Neoplasms

Skin and Connective Tissue Diseases

All Conditions

Symptoms and General Pathology

Digestive System Diseases

Gland and Hormone Related Diseases

Nervous System Diseases

Heart and Blood Diseases

Diseases and Abnormalities at or Before Birth

Nutritional and Metabolic Diseases

Immune System Diseases

Rare Diseases

Breast Neoplasms

Syndrome

Pancreatic Neoplasms

Melanoma

Pancreatitis

Pancreatitis, Chronic

Ataxia

Cerebellar Ataxia

Telangiectasis

Ataxia Telangiectasia

Peutz-Jeghers Syndrome

Nevus

Colorectal Neoplasms

Colorectal Neoplasms, Hereditary Nonpolyposis

Gastrointestinal Neoplasms

Digestive System Neoplasms

Endocrine Gland Neoplasms

Gastrointestinal Diseases

Pancreatic Diseases

Endocrine System Diseases

Intestinal Neoplasms

Neoplastic Syndromes, Hereditary

Colonic Diseases

Intestinal Diseases

Genetic Diseases, Inborn

DNA Repair-Deficiency Disorders

Metabolic Diseases

Intestinal Polyposis

Lentigo

Melanosis

Hyperpigmentation

Pigmentation Disorders

Skin Diseases

Pancreatic Cancer

Hereditary Pancreatitis

Gastrointestinal Agents

All Drugs and Chemicals

Amino Acids

Pancrelipase

Pancreatin

Secretin

Hormones

Hormone Antagonists

Serine

High Risk Group 2 (familial pancreatic cancer relatives):

1. \> 55 years old or 10 years younger than the age of youngest relative with pancreatic cancer, and
2. come from a family with 2 or more members with a history of pancreatic cancer (2 of which have a first-degree relationship consistent with familial pancreatic cancer), and
3. have a first-degree relationship with at least one of the relatives with pancreatic cancer.

If there are 2 or more affected blood relatives, at least 1 must be a first-degree relative of the individual being screened

High Risk Group 3 (Group 1 germline mutation carriers with an associated with an estimated lifetime risk of pancreatic cancer of \~10% or higher):

a. \> 50 years old or 10 years younger than the age of the youngest relative affected, if pancreatic cancer is in family, and b. The Patient is a carrier of a confirmed BRCA2, ATM or PALB2 mutation, regardless of family history of pancreatic cancer. b.\> Individual is a carrier of a confirmed FAMMM (p16/CDKN2A) mutation, age 40 years or older, regardless of family history of pancreas cancer.

High Risk Group 4 (Group 2 germline mutation carriers with an associated with an estimated lifetime risk of pancreatic cancer of \~5%):

1. \> 50 years old or 10 years younger than the age of the youngest relative with pancreatic cancer, and
2. The patient is a carrier of a confirmed BRCA1 or HNPCC (hereditary non-polyposis colorectal cancer or Lynch syndrome, hMLH1, hMSH2, PMS1, hMSH6, EpCAM) gene mutation, and there is \> 1 pancreatic cancer in the family, one of whom is a first- or second-degree relative of the subject to be screened.

High risk group 5 (hereditary pancreatitis) with confirmed gene mutations that predispose to chronic pancreatitis, such as PRSS1, PRSS2, CTRC) and age 50 years or older (these patients have an estimated lifetime risk for pancreatic cancer of 40%) or twenty-years since their first attack of pancreatitis, whichever age is younger.

1. At least 30 years old, and
2. at least 2 of 3 criteria diagnostic of Peutz-Jeghers syndrome (characteristic intestinal hamartomatous polyps, mucocutaneous melanin deposition, or family history of Peutz-Jeghers syndrome), or,
3. known STK11 gene mutation carrier

1. are undergoing routine EGD or Colonoscopy; or Endoscopic Ultrasound (EUS) and/or Endoscopic Retrograde Cholangiopancreatography (ERCP) for non-pancreatic indications as part of their standard medical care, and
2. have no clinical or radiologic suspicion of pancreatic disease (chronic pancreatitis or pancreatic cancer)

1. are undergoing EUS and/or ERCP for evaluation and/or treatment of suspected or proven chronic pancreatitis as part of their standard medical care, and,
2. have no clinical or radiologic suspicion of pancreatic cancer

a. are undergoing EUS and/or ERCP for evaluation and/or treatment of suspected or proven pancreatic ductal adenocarcinoma (based on clinical and radiologic evidence)

are undergoing EUS and/or ERCP for evaluation and/or treatment of suspected or proven pancreatic cancer precursor, intraductal papillary mucinous neoplasm (based on clinical presentation and radiologic or prior EUS or radiologic evidence of a dilated main pancreatic duct and/or pancreatic cystic lesion communicating with the pancreatic ductal system).

inject Secretin to stimulate pancreatic digestive fluid, which is collected in duodenum near ampulla via endoscope suction port. This fluid will be assessed for biomarkers.

MRI abdomen with contrast (MRCP) will be clinically indicated for abnormal novel CA-19-9 lab results.

A tumor marker gene test that will be used to stratify individuals into one of several circulating tumor marker reference ranges for CA19-9. The variants in the genes FUT3 and FUT2 affect the levels of CA19-9.

Tumor marker gene test with CA19-9

Hilary Cosby, RN

Scott Merenda, BSN

James Farrell, MD

Hilary Cosby, RN, CGRN

Michael Goggins, MD

Marcia I Canto, MD

Emily Blair

Chinedu Ukaegbu

Sapna Syngal, MD

Erika Koeppe, MS

Elena Stoffel, MD

Tiffany Lam

Fay Kastrinos, MD

Barbara Heaton

Wendy Brock, RN

Amitabh Chak, MD

Maureen DeMarshall, RN

Daniel Clay

Bryson Katona, MD

Christine Decapite

Sara Booz

Randall Brand, MD

Johns Hopkins clinical research office quality assurance group will monitor and audit this study at Johns Hopkins. The Sub Investigator at each site will be responsible for internal monitoring at their site.

The Sub Investigator at each site will be responsible for internal monitoring at their site. The site sub Investigator and study team will report any serious adverse events to Principal Investigator and annually report adverse events.

Evaluation of the effect of diagnostic tests for pancreatic cancer

No masking of the diagnostic test results

The Cancer of the Pancreas Screening-5 CAPS5)Study

Aim #3: To determine the prevalence of pancreatic lesions, pancreatic fluid mutations and circulating pancreatic epithelial cells among a large cohort of high-risk individuals undergoing pancreatic screening and surveillance of a new cohort in which screening is begun at age \>55.

Aim #4 To evaluate the diagnostic performance of a tumor marker gene test to personalize the normal reference range of tumor markers such as CA19-9 for patients undergoing pancreatic surveillance.

Aim #1: To evaluate pancreatic fluid mutations and circulating pancreatic epithelial cells as accurate markers of neoplasia by comparing their prevalence in cases with sporadic pancreatic neoplasia to healthy and disease controls.

Aim #2: To compare the prevalence of pancreatic fluid mutations and circulating pancreatic epithelial cells among a prospective cohort of individuals with sporadic pancreatic cysts undergoing pancreatic surveillance.

ChiRhoClin, Inc.

National Cancer Institute (NCI)

National Institutes of Health (NIH)

Johns Hopkins University

Adenocarcinoma

Neoplasms, Cystic, Mucinous, and Serous

Neoplasms, Glandular and Epithelial

Neoplasms by Histologic Type

Fifteen subjects will be randomly selected to undergo S-MRI prior to surgery. These subjects would receive Secretin, administered by IV bolus injection over 1 minute followed by a 30 second saline flush.

Fifteen subjects will be selected as controls, undergoing MRI without secretin-enhancement and matched for age, sex, race and tumor-type.

Subjects will each undergo an S-MRI evaluation, at a dose of 0.2 ucg/kg per exam. Secretin will be administered by IV bolus injection over 1 minute followed by a 30 second saline flush. The maximum dose of secretin will be 18.5 ucg.

Elizabeth Hecht, MD

The aim of the study is to evaluate the utility of secretin-enhanced MRI (S-MRI) in detecting and measuring pancreatic lesions in patients with known adenocarcinoma or Intraductal papillary mucinous neoplasm (IPMN) lesions. The hypothesis is that S-MRI is superior to MRI without secretin enhancement (N-MRI) in increasing tumor conspicuity, allowing for improved identification and more accurate measurement of lesions or precursor lesions in the pancreas.

Pancreatic cancer remains the fourth leading cause of cancer-related death in the United States and is marked by advanced stage at diagnosis and a high mortality rate. Intraductal papillary mucinous neoplasm (IPMN) is a cystic lesion that can be potentially cancerous, leading to pancreatic adenocarcinoma. Currently, there is no existing imaging modality that is both sensitive and cost-effective enough in accurately measuring or detecting adenocarcinoma and IPMN. Improving the methods used in identification and localization of this disease is critical.

Secretin, a hormone produced by duodenal mucosal cells increases blood-flow to the pancreas. The investigators' hypothesis is that as secretin increases blood flow to the pancreas, there will be increased conspicuity in areas of dysplasia/cancer where there is minimal blood-flow, enhancing tumor detection. The investigators are conducting a prospective, randomized-control pilot study of thirty subjects with IPMN or pancreatic cancer who are undergoing surgical resection at Columbia University's Pancreas Center. Fifteen subjects will be randomly selected to undergo S-MRI prior to surgery and fifteen subjects will be selected as controls, undergoing MRI without secretin-enhancement and matched for age, sex, race and tumor-type. The investigators will first evaluate if secretin allows for increased tumor conspicuity, enhanced visualization of the lesion, by comparing the calculated tumor conspicuity of S-MRI to N-MRI groups.

The investigators will then assess if S-MRI imaging allows for increased accuracy in lesion measurements by looking at the concordance in measurements between S-MRI and tumor specimens post-resection as compared to the concordance in measurements between N-MRI and tumor specimens post-resection.

Secretin-enhanced Magnetic Resonance Imaging (S-MRI) for Pancreatic Cancer Detection

MRI With Secretin Enhancement to Increase Conspicuity of Pancreatic Cancer

The primary outcome is whether S-MRI allows for better tumor detection secondary to anticipated increased conspicuity of tumor due to secretin's effect on increasing blood flow to the normal pancreas as compared to N-MRI. Determining S-MRI's efficacy versus that of N-MRI will be carried out by comparing tumor conspicuity measurements in S-MRI and N-MRI groups. Tumor conspicuity will be measured by calculating the contrast to noise ratio, placing region of interest (ROI) on tumor and adjacent tissue and dividing by image noise.

The secondary outcome will be the discrepancy in tumor size estimated from MRI and "confirmed" from post-surgical specimens. Tumor size estimated from MRI scans will be determined by measuring the greatest linear dimension (metric) of the lesion. Tumor size estimated by pathology will be directly measured using a linear scale (metric), taking the greatest linear dimension of the resected tumor. The discrepancy in estimated versus "confirmed" tumor size will be compared between S-MRI and N-MRI groups.

Elizabeth Hecht

Associate Professor of Clinical Radiology

Duodenopancreatic aspiration after secretin stimulation will be performed followed by endoscopic ultrasound-guided fine needle aspiration (EUS-FNA)

Endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) will be performed followed by duodenopancreatic aspiration after secretin stimulation

Secretin will be administered intravenous during 1 minute at a dose of 0,2 μg/Kg previous to the endoscopic procedure.

Endoscopic aspiration of duodenopancreatic juice after secretin stimulation

Endoscopic aspiration

Endoscopic ultrasound-guided fine needle aspiration of intraductal papillary mucinous intraductal neoplasia (IPMN).

Endoscopic ultrasound-guided fine needle aspiration

Àngels Ginès

Àngels Ginès, MD

Study to evaluate aspiration of duodenopancreatic juice after secretin stimulation (ADPJ-secr)versus endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) for molecular analysis of intraductal papillary mucinous intraductal neoplasia.

Aspiration of Duodenopancreatic Juice After Secretin Stimulation vs Endoscopic Aspiration for Molecular Analysis of Intraductal Papillary Mucinous Intraductal Neoplasia.

Aspiration of Duodenopancreatic Juice After Secretin Stimulation (ADPJ-secr-) vs Endoscopic Aspiration (EUS-FNA) for Molecular Analysis of Intraductal Papillary Mucinous Intraductal Neoplasia (IPMN).

In intracystic fluid obtained by EUS-FNA versus pancreatic juice obtained by ADPJ-secr after both techniques.

In samples obtained by EUS-FNA versus ADPJ-secr after performing both techniques, in the subgroup of patients undergoing pancreatic resection within 12 months after study entry.

In samples obtained by EUS-FNA versus ADPJ-secr after performing both techniques.

A sample is defined as suitable when it is read by the Qubit fluorometer, which only detects full double-stranded DNA suitable for molecular analysis.

In samples obtained by EUS-FNA versus ADPJ-secr within 12 months of study entry.

In samples obtained by both techniques under study (ADPJ-secr vs EUS-FNA) who have advanced neoplasia in the surgical resection specimen after surgery performed within 12 months after study inclusion.

Advanced neoplasia is defined as the presence of IPMN with high-grade dysplasia or IMPN with associated invasive carcinoma according to Lokuhetty D, et al. Digestive SystemTumours: WHO Classification of Tumours, International Agency for Research on Cancer, 2019.

In samples obtained by both techniques under study (ADPJ-secr vs EUS-FNA) who do not have advanced neoplasia in the surgical resection specimen after surgery performed within 12 months after inclusion in the study.

Advanced neoplasia is defined as the presence of IPMN with high-grade dysplasia or IPMN with associated invasive carcinoma according to Lokuhetty D, et al. Digestive System Tumours: WHO Classification of Tumours, International Agency for Research on Cancer, 2019.

To compare if diameter of the largest cystic lesion in mm is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if median maximum diameter of the main pancreatic duct assessed by EUS and measured in mm is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients that present a segmental main pancreatic duct dilatation assessed by EUS is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of cystic lesions located in the pancreatic head, pancreatic body or pancreatic tail assessed by EUS are different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients with \> 1 pancreatic cystic lesion assessed by EUS is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients that present mural nodules assessed by EUS is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients that present features of chronic pancreatitis assessed by EUS is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients that present intraductal calcifications assessed by EUS is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients that present pancreatic atrophy assessed by EUS is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if median of age measured in years is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of male or female patients are different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients with reported active smoking is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients with high risk chronic alcohol consumption (\> 21 standard drinks for men, \> 14 standard drinks for women) is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients with hypertension is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients with type 2 diabetes mellitus is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients with chronic heart failure is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients with chronic liver disease is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients with chronic kidney disease is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients with previous neoplasm in past medical history is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients with history of acute pancreatitis in past medical history is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients with history of chronic pancreatitis in past medical history is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients with history of pancreatic cancer in first degree relatives is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if time since diagnosis of IPMN measured in years is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportions of patients with MD-IPMN, BD-IPMN or mixed-type IPMN are different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if mean blood levels of amylase measured in U/L is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if mean blood levels of lipase measured in U/L is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if mean blood levels of creatinine measured in mg/dl is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if mean blood levels of total bilurrubin measured in mg/dl is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if mean blood levels of AST measured in U/L is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if mean blood levels of ALT measured in U/L is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if mean blood levels of GGT measured in U/L is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if mean blood levels of alkaline phosphatase measured in U/L is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if mean blood levels of hemoglobin measured in g/l is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if mean blood total count of platelets measured in units per microliter is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if mean blood levels of CA 19.9 measured in U/L is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if mean blood levels of CEA measured in U/L is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if mean blood levels of glycated hemoglobin measured in % is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]).

To compare if the proportion of patients with adverse effects associated with the techniques under study at 24 hours and 7 days is different between both groups of study (mutated GNAS/KRAS versus non-mutated GNAS/KRAS \[wild type\]). Adverse effects will be reported following the American Society of Gastrointestinal Endoscopy (ASGE) (P.B. Cotton, et al. Gastrointest Endosc, 2010) and the WHO Toxicity Grading Scale for Determining the Severity of Adverse Events, 2003.

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
The Cancer of the Pancreas Screening-5 CAPS5)Study	NCT02000089	Pancreas Cancer Peutz-Jeghers S... Gene Mutation Germline Mutati... Lynch Syndrome	Secretin MRI Tumor marker ge...	18 Years -	Johns Hopkins University
Secretin-enhanced Magnetic Resonance Imaging (S-MRI) for Pancreatic Cancer Detection	NCT01094626	Pancreatic Canc... Intraductal Pap...	Secretin	18 Years - 75 Years	Columbia University
Aspiration of Duodenopancreatic Juice After Secretin Stimulation vs Endoscopic Aspiration for Molecular Analysis of Intraductal Papillary Mucinous Intraductal Neoplasia.	NCT05914077	Intraductal Pap...	Secretin Endoscopic aspi... Endoscopic ultr...	18 Years -	Fundacion Clinic per a la Recerca Biomédica
The Cancer of the Pancreas Screening-5 CAPS5)Study	NCT02000089	Pancreas Cancer Peutz-Jeghers S... Gene Mutation Germline Mutati... Lynch Syndrome	Secretin MRI Tumor marker ge...	18 Years -	Johns Hopkins University

Spots Global Cancer Trial Database for secretin

Every month we try and update this database with for secretin cancer trials from around the world to help patients and their families find trials that might be right for them.
We offer this 100% free of charge and do not endorse any of the trials listed here, we hope it helps you or a loved one.

Spots Global Cancer Trial Database for secretin

Every month we try and update this database with for secretin cancer trials from around the world to help patients and their families find trials that might be right for them. We offer this 100% free of charge and do not endorse any of the trials listed here, we hope it helps you or a loved one.

Every month we try and update this database with for secretin cancer trials from around the world to help patients and their families find trials that might be right for them.
We offer this 100% free of charge and do not endorse any of the trials listed here, we hope it helps you or a loved one.