aug;57(2):146-50. doi: 10.1054/mehy.2001.1316.
- Pleasance E, Titmuss E, Williamson L, Kwan H, Culibrk L, Zhao EY, Dixon K, Fan K, Bowlby R, Jones MR, Shen Y, Grewal JK, Ashkani J, Wee K, Grisdale CJ, Thibodeau ML, Bozoky Z, Pearson H, Majounie E, Vira T, Shenwai R, Mungall KL, Chuah E, Davies A, Warren M, Reisle C, Bonakdar M, Taylor GA, Csizmok V, Chan SK, Zong Z, Bilobram S, Muhammadzadeh A, D'Souza D, Corbett RD, MacMillan D, Carreira M, Choo C, Bleile D, Sadeghi S, Zhang W, Wong T, Cheng D, Brown SD, Holt RA, Moore RA, Mungall AJ, Zhao Y, Nelson J, Fok A, Ma Y, Lee MKC, Lavoie JM, Mendis S, Karasinska JM, Deol B, Fisic A, Schaeffer DF, Yip S, Schrader K, Regier DA, Weymann D, Chia S, Gelmon K, Tinker A, Sun S, Lim H, Renouf DJ, Laskin J, Jones SJM, Marra MA. Pan-cancer analysis of advanced patient tumors reveals interactions between therapy and genomic landscapes. Nat Cancer. 2020 Apr;1(4):452-468. doi: 10.1038/s43018-020-0050-6. Epub 2020 Apr 13.
- Polonsky KS. Dynamics of insulin secretion in obesity and diabetes. Int J Obes Relat Metab Disord. 2000 Jun;24 Suppl 2:S29-31. doi: 10.1038/sj.ijo.0801273.
- Sharma A, Chari ST. Pancreatic Cancer and Diabetes Mellitus. Curr Treat Options Gastroenterol. 2018 Dec;16(4):466-478. doi: 10.1007/s11938-018-0197-8.
- Shlomai G, Neel B, LeRoith D, Gallagher EJ. Type 2 Diabetes Mellitus and Cancer: The Role of Pharmacotherapy. J Clin Oncol. 2016 Dec 10;34(35):4261-4269. doi: 10.1200/JCO.2016.67.4044. Epub 2016 Nov 7.
- Templeman NM, Flibotte S, Chik JHL, Sinha S, Lim GE, Foster LJ, Nislow C, Johnson JD. Reduced Circulating Insulin Enhances Insulin Sensitivity in Old Mice and Extends Lifespan. Cell Rep. 2017 Jul 11;20(2):451-463. doi: 10.1016/j.celrep.2017.06.048.
- Tsujimoto T, Kajio H, Sugiyama T. Association between hyperinsulinemia and increased risk of cancer death in nonobese and obese people: A population-based observational study. Int J Cancer. 2017 Jul 1;141(1):102-111. doi: 10.1002/ijc.30729. Epub 2017 Apr 22.
- Wang F, Qi XM, Wertz R, Mortensen M, Hagen C, Evans J, Sheinin Y, James M, Liu P, Tsai S, Thomas J, Mackinnon A, Dwinell M, Myers CR, Bartrons Bach R, Fu L, Chen G. p38gamma MAPK Is Essential for Aerobic Glycolysis and Pancreatic Tumorigenesis. Cancer Res. 2020 Aug 15;80(16):3251-3264. doi: 10.1158/0008-5472.CAN-19-3281. Epub 2020 Jun 24.
- Wang M, Li J, Lim GE, Johnson JD. Is dynamic autocrine insulin signaling possible? A mathematical model predicts picomolar concentrations of extracellular monomeric insulin within human pancreatic islets. PLoS One. 2013 Jun 14;8(6):e64860. doi: 10.1371/journal.pone.0064860. Print 2013.
- Yan L, Raj P, Yao W, Ying H. Glucose Metabolism in Pancreatic Cancer. Cancers (Basel). 2019 Sep 29;11(10):1460. doi: 10.3390/cancers11101460.
- Yuan C, Rubinson DA, Qian ZR, Wu C, Kraft P, Bao Y, Ogino S, Ng K, Clancy TE, Swanson RS, Gorman MJ, Brais LK, Li T, Stampfer MJ, Hu FB, Giovannucci EL, Kulke MH, Fuchs CS, Wolpin BM. Survival among patients with pancreatic cancer and long-standing or recent-onset diabetes mellitus. J Clin Oncol. 2015 Jan 1;33(1):29-35. doi: 10.1200/JCO.2014.57.5688. Epub 2014 Nov 17.
- Zhang AMY, Magrill J, de Winter TJJ, Hu X, Skovso S, Schaeffer DF, Kopp JL, Johnson JD. Endogenous Hyperinsulinemia Contributes to Pancreatic Cancer Development. Cell Metab. 2019 Sep 3;30(3):403-404. doi: 10.1016/j.cmet.2019.07.003. Epub 2019 Aug 1. No abstract available.
- Siegel RL, Miller KD, Fuchs HE, Jemal A. Cancer Statistics, 2021. CA Cancer J Clin. 2021 Jan;71(1):7-33. doi: 10.3322/caac.21654. Epub 2021 Jan 12.
- Stott M, Stefanova I, Oldfield L, Evans A, Birch-Ford J, Rao R, Greenhalf W, Halloran C, Costello E. Prevalence of New-Onset Diabetes in Patients Undergoing Pancreatic Surgery and the Association of Glucose Dysregulation With Complications in Pancreatic Cancer. Ann Surg Open. 2025 Jun 11;6(2):e584. doi: 10.1097/AS9.0000000000000584. eCollection 2025 Jun.
- Choe HJ, Han KD, Park JH, Lee J, Kwak MK, Choi YM, Moon SJ, Hong EG. Underweight and Mortality in Type 2 Diabetes: A Nationwide Retrospective Cohort Study. J Cachexia Sarcopenia Muscle. 2025 Dec;16(6):e70145. doi: 10.1002/jcsm.70145.
Datoer for undersøgelser
Disse datoer sporer fremskridtene for indsendelser af undersøgelsesrekord og resumeresultater til ClinicalTrials.gov. Studieregistreringer og rapporterede resultater gennemgås af National Library of Medicine (NLM) for at sikre, at de opfylder specifikke kvalitetskontrolstandarder, før de offentliggøres på den offentlige hjemmeside.
Studer store datoer
Studiestart (Faktiske)
16. april 2024
Primær færdiggørelse (Anslået)
1. oktober 2028
Studieafslutning (Anslået)
1. oktober 2028
Datoer for studieregistrering
Først indsendt
10. november 2021
Først indsendt, der opfyldte QC-kriterier
22. november 2021
Først opslået (Faktiske)
24. november 2021
Opdateringer af undersøgelsesjournaler
Sidste opdatering sendt (Faktiske)
14. september 2026
Sidste opdatering indsendt, der opfyldte kvalitetskontrolkriterier
10. september 2026
Sidst verificeret
1. september 2026
Mere information
Begreber relateret til denne undersøgelse
Nøgleord
Yderligere relevante MeSH-vilkår
- Sygdomme i det endokrine system
- Neoplasmer efter sted
- Neoplasmer
- Metaboliske sygdomme
- Neoplasmer i fordøjelsessystemet
- Sygdomme i fordøjelsessystemet
- Glukosemetabolismeforstyrrelser
- Neoplasmer i endokrine kirtler
- Pancreassygdomme
- Ernæringsmæssige og metaboliske sygdomme
- Bugspytkirtel neoplasmer
- Hyperglykæmi
- Sundhedstjenester Administration
- Sundhedsvæsenets kvalitet, adgang og evaluering
- Sundhedskvalitet
- Kvalitetsindikatorer, sundhedsvæsenet
- Standard for pleje
Andre undersøgelses-id-numre
- H21-03061
Lægemiddel- og udstyrsoplysninger, undersøgelsesdokumenter
Studerer et amerikansk FDA-reguleret lægemiddelprodukt
Ingen
Studerer et amerikansk FDA-reguleret enhedsprodukt
Ingen
produkt fremstillet i og eksporteret fra U.S.A.
Ingen
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