- ICH GCP
- Registro de ensaios clínicos dos EUA
- Ensaio Clínico NCT05132244
Monitorando e Gerenciando os Níveis de Glicose em Pessoas com Câncer de Pâncreas (PEGASUS)
Estudo de Avaliação e Regulação da Glicose do Câncer Pancreático
Este estudo investigará se é ou não viável monitorar e gerenciar de perto os níveis de glicose em pessoas com câncer pancreático. Ele também investigará o impacto que o gerenciamento de glicose pode ter no câncer de pâncreas.
Este é um estudo piloto que usará monitores contínuos de glicose (CGM) para monitorar os níveis de glicose em aproximadamente 50 participantes com câncer pancreático. Os participantes receberão quimioterapia padrão com uma combinação de até quatro medicamentos para tratar o câncer de pâncreas: oxaliplatina, irinotecano, 5-fluorouracil e leucovorina (FOLFIRINOX). Para tratar níveis elevados de glicose, os participantes serão distribuídos aleatoriamente em um dos dois grupos: Grupo 1 receberá tratamento anti-hiperglicêmico orientado por um endocrinologista com o objetivo de manter os níveis de glicose entre 4 e 10 mmol/L; O Grupo 2 receberá tratamento anti-hiperglicêmico se seus níveis de glicose estiverem acima de 15 mmol/L, que é o tratamento padrão. Os participantes dos Grupos 1 e 2 receberão tratamentos anti-hiperglicêmicos padrão: metformina, insulina, agonistas do receptor do peptídeo-1 semelhante ao glucagon (GLP-1), inibidores do cotransportador de glicose e sódio (SGLT2) e dipeptidil peptidase 4 (DPP- 4) inibidores.
Após 4 ciclos de FOLFIRINOX, o CGM será removido, mas quaisquer tratamentos anti-hiperglicêmicos continuarão conforme necessário. Se os participantes descontinuarem o tratamento com FOLFIRINOX, eles continuarão a ser acompanhados para sobrevivência e subsequente terapia anticancerígena e continuarão o acompanhamento para problemas relacionados à glicose, a critério de seu endocrinologista e/ou oncologista médico.
Visão geral do estudo
Status
Intervenção / Tratamento
Tipo de estudo
Inscrição (Estimado)
Estágio
- Não aplicável
Contactos e Locais
Contato de estudo
- Nome: Daniel Renouf, MD, MPH
- Número de telefone: 800-663-3333
- E-mail: drenouf@bccancer.bc.ca
Locais de estudo
-
-
British Columbia
-
Vancouver, British Columbia, Canadá, V5Z 4E6
- Recrutamento
- British Columbia Cancer
-
Investigador principal:
- Daniel Renouf, MD, MPH
-
Contato:
- Daniel Renouf, MD, MPH
- Número de telefone: 800-663-3333
- E-mail: drenouf@bccancer.bc.ca
-
-
Ontario
-
Toronto, Ontario, Canadá, M5G 2M9
- Recrutamento
- Princess Margaret Cancer Centre
-
Contato:
- Erica Tsang, MD, MPH
- Número de telefone: 416-946-2000
- E-mail: erica.tsang@uhn.ca
-
Contato:
- Robert Grant, MD
- Número de telefone: 416-946-2000
- E-mail: robert.grant@uhn.ca
-
-
Critérios de participação
Critérios de elegibilidade
Idades elegíveis para estudo
Aceita Voluntários Saudáveis
Descrição
Critério de inclusão:
- Diagnóstico histológico/citológico de adenocarcinoma ductal pancreático (PDAC).
- Planejado para receber terapia sistêmica de primeira linha com FOLFIRINOX.
- Idade maior ou igual a 18 anos.
- Status de desempenho do Eastern Cooperative Oncology Group (ECOG) 0-1.
Medula óssea e função de órgãos adequadas, conforme definido pelos seguintes valores laboratoriais:
- Contagem absoluta de neutrófilos (ANC) maior ou igual a 1,5 x 10^9/L.
- Contagem de plaquetas maior ou igual a 75 x 10^9/L.
- Hemoglobina maior ou igual a 9,0 g/dL.
- Taxa de filtração glomerular (TFG) estimada pela equação de Cockroft-Gault OU coleta de urina de 24 horas maior ou igual a 40 ml/min.
- Depuração de creatinina maior ou igual a 40 mL/min usando a fórmula de Cockcroft-Gault.
- Potássio dentro dos limites normais ou corrigido com suplementos.
- Razão normalizada internacional (INR) menor ou igual a 1,5.
- Bilirrubina sérica total menor ou igual a 2 x limite superior do normal (LSN) (qualquer bilirrubina elevada deve ser assintomática na inscrição), exceto para participantes com síndrome de Gilbert documentada, que só podem ser incluídos se a bilirrubina total for menor ou igual a 3 x LSN ou bilirrubina direta menor ou igual a 1,5 x LSN).
- Alanina aminotransferase (ALT) e aspartato aminotransferase (AST) menor ou igual a 2,5 x LSN (ou menor ou igual a 5 x LSN se houver metástases hepáticas).
- Capaz de compreender e assinar voluntariamente o formulário de consentimento informado.
- Capaz de cumprir o cronograma de visitas do estudo e outros requisitos do protocolo.
- Capaz de engolir medicamentos orais e não tem contra-indicações para injeções subcutâneas de insulina.
- Doença mensurável ou avaliável por Critérios de Avaliação de Resposta em Tumores Sólidos (RECIST) 1.1 na linha de base.
- Expectativa de vida de mais de 90 dias, conforme julgado pelo médico do estudo.
Critério de exclusão:
- Ausência de metástases distantes ou linfonodais. Participantes com PDAC limítrofe ressecável ou localmente avançado não são elegíveis.
- Recebeu terapia sistêmica anterior (quimioterapia ou qualquer outro agente anticancerígeno) para tratamento de PDAC metastático. Os participantes que receberam quimioterapia adjuvante após a ressecção cirúrgica da doença em estágio inicial são elegíveis.
- Atualmente recebendo terapia anti-câncer (quimioterapia ou qualquer outro agente anti-câncer).
- Não adequado para quimioterapia combinada, conforme julgado pelo médico do estudo.
- Presença de metástases cerebrais.
- Diagnóstico conhecido de diabetes tipo I onde já está indicado o controle glicêmico rigoroso e acompanhamento endocrinológico de perto.
- Diagnóstico conhecido de diabetes tipo II e já acompanhado por Endocrinologista.
- Participantes do sexo feminino com teste de gravidez positivo.
- Participantes que não são seguros para incluir no estudo conforme julgado pelo médico do estudo por qualquer motivo médico ou não médico.
- Incapaz de cumprir as avaliações e acompanhamento do estudo.
Plano de estudo
Como o estudo é projetado?
Detalhes do projeto
- Finalidade Principal: Tratamento
- Alocação: N / D
- Modelo Intervencional: Atribuição de grupo único
- Mascaramento: Nenhum (rótulo aberto)
Armas e Intervenções
Grupo de Participantes / Braço |
Intervenção / Tratamento |
|---|---|
|
Experimental: Glucose Measurements via Blood Draws
Participants will have glucose levels measured using blood drawn prior to each cycle of systemic therapy.
|
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.
|
O que o estudo está medindo?
Medidas de resultados primários
Medida de resultado |
Descrição da medida |
Prazo |
|---|---|---|
|
Proportion of participants who experience at least one episode of hyperglycemia
Prazo: From baseline (up to 2 weeks prior to first dose) until progression of disease, assessed up to 24 months.
|
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%.
|
From baseline (up to 2 weeks prior to first dose) until progression of disease, assessed up to 24 months.
|
|
Percentage of glucose measurements above the target range
Prazo: From baseline (up to 2 weeks prior to first dose) until progression of disease, assessed up to 24 months.
|
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%.
|
From baseline (up to 2 weeks prior to first dose) until progression of disease, assessed up to 24 months.
|
Medidas de resultados secundários
Medida de resultado |
Descrição da medida |
Prazo |
|---|---|---|
|
Overall response rate (ORR) of the cohort, as defined by RECIST 1.1
Prazo: From the date of the screening scan (within 28 days of first dose) until the date of confirmed progression, assessed up to 24 months.
|
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.
|
From the date of the screening scan (within 28 days of first dose) until the date of confirmed progression, assessed up to 24 months.
|
|
Progression-free survival (PFS) of the cohort from the initiation of first-line systemic therapy
Prazo: 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.
|
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 from the initiation of first-line systemic therapy
Prazo: 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.
|
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.
|
Outras medidas de resultado
Medida de resultado |
Descrição da medida |
Prazo |
|---|---|---|
|
Overall response rate (ORR) of the cohort, as defined by RECIST 1.1 and stratified by prognostic and metabolic gene expression subtypes of PDAC
Prazo: From the date of the screening scan (within 28 days of first dose) until the date of confirmed progression, assessed up to 24 months.
|
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.
|
From the date of the screening scan (within 28 days of first dose) until the date of confirmed progression, assessed up to 24 months.
|
|
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
Prazo: 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 prognostic and metabolic gene expression subtypes of PDAC.
|
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 prognostic and metabolic gene expression subtypes of PDAC from the initiation of first-line systemic therapy
Prazo: 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 prognostic and metabolic gene expression subtypes of PDAC.
|
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.
|
|
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
Prazo: From the date of the screening scan (within 28 days of first dose) until the date of confirmed progression, assessed up to 24 months.
|
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.
|
From the date of the screening scan (within 28 days of first dose) until the date of confirmed progression, assessed up to 24 months.
|
|
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
Prazo: 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
Prazo: 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.
|
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.
|
|
Amount of insulin, measured in molar, for participants from screening until the end of study visit
Prazo: From the date of screening blood sample collection until the date of the end of study blood sample collection (an average of 6 months).
|
The quantity of insulin, measured in molar from immunoassays, from blood samples collected throughout the study.
|
From the date of screening blood sample collection until the date of the end of study blood sample collection (an average of 6 months).
|
|
Amount of proinsulin, measured in molar, for participants from screening until the end of study visit
Prazo: 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).
|
The quantity of proinsulin, measured in molar from immunoassays, from blood samples collected throughout the study.
|
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).
|
|
Amount of C-peptide, measured in molar, for participants from screening until the end of study visit
Prazo: 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).
|
The quantity of C-peptide, measured in molar from immunoassays, from blood samples collected throughout the study.
|
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).
|
|
Amount of circulating biomarkers, measured in molar, for participants from screening until the end of study visit
Prazo: 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).
|
The quantity of circulating biomarkers, measured in molar from immunoassays, from blood samples collected throughout the study.
|
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).
|
Colaboradores e Investigadores
Patrocinador
Colaboradores
Investigadores
- Investigador principal: Daniel Renouf, MD, MPH, BC Cancer
Publicações e links úteis
Publicações Gerais
- Sharma A, Smyrk TC, Levy MJ, Topazian MA, Chari ST. Fasting Blood Glucose Levels Provide Estimate of Duration and Progression of Pancreatic Cancer Before Diagnosis. Gastroenterology. 2018 Aug;155(2):490-500.e2. doi: 10.1053/j.gastro.2018.04.025. Epub 2018 Apr 30.
- 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.
Datas de registro do estudo
Datas Principais do Estudo
Início do estudo (Real)
Conclusão Primária (Estimado)
Conclusão do estudo (Estimado)
Datas de inscrição no estudo
Enviado pela primeira vez
Enviado pela primeira vez que atendeu aos critérios de CQ
Primeira postagem (Real)
Atualizações de registro de estudo
Última Atualização Postada (Real)
Última atualização enviada que atendeu aos critérios de controle de qualidade
Última verificação
Mais Informações
Termos relacionados a este estudo
Palavras-chave
Termos MeSH relevantes adicionais
- Doenças do Sistema Endócrino
- Neoplasias por local
- Neoplasias
- Doenças Metabólicas
- Neoplasias do Aparelho Digestivo
- Doenças do aparelho digestivo
- Distúrbios do Metabolismo da Glicose
- Neoplasias das Glândulas Endócrinas
- Doenças pancreáticas
- Doenças Nutricionais e Metabólicas
- Neoplasias Pancreáticas
- Hiperglicemia
- Administração de Serviços de Saúde
- Qualidade, acesso e avaliação da assistência médica
- Qualidade de assistência médica
- Indicadores de qualidade, assistência médica
- Padrão de atendimento
Outros números de identificação do estudo
- H21-03061
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Estuda um produto de dispositivo regulamentado pela FDA dos EUA
produto fabricado e exportado dos EUA
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