Neoplasms

All Conditions

Nervous System Diseases

Gland and Hormone Related Diseases

Behaviors and Mental Disorders

Musculoskeletal Diseases

Rare Diseases

Carcinoma

Pituitary Diseases

Aggression

Acromegaly

Pituitary Neoplasms

Prolactinoma

Neoplasms, Glandular and Epithelial

Neoplasms by Histologic Type

Hypothalamic Diseases

Brain Diseases

Central Nervous System Diseases

Endocrine System Diseases

Endocrine Gland Neoplasms

Hypothalamic Neoplasms

Supratentorial Neoplasms

Brain Neoplasms

Central Nervous System Neoplasms

Nervous System Neoplasms

Pituitary Cancer

Gerald Raverot, MD PhD

Emmanuel Jouanneau, MD PhD

The purpose of this study is to observe predictors of pituitary tumor recurrence and markers of persistent disease activity through computerized collection of comprehensive demographic, therapeutic, pathologic and outcome information on patients harboring pituitary mass lesions of all types.

DNA and pituitary tumor frozen sample (Neurobiotec Biological Resource Centre (BRC) of Hospices Civils de Lyon (HCL))

PITUItary Carcinoma or Aggressive Tumors REgistry -Lyon

PITUItary Carcinomas or Aggressive Tumors REgistry: Monocentric Study Form a Cohort of Patient Operated on for Pituitary Tumors in University Hospital of Lyon (France)

Clinical, biochemical et imaging evaluation of a cohort of patient operated in the referral center for pituitary tumor.

Identification of recurrence or progression an analysis of the clinicopathological classification.

Evaluation of the different therapeutic strategies (med, surgery, chemotherapies, radiation therapy) to prevent recurrence or tumor progression.

Analysis of the expression of SST receptors in GH, PRL and ACTH secreting pituitary tumors: SSTR expression accessed by immunohistochemistry of the pituitary tumor.

Evaluation of the response to somatostatine analogs: somatostatine analogs efficacy evaluated by normalization of hormone hypersecretion in ACTH, GH and PRL secreting pituitary tumor.

Evaluation of MGMT expression (accessed by immunohistochemistry of the pituitary tumor) and response to temozolomide treatment (evaluated according to RECIST criteria) for patient presenting multirecurrent tumors resistant to conventional treatment.

Hospices Civils de Lyon

Symptoms and General Pathology

Skin and Connective Tissue Diseases

Nutritional and Metabolic Diseases

Syndrome

Adenoma

Cushing Syndrome

Lipodystrophy

Adrenocortical Hyperfunction

Adrenal Gland Diseases

Cushing's Syndrome

Hyperadrenalism

Anti-Inflammatory Agents

All Drugs and Chemicals

Hypoglycemic Agents

Hydrocortisone

Hydrocortisone 17-butyrate 21-propionate

Hydrocortisone acetate

Hydrocortisone hemisuccinate

Insulin

Insulin, Globin Zinc

Glucocorticoids

Hormones

Hormone Antagonists

normal weight metabolic healthy patients having partial nephrectomy with small AT Biopsy.

obese individuals already included and having biopsies of VAT and SCAT stocked.

The purpose of this trial is to investigate the impact of cortisol on adipose tissue functions, distribution and morphology. Patient with endogenous blood cortisol excess exhibit changes in adipose tissue, with fat gain in the upper trunk, face and neck leading to visceral obesity and features of the metabolic syndrome. The aims of this study will be

* to compare the pattern of gene expression between visceral and subcutaneous adipose tissue in Cushing patients requiring an adrenalectomy as cortisol adenoma treatment;
* to compare these patterns of gene expression with those of two control populations:1/ healthy metabolic subjects having a partial nephrectomy, 2/obese patients with similar degree of insulin resistance.

analyze the role of glucocorticoid in AT distribution.

Bruno Feve, PhD

Cushing's syndrome is a rare disease resulting from chronic exposure to glucocorticoids (endogenous or iatrogenic) with abnormal fat distribution (lipodystrophy). Glucocorticoids regulate the functions of adipose tissue (AT) targeting adipocyte differentiation as well as anabolic, catabolic and secretory pathways of the adipocyte. However, the mechanisms by which glucocorticoids differentially disrupt the development or metabolism of AT between deep and superficial deposits remain unknown. Among the main effectors of the glucocorticoid signaling pathway, 11 beta-hydroxysteroid deshydrogenase (11beta-HSD1) , that regenerate cortisol from cortisone, is likely a key step in the biological effect of glucocorticoids in AT. Identifying these mechanisms of action of glucocorticoids on different fat depots requires the comparison with fatty deposits derived from two types of control populations: 1/ normal weight individuals without inflammatory or metabolic disorder (controls1); 2/individuals obese matched for the level of insulin resistance (controls2).

Hypothesis: Excess glucocorticoids cause abnormal fat distribution via a direct effect on the various deposits of AT, leading secondarily to insulin resistance.

Primary endpoint: To compare gene expression of glucocorticoid signaling between the visceral AT (VAT) of Cushing patients with that of controls1 (matched for age and sex).

Secondary endpoints:

1. For patients with Cushing and controls1, to compare their respective subcutaneous AT (SCAT) and VAT for:

   * The expression of genes involved in differentiation and inflammation of the AT,
   * Morphological aspects: adipocyte size, fibrosis, inflammation, immunohistochemistry.
2. Same parameters for Cushing patients and controls2 (matched for sex, age + / -5, HOMA-R + / -1), to differentiate the specific effects of glucocorticoid from the effects of insulin resistance,
3. To compare these parameters between SCAT and VAT from Cushing patients. Methodology and experimental design: non-randomized comparative multicenter study with constitution of a biological collection.

Patients will be recruited in endocrinology before adrenalectomy and controls1 in urology. They will have a preoperative assessment and sampling of perirenal AT and SCAT at surgery. Controls2 are already included in the CRC2007-P050318 and will be drawn for matching.

Number of patients needed: We assume the relative gene expression of 11β-HSD1 in the VAT not exposed to glucocorticoids = 0.81 ± 0.121. Our recruitment potential of Cushing patients is 30 patients. With 30 patients per group, we will be able to detect a difference in 11β-HSD1 gene expression in the VAT of Cushing patients at least 15% higher compared to controls1.

Pattern of Gene Expression in Adipose Tissue From Patients With Cushing Syndrome

Comparative Study of Subcutaneous and Visceral Adipose Tissue in Patients Affected by Cushing Syndrome Versus 2 Controls Population

Comparison of glucocorticoid pathway genes expression between visceral adipose tissue of Cushing patients and that of normal weight controls matched on sex and age.

For patients with Cushing and controls1, to compare their respective SCAT and VAT for:

* The expression of genes involved in differentiation and inflammation of the AT,
* Morphological aspects: adipocyte size, fibrosis, inflammation, immunohistochemistry.

Comparison of these same parameters(secondary outcome n°1) between Cushing patients and controls2 (matched for sex, age + / -5, HOMA-R + / -1), to differentiate the specific effects of glucocorticoid from the effects of insulin resistance

To compare these parameters between SCAT and VAT from Cushing patients

Assistance Publique - Hôpitaux de Paris

Heart and Blood Diseases

Diabetes Mellitus, Type 2

Diabetes Mellitus

Hypertension

Facies

Glucose Intolerance

Hyperglycemia

Adrenocortical Carcinoma

Adenocarcinoma

Adrenal Cortex Neoplasms

Adrenal Gland Neoplasms

Adrenal Cortex Diseases

Antineoplastic Agents

Vasoconstrictor Agents

Respiratory System Agents

Pembrolizumab

Epinephrine

Racepinephrine

Epinephryl borate

Antineoplastic Agents, Immunological

Immune Checkpoint Inhibitors

Participants will be treated on Day -3 to Day 1 (Cohort 1 under fasting conditions) or Day -6 to Day 1 (Cohort 2 under fed conditions) for Cycle 1 only. During the lead-in period, 300 mg relacorilant will be administered daily for 4 -7 days. Patients will receive their first pembrolizumab infusion on Cycle 1 Day 1. The participants will then receive combined treatment from Cycle 1 Day 1 until confirmed PD or unacceptable toxicity. Pembrolizumab will be administered every 6 weeks (on Day 1 of each 42-day cycle) and relacorilant will be administered daily. Optional Cohort 3 will lead-in with 400 mg relacorilant once daily for 7 days and combined treatment of relacorilant and pembrolizumab, depending on PD and toxicity.

Relacorilant, 100 mg soft gel capsules orally once daily

Relacorilant

Pembrolizumab 400 mg infusion every 6 weeks

Andreas G Moraitis, MD

This study will investigate the safety and efficacy of Relacorilant in combination with Pembrolizumab for Patients with Adrenocortical Carcinoma which Produces Too Much Stress Hormone (Cortisol).

Relacorilant is a small molecule antagonist of the glucocorticoid receptor (GR).

The goal of this study is to assess the safety and efficacy of relacorilant when given in combination with pembrolizumab in patients with advanced adrenocortical carcinoma (ACC) which produces too much stress hormone (cortisol). Too much stress hormone (cortisol) is also called glucocorticoid (GC) excess.

Eligible patients are those with advanced ACC that produces too much cortisol.

Patients will receive treatment until progressive disease (PD) (per RECIST v1.1) is confirmed, experience unmanageable toxicity, or until other treatment discontinuation criteria are met. All patients will be followed for documentation of disease progression, survival information (i.e., date and cause of death) and subsequent treatment.

Study of Relacorilant in Combination With Pembrolizumab for Patients With Adrenocortical Carcinoma Which Produces Too Much Stress Hormone (Cortisol)

A Phase 1b, Open-Label Study of Relacorilant in Combination With Pembrolizumab for Patients With Adrenocortical Carcinoma With Excess Glucocorticoid Production

Evaluate the percentage of patients with a dose-limiting toxicity

Evaluate the non-progression rate (NPR) per RECIST v1.1

Evaluate progression-free survival (PFS) per RECIST v1.1

Adverse events (AEs) by severity grade using the National Cancer Institute Common Terminology Criteria for Adverse Events Version 5.0 (NCI CTCAE v5.0)

Plasma concentrations of relacorilant in combination with pembrolizumab will be calculated in patients with advanced ACC and glucocorticoid excess

Corcept Therapeutics

To determine the outcomes of patients with different pituitary disorders whether they are managed medically, surgically or expectantly.

A chart audit of around 1500 patients seen in two specific clinics, the Medical Pituitary Clinic and the combined Endocrine/Neurosurgical Pituitary Clinic at the University of Alberta Hospital, will be performed to determine the effectiveness of various treatment strategies on the long term outcome of specific pituitary disorders. The investigator's will collect retrospective demographic (age, sex, ethnicity), clinical (mode of presentation, hormonal parameters) and therapeutic outcome (surgical, medical, expectant and / or radiation treatment; co-morbidities and complications) of patients seen in these two clinics between January 2000 and December 2020.

Long Term Outcome Study in Patients With Pituitary Disorders

Using clinical, biochemical and imaging studies of a cohort of surgically operated patients to identify prognostic factors of tumor recurrence

University of Alberta

Edotreotide

Radiopharmaceuticals

To give Ga-68 DOTATOC in pituitary patients doing PET/CT

They are compared with Ga-68 DOTATOC PET performed in another study on patients with no pituitary disease.

The intervention is to administer Ga-68 DOTATOC in pituitary patients doing PET/CT

Gallium-68 DOTATOC PET

Helena Filipsson Nyström, Ass Prof

Title: Gallium (GA) -68-DOTATOC -PET (positron emission tomography) in the management of pituitary tumours Medical product: Ga-68-DOTATOC in PET/computer tomography (CT) Route of administration: Intravenously Diseases of interest: Pituitary tumours Aim: To study the detection of pituitary tumours with Ga-68-DOTATOC -PET (Ga-PET) and to correlate the tracer expression to somatostatin receptor (sst) occurrence Study design: Prospective non-randomised case-control study with open design with GA-PET before and after pituitary surgery in patients with pituitary tumours Study population: patients with acromegaly (n=10), Cushing's' disease of pituitary origin (n=10), TSH (thyreotropin) producing tumours (TSHomas) (n=5) and non-functioning pituitary adenomas (NFPA) (n=20) Number of patients: 45 Inclusion criteria: Adult man or woman (over 18 years) and naïve, unoperated pituitary tumour with growth hormone (GH) or adrenocorticotrophic hormone (ACTH)) or TSH production or NFPA without treatment with somatostatin analogues (SSA) or dopamine agonists.

Exclusion criteria: Patient who may not attend to the protocol according to the investigators opinion. Pregnancy or lactating. Isolated prolactin producing tumours. Overproduction of gonadotropins. Carcinoids ie ectopic corticotrophin realising factor (CRF) production. Known or suspected allergy to the trial product or related products.

Controls: Adult patients with Thyroid associated ophthalmopathy (TAO) before iv steroid infusion (part of another study see this protocol)- Study variables: Tumour detection, Tracer uptake as Standardised uptake value (SUV) max (SUVmax), SUV hotspot and SUV mean in regions of interests (ROIs) Time schedule: Recruitment of patients 2015-2017. Study termination 3 years later

Background The most common cause to pituitary insufficiency is the pituitary adenoma (PA). PA may be divided into hormone producing PAs and non-functioning PAs (NFPA). Normal pituitary tissue, as well as tissues from PAs, expresses somatostatin receptors (sst). Five subtypes of sst receptors has been characterized.

Magnetic resonance tomography (MRI) presents anatomy, while in vivo diagnostics with somatostatin receptor scintigraphy (SRS) or position emission tomography (PET) reflect the functional properties of the tissue. The SRS have earlier been evaluated for diagnostics of pituitary diseases and has low discriminative ability to differ tumor tissue from normal pituitary tissue even though some secretory tumors and NFPA are seen. The superiority of the PET in diagnostics compared to the SRS is based on higher spatial resolution and a higher tumor to background ratio. Therefore it is of large interest to study Gallium 68 DOTATOC (Ga-PET) i small tumours that exhibit sst, such as in the pituitary, where high resolution is essential to discriminate from normal tissue and to evaluated residual tumor tissue postoperatively.

Aim with the project

To evaluate Ga-PET in the management of pituitary tumors and to seek the answer to the following questions:

1. Is the method of value in primary diagnostics in PAs? Does Ga-PET contribute with more functional information than that given from an conventional MRI?
2. Is the method of value in the follow-up, the detection of residual tumor tissue, and increase the possibility to differ scar tissue from true tumor?
3. Can relapses of PA be detected earlier with Ga-PET than with conventional MRI?
4. Are some of the sub-groups easier to detect that others??
5. Can the pathological-anatomical findings and the immunochemical expression of sst be correlated to the PET findings?
6. Can the treatment with somatostatin analogues be designed from the PET investigation and the sst analysis?

Method The aim is to recruit 10 patients with acromegaly (GH-producing PA), 10 patients with Cushing's disease (ACTH-producing PA), 5 patients with TSH-producing PA (TSHoma) and 20 patients with NFPA and to do Ga-PET before and after the pituitary surgery. In the Cushing patients, the TSHomas and in NFPA Ga-PET will also be dome after 3 years postoperatively to detect recurrences. At surgery, pituitary tissue is taken to investigate hormonal expression, sst and for further molecular genetic studies. At all PET occasions blood specimens from the patients are collected for future analyses. They will be kept in a freezer.

If difficulties to separate the Ga-Pet up-take in tumors from normal pituitary tissue the tumor expression may be enhanced by a somatostatin injection before Ga-PET that suppresses normal tissue.

The pituitary PET of pituitary tumours patients will be compared with the pituitary of patients with thyroid associated tumours performing PET according to the similar protocol in Another study

Significance This study is a pilot study. Ga-PET has not been used in pituitary tumors but there is known from studies in patients with gastrointestinal neuroendocrine tumors that the pituitary is seen on GA-PET. This is a "proof of concept". It addresses some of the clinical problems in the management of pituitary tumors. If the questions addressed in this study will be answered in advantage for PET, PET may be a routine investigation and the patients may avoid invasive procedures and repeated MRI. In addition, the patients may have better information regarding cure or not. If not, the treatment may be tailored from the sst receptor expression. This is of great importance for the patients and for the health care system.

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
PITUItary Carcinoma or Aggressive Tumors REgistry -Lyon	NCT02854228	Pituitary Tumor		-	Hospices Civils de Lyon
Pattern of Gene Expression in Adipose Tissue From Patients With Cushing Syndrome	NCT01688349	Cushing Syndrom...	analyze the rol...	18 Years -	Assistance Publique - Hôpitaux de Paris
Pattern of Gene Expression in Adipose Tissue From Patients With Cushing Syndrome	NCT01688349	Cushing Syndrom...	analyze the rol...	18 Years -	Assistance Publique - Hôpitaux de Paris
Study of Relacorilant in Combination With Pembrolizumab for Patients With Adrenocortical Carcinoma Which Produces Too Much Stress Hormone (Cortisol)	NCT04373265	Adrenocortical ...	Relacorilant Pembrolizumab	18 Years -	Corcept Therapeutics
Long Term Outcome Study in Patients With Pituitary Disorders	NCT03665064	Pituitary Disea... Pituitary Neopl...		-	University of Alberta
Ga-68-DOTATOC -PET in the Management of Pituitary Tumours	NCT02419664	Pituitary Tumou...	Gallium-68 DOTA...	18 Years -	Göteborg University
PITUItary Carcinoma or Aggressive Tumors REgistry -Lyon	NCT02854228	Pituitary Tumor		-	Hospices Civils de Lyon
Long Term Outcome Study in Patients With Pituitary Disorders	NCT03665064	Pituitary Disea... Pituitary Neopl...		-	University of Alberta

Spots Global Cancer Trial Database for cushing

Every month we try and update this database with for cushing 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 cushing

Every month we try and update this database with for cushing 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 cushing 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.