Neoplasms

All Conditions

Carcinoma

Carcinoma, Squamous Cell

Squamous Cell Carcinoma of Head and Neck

Neoplasms, Glandular and Epithelial

Neoplasms by Histologic Type

Neoplasms, Squamous Cell

Head and Neck Neoplasms

All Drugs and Chemicals

Phosphoinositide-3 Kinase Inhibitors

Enzyme Inhibitors

Participants receive Alpelisib PO QD for 14-21 days in the absence of disease progression of unacceptable toxicity and then undergo surgery. Participants may receive Alpelisib for up to 28 days if surgery is delayed.

Alpelisib

Laboratory Biomarker Analysis

Pharmacodynamic Study

Therapeutic Conventional Surgery

Ricklie Julian, MD

This phase II trial studies how well alpelisib works in treating participants with human papillomavirus(HPV)-associated stage I-IVA head and neck cancer that can be removed by surgery. Alpelisib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.

PRIMARY OBJECTIVES:

I. To assess the preliminary efficacy of neoadjuvant Alpelisib (BYL719) in patients with transorally-resectable, HPV+ head and neck squamous cell carcinoma (HNSCC), as measured by quantitative change in tumor size (change in T) following 14-21 days of treatment.

II. To evaluate the relationship between genomic PIK3CA activation to change in T.

SECONDARY OBJECTIVES:

I. To describe the tolerability of brief neoadjuvant exposure to BYL719. II. To assess the effect of BYL719 on the tumoral Ki-67 proliferation index. III. To evaluate viral and molecular mediators of response and resistance to BYL719, including viral messenger ribonucleic acid (mRNA), E6 and E7 oncoproteins, and phosphorylated (p)HER3.

OUTLINE:

Participants receive Alpelisib orally (PO) once daily (QD) for 14-21 days in the absence of disease progression of unacceptable toxicity and then undergo surgery. Participants may receive Alpelisib for up to 28 days if surgery is delayed.

After completion of study treatment, participants are followed up for up to 12 weeks.

Alpelisib in Treating Participants With Transorally Resectable HPV-Associated Stage I-IVA Oropharyngeal Cancer

Biomarker Modulation by Alpelisib (BYL719) in Transorally Resectable, HPV-Associated HNSCC: A Phase II Window Trial

Measurable index lesions on paired, pre-and post-treatment computed tomography scans (delta change in T) with size treated as a continuous variable. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), \>=30% decrease in the sum of the longest diameter of target lesions; Progressive disease (PD) is the sum of target lesions have increased by \>=20% and \>=5 mm from nadir; Stable disease (SD) neither sufficient shrinkage to qualify for PR not sufficient increase to qualify for PD, taking as reference the smallest sum diameters while on study.

Will compare percent change in tumor size (change in T) in patients with genomic PIK3CA pathway alteration (PIK3CA mutation, amplification, and fluorescence in situ hybridization \[FISH\] for PTEN loss) versus no genomic activation.

Will be reported descriptively, including tabulation of toxicities according to National Cancer Institut (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 4.

The safety of this window intervention will be reported descriptively, including tabulation of toxicities according to NCI CTCAE v.4.03, surgical complications, and length of hospital stay.

We hypothesize that BYL719 will reduce HPV mRNA, and this will correlate with decrease in tumor size.

We hypothesize that BYL719 will decrease tumoral E6 and E7 oncoprotein levels, and this will correlate with decrease in tumor size

We hypothesize that pHER3 is a resistance mechanism for BYL719, and that pHER3 will be upregulated in non-responders.

We hypothesize that HER3/PI3K dimerization is a resistance mechanism for BYL719, and that dimers will be upregulated in non-responders.

National Cancer Institute (NCI)

University of Arizona

Only AEs meeting one of the following criteria were collected.

* Any AE that is Grade 3 or higher, regardless of relationship to the study drug
* Any intolerable Grade 2 AE
* Any Grade AE resulting in holding or dose-reducing BYL719
* Any Grade 2 laboratory or vital sign values that are deemed clinically significant by the treating investigator
* Any Grade AE in the following categories of interest:

  * Rash
  * Diarrhea
  * Pneumonitis
  * Hyperglycemia

Participants receive Alpelisib PO QD for 10-21 days in the absence of disease progression of unacceptable toxicity and then undergo surgery. Participants may receive Alpelisib for up to 28 days if surgery is delayed.

Alpelisib: Given PO

Laboratory Biomarker Analysis: Correlative studies

Pharmacodynamic Study: Correlative studies

Therapeutic Conventional Surgery: Undergo surgery

Treatment (Alpelisib)

Age, Continuous

Sex: Female, Male

Ethnicity (NIH/OMB)

Race (NIH/OMB)

United States

Region of Enrollment

This study stopped accrual early as the investigational product (IP) manufacturer, Novartis, terminated the study stopping provision of IP. 6 out of 20 subjects were accrued, 5 of which completed study. Due to early termination with few patients, only the counts of events have been calculated and no testing was done.

Stable disease

Partial response

Complete response

Progressive disease

Non-evaluable

Quantitative Change in the Sum of Response Evaluation Criteria in Solid Tumors (RECIST) -

Change in tumor size is presented here. Correlative analysis for this outcome will be completed in the upcoming months.

Percent Change in Tumor Size (Change in T) in Patients With Genomic PIK3CA Pathway Alteration (PIK3CA Mutation, Amplification, and Fluorescence in Situ Hybridization [FISH] for PTEN Loss)

Diarrhea

Creatinine Increased

Acute Kidney Injury

Maculopapular rash

Hyperglycemia

Percentage of Participants With Adverse Events

Surgical Complications

Length of Hospital Stay

Data was not collected for this outcome measure.

Changes in Pre- and Post-treatment Tumor Levels of Human Papillomavirus (HPV) Messenger Ribonucleic Acid (mRNA) (Quantitative Polymerase Chain Reaction [qPCR])

data was not collected for this outcome measure

Changes in Pre- and Post-treatment Tumor Levels of E6 and E7 Oncoproteins

Changes in Pre- and Post-treatment Tumor Levels of Phospho - Human Epidermal Growth Factor Receptor 3 (HER3)

Data was not collected for this outcome measure

Changes in Pre- and Post-treatment Tumor Levels of HER3/PI3K Dimers (Monogram)

Overall Study

Nervous System Diseases

Diseases and Abnormalities at or Before Birth

Skin and Connective Tissue Diseases

Rare Diseases

Neurofibromatoses

Neurofibromatosis 1

Nerve Sheath Neoplasms

Neurofibrosarcoma

Neoplasms, Nerve Tissue

Nervous System Neoplasms

Peripheral Nervous System Neoplasms

Peripheral Nervous System Diseases

Neuromuscular Diseases

Fibrosarcoma

Neoplasms, Fibrous Tissue

Neoplasms, Connective Tissue

Neoplasms, Connective and Soft Tissue

Sarcoma

Neurofibroma

Neurofibromatosis

Neurofibromatosis Type 1

Malignant Peripheral Nerve Sheath Tumor

Soft Tissue Sarcoma

Patients receive telaglenastat hydrochloride PO BID on days 1-28. Cycles repeat every 28 days in the absence of disease progression or unacceptable toxicity. Patients also undergo CT, MRI, or PET/CT during screening and on study, and collection of blood samples during screening and on study.

Biospecimen Collection

Computed Tomography

Magnetic Resonance Imaging

Positron Emission Tomography

Telaglenastat Hydrochloride

Funda Meric-Bernstam

This phase II trial studies how well glutaminase inhibitor telaglenastat hydrochloride (CB-839 HCl) works in treating patients with specific genetic mutations and solid tumors or malignant peripheral nerve sheath tumors that have spread to other places in the body (metastatic) or cannot be removed by surgery (unresectable). Glutaminase converts an amino acid (building block of proteins) called glutamine to glutamate, which can support several cellular pathways. Telaglenastat hydrochloride works by blocking glutamine activity needed for the growth of cells. When this activity is blocked, the growth of cancer cells may stop and the cancer cells may then die. Cancer is caused by changes (mutations) to genes that control the way cells function and uncontrolled cell growth may result in tumor formation. Specific genetic mutations studied in this clinical trial are NF1 mutation for malignant peripheral nerve sheath tumors, and NF1, KEAP1/NRF2, or STK11/LKB1 mutation for other solid tumors. Telaglenastat hydrochloride may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.

PRIMARY OBJECTIVE:

I. To assess the best overall response rate (BORR) achieved by 6 months of telaglenastat (CB-839) hydrochloride (HCl) treatment in specific pathway aberrant tumors (MPNST, NF1, KEAP1/NRF2 \& STK11/ LKB1).

SECONDARY OBJECTIVES:

I. To determine the safety, progression-free survival (PFS), time to progression (TTP) and overall survival (OS).

II. To determine the overall response rate (ORR) (highest objective response achieved between start of therapy and progression), time to response (TTR) and clinical benefit rate (CBR) of telaglenastat (CB-839)HCl.

III. To assess pharmacodynamic changes and adaptive responses and correlate with response to treatment as well as disease progression (correlative objective).

EXPLORATORY OBJECTIVES:

I. Correlate fludeoxyglucose F-18 (18-F FDG) positron emission tomography (PET)/computed tomography (CT) pre-therapy and 8-weeks post-therapy response to telaglenastat (CB-839) HCl therapy.

II. Evaluate changes in level of circulating tumor deoxyribonucleic acid (DNA) at baseline, one month on-treatment and time of progression (Molecular Characterization Laboratory \[MoCHA Labs\]) to treatment response.

III. Quantify the peripheral blood concentrations of the metabolites: aspartate, glutamate, glutamine and arginine (@Mayo clinic Oncometabolomics core) and correlate with response.

IV. Evaluate the pharmacodynamic (PD) effect of telaglenastat (CB-839) HCl on systemic levels of the tricarboxylic acid (TCA) cycle metabolites in peripheral blood (baseline and one month) as part of the protocol.

V. Evaluate tumor by reverse phase protein array (@core facility at MD Anderson) and ribonucleic acid (RNA) sequencing (seq) to evaluate changes from pre-treatment, during treatment and post treatment specimens.

VI. Perform patient-derived tumor xenograft (PDX) modelling-co-clinical trials (@Dr. Funda Meric-Bernstam's lab MD Anderson) to understand response/resistance mechanisms and also evaluate combination therapies for future development.

OUTLINE:

Patients receive telaglenastat hydrochloride orally (PO) twice daily (BID) on days 1-28. Cycles repeat every 28 days in the absence of disease progression or unacceptable toxicity. Patients also undergo CT, magnetic resonance imaging (MRI), or PET/CT during screening and on study, and collection of blood samples during screening and on study.

After completion of study treatment, patients are followed up every 3 months thereafter.

Testing Whether Cancers With Specific Mutations Respond Better to Glutaminase Inhibitor, Telaglenastat Hydrochloride, Anti-Cancer Treatment, BeGIN Study

A Phase II Basket Trial of Glutaminase Inhibitor (BEGIN) Telaglenastat (CB-839) HCL in Patients With NF1 Aberrations, NF1 Mutant Malignant Peripheral Nerve Sheath Tumors (MPNST), KEAP1/NRF2 and LKB1 Aberrant Tumors

NCI is committed to sharing data in accordance with NIH policy. For more details on how clinical trial data is shared, access the link to the NIH data sharing policy page

Will assess PD changes before and after treatment using the Wilcoxon signed rank test. Will correlate these changes with response to treatment using Wilcoxon rank sum test. Will also perform a receiver operating characteristic curve analysis.

Will be based on Response Evaluation Criteria in Solid Tumors version 1.1.

Will be assessed by Common Terminology Criteria for Adverse Events version 5.0. Will tabulate toxicity by cohort, type, severity and attribution.

Will estimate using the Kaplan-Meier method with time zero set to cycle 1, day 1 (C1D1). Will estimate the medians and select probabilities along with 95% confidence intervals. If more than a handful of patients die without progression, will use Aalen-Johansen estimates to adjust for the competing risk of death.

Will estimate the medians and select probabilities along with 95% confidence intervals. If more than a handful of patients die without progression, will use Aalen-Johansen estimates to adjust for the competing risk of death.

Will estimate using the Kaplan-Meier method with time zero set to C1D1. Will estimate the medians and select probabilities along with 95% confidence intervals. If more than a handful of patients die without progression, will use Aalen-Johansen estimates to adjust for the competing risk of death.

Digestive System Diseases

Adenocarcinoma

Esophageal Squamous Cell Carcinoma

Esophageal Neoplasms

Gastrointestinal Neoplasms

Digestive System Neoplasms

Gastrointestinal Diseases

Esophageal Diseases

Esophageal Cancer

Antineoplastic Agents

Pembrolizumab

Antineoplastic Agents, Immunological

Immune Checkpoint Inhibitors

Starting 14 days after completion of standard of care chemoradiotherapy, participants receive epacadostat PO BID during weeks 3-8 and pembrolizumab IV over 30 minutes on day 1 of weeks 3 and 6 in the absence of disease progression or unacceptable toxicity.

Epacadostat

Joseph Chao, MD

This phase II trial studies the side effects of epacadostat and pembrolizumab and to see how well they work before surgery in treating participants with stage II-III esophageal or gastroesophageal cancer. Epacadostat may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Monoclonal antibodies, such as pembrolizumab, may interfere with the ability of the tumor cells to grow and spread. Giving epacadostat and pembrolizumab before surgery may work better in treating participants with stage II-III esophageal or gastroesophageal cancer.

PRIMARY OBJECTIVES:

I. To establish that the combination of epacadostat and pembrolizumab will lead to an increase in tumor infiltrating cytotoxic T-cells and circulating cytotoxic T cells and a reduction in immunosuppressive Tregs and myeloid-derived suppressor cells (MDSCs) in esophageal/gastroesophageal junction (GEJ) tumors that can arise after treatment with neoadjuvant chemoradiation.

II. To assess safety and tolerability of pembrolizumab and epacadostat (immunotherapy) in this patient population.

SECONDARY OBJECTIVES:

I. To evaluate pathologic complete response rate (path CR) and correlate with tumor T-cell response.

II. To evaluate complete clinical response rate (clinical CR) and subsequent avoidance of esophagectomy and correlate with tumor T-cell response.

III. To evaluate toxicities with the combination of pembrolizumab and epacadostat in this treatment setting.

IV. To evaluate disease-free survival (DFS) and overall survival (OS) in this treatment population.

EXPLORATORY OBJECTIVES:

I. To measure changes in whole genome serum micro ribonucleic acid (miRNA) signatures before and after protocol therapy and correlate with tumor/immune/stromal cell miRNA expression profiling determined by deep sequencing.

II. To assess the role of circulating miR-23a as serum biomarker given its role as an oncomir in esophagastric cancer and reporting in the literature of suppressing tumor cytotoxic T cells in preclinical models.

III. To correlate diversity in the gut microbiome with path CR and clinical CR after treatment with pembrolizumab and epacadostat.

IV. To measure serial plasma kynurenine/tryptophan ratio levels as a pharmacodynamic marker of increased IDO1 activity and response.

V. Association of PD-L1 expression, microsatellite stability and/or IDO1 expression and pathological complete response (pCR) rate.

OUTLINE:

Starting 14 days after completion of standard of care chemoradiotherapy, participants receive epacadostat orally (PO) twice daily (BID) during weeks 3-8 and pembrolizumab intravenously (IV) over 30 minutes on day 1 of weeks 3 and 6 in the absence of disease progression or unacceptable toxicity.

After completion of study treatment, participants are followed up at one month and then every 3 months in year 1, every 4 months in year 2, and every 6 months in year 3.

Epacadostat and Pembrolizumab Before Surgery in Treating Participants With Stage II-III Esophageal or Gastroesophageal Cancer

A Phase 2 Trial of Neoadjuvant Pembrolizumab in Combination With Epacadostat (INCB024360) in Patients With Non-Metastatic Esophageal/Gastroesophageal Squamous Cell and Adenocarcinomas Treated With Neoadjuvant Chemoradiation: A Window-Of-Opportunity Study

Patient demographics and baseline disease/prior treatment characteristics will be summarized using descriptive statistics. Descriptive statistics will be used to summarize the gene expression profile in tissue/blood. Changes in these measures during and after treatment (when measured) will also be summarized by descriptive statistics and tables/plots. Various statistical analyses will be used to explore the association between these gene expression measures (at different time points and the changes over time) with clinical outcomes. For the exploratory correlation of these endpoints with response, analyses comparing groups of participants defined by response may be conducted by two-sample t-test or Wilcoxon rank sum test.

All participants evaluable for toxicity will be included in the toxicity analysis. Observed toxicities will be summarized in terms of type (organ affected or laboratory determination), severity, time of onset, duration, probable association with the study treatment and reversibility or outcome.

Will be defined as no residual cancer cells, including lymph nodes under pathologic examination of the surgically resected specimen and/or a Tumor Regression Score of 0 by the College of American Pathologists (CAP) Cancer Protocol for Esophageal Carcinoma. Pathological response will be determined per CAP Cancer Protocols and will utilize a modified Ryan scheme. For pathological CR, all participants evaluable for response will be included in the analysis. Pathological CR rate will be estimated by the proportion of participants achieving pathological CR along with the 95% exact binomial confidence interval.

Defined as no radiographic evidence of disease of positron emission tomography/computed tomography (PET/CT) or CT imaging. For clinical CR, all participants evaluable for response will be included in the analysis. Clinical CR rate will be estimated by the proportion of participants achieving clinical CR along with the 95% exact binomial confidence interval.

DFS will be determined using the Kaplan-Meier method.

OS will be determined using the Kaplan-Meier method.

City of Hope Medical Center

Symptoms and General Pathology

Heart and Blood Diseases

Blood and Lymph Conditions

Immune System Diseases

Recurrence

Waldenstrom Macroglobulinemia

Neoplasms, Plasma Cell

Hemostatic Disorders

Blood Coagulation Disorders

Vascular Diseases

Paraproteinemias

Blood Protein Disorders

Hematologic Diseases

Hemorrhagic Disorders

Lymphoproliferative Disorders

Lymphatic Diseases

Immunoproliferative Disorders

Anticoagulants

Anti-Infective Agents

Other Dietary Supplements

Amino Acids

Citric Acid

Sodium Citrate

Ibrutinib

Ixazomib

Glycine

Tyrosine Kinase Inhibitors

Protein Kinase Inhibitors

HIV Protease Inhibitors

Protease Inhibitors

Neurotransmitter Agents

Citrate

Tyrosine

Patients receive ixazomib citrate PO on days 1, 8, and 15 and ibrutinib PO daily on days 1-28. Treatment repeats every 28 days for up to 24 cycles in the absence of disease progression or unacceptable toxicity.

Ixazomib Citrate

Pharmacokinetic Study

Asher A Chanan-Khan

This phase II trial studies the side effects of ibrutinib citrate when given with ixazomib, and determines how well they work in treating patients with Waldenstrom macroglobulinemia that is newly diagnosed, has come back (recurrent) or does not respond to treatment (refractory). Enzyme inhibitors, such as ibrutinib and ixazomib citrate, may stop the growth of cancer cells by blocking some of the enzymes needed for cell growth.

PRIMARY OBJECTIVE:

I. To determine the efficacy (as assessed by complete response \[CR\] rate) of the combination of ixazomib citrate (ixazomib) and ibrutinib in Waldenstrom macroglobulinemia (WM) patients.

SECONDARY OBJECTIVES:

I. To assess the overall response rate (ORR=partial response \[PR\] or better) in WM patients treated with ixazomib and ibrutinib.

II. To assess the time to progression (TTP) in WM patients treated with ixazomib and ibrutinib.

III. To further characterize the safety and toxicity of the combination of ibrutinib and ixazomib.

IV. To assess the overall survival (OS) in WM patients treated with ixazomib and ibrutinib.

CORRELATIVE RESEARCH OBJECTIVES:

I. To determine the role of members of the BTK signalosome in achievement or lack thereof of response to ibrutinib and ixazomib.

II. To explore biologic effects of ibrutinib and ixazomib on microenvironment in WM and correlate with response to treatment.

OUTLINE:

Patients receive ixazomib citrate orally (PO) on days 1, 8, and 15 and ibrutinib PO daily on days 1-28. Treatment repeats every 28 days for up to 24 cycles in the absence of disease progression or unacceptable toxicity.

After completion of study treatment, patients are followed up every 3 months for up to 2 years.

Ibrutinib and Ixazomib Citrate in Treating Newly Diagnosed, Relapsed or Refractory Waldenstrom Macroglobulinemia

Phase II Study of Ibrutinib in Combination With Ixazomib in Patients With Waldenström Macroglobulinemia

15 protein/genes associated with BTK-signaling will be assessed and their levels from baseline samples will be compared with levels from samples during treatment. Changes over time will be evaluated using paired sample approaches (Wilcoxon signed rank test). Baseline levels will be correlated with response (responder versus \[vs.\] non-responder) using Wilcoxon rank sum tests.

Blood samples \& bone marrow aspirate to be taken from participants. The study will explore biologic effects of ibrutinib and ixazomib on microenvironment in WM and correlate with response to treatment. Immunophenotyping of tumor infiltrating lymphocytes (TILs) using the Multi-Omyx TILs platform. This will identify 17 different types of TILs from BM samples collected at baseline and then after one cycle of treatment. This data is represented as % and actual cell counts. Next, identification of 4 types of T-cells from the blood. This will be done from peripheral blood samples collected at Baseline and then after one cycle of treatment with ixazomib + ibrutinib (Ixa+Ibr). Next, BTK receptor occupancy: This is a competitive-binding assay essentially and will be performed in CD19+/CD138+ WM cells collected at baseline and then after one cycle of treatment with Ixa+Ibr. Readout is % occupancy. Values to be correlated with response (responder vs. non-responder) using Wilcoxon rank sum tests.

Complete response rate to be defined as an objective status of CR at any time, where confirmation of the complete response status is required on two consecutive evaluations with a second immunofixation before calling the patient a CR. The proportion of successes will be estimated by the number of successes divided by the total number of evaluable patients. 95% confidence intervals for the true success proportion will be calculated according to the approach of Duffy and Santner.

Overall response rate will be estimated by the total number of patients who achieve a CR, very good partial response (VGPR), or partial response (PR) divided by the total number of evaluable patients. All evaluable patients will be used for this analysis. Exact binomial 95% confidence intervals for the true overall response rate will be calculated.

The distribution of time to progression will be estimated using the method of Kaplan-Meier.

The distribution of overall survival will be estimated using the method of Kaplan-Meier.

The maximum grade for each type of AE will be recorded for each patient, and frequency tables will be reviewed to determine patterns. Additionally, the relationship of the AE(s) to the study treatment will be taken into consideration.

Mayo Clinic

Colorectal Neoplasms

Intestinal Neoplasms

Colonic Diseases

Intestinal Diseases

Rectal Diseases

Irinotecan

Antibodies

Antibodies, Monoclonal

Cetuximab

Camptothecin

Immunoglobulins

Immunoglobulins, Intravenous

Immunoglobulin G

Immunologic Factors

Topoisomerase I Inhibitors

Patients receive irinotecan hydrochloride IV over 90 minutes and cetuximab IV over 1-2 hours on days 1 and 15, and utomilumab IV over 1 hour on day 2. Cycles repeat every 28 days in the absence of disease progression or unacceptable toxicity.

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
Alpelisib in Treating Participants With Transorally Resectable HPV-Associated Stage I-IVA Oropharyngeal Cancer	NCT03601507	CDKN2A-p16 Posi... HPV Positive Or... Stage I Orophar... Stage II Oropha... Stage III Oroph... Stage IVA Oroph...	Alpelisib Laboratory Biom... Pharmacodynamic... Therapeutic Con...	-	University of Arizona
Testing Whether Cancers With Specific Mutations Respond Better to Glutaminase Inhibitor, Telaglenastat Hydrochloride, Anti-Cancer Treatment, BeGIN Study	NCT03872427	Advanced Malign... Metastatic Mali... NF1 Mutation Po... Unresectable Ma...	Biospecimen Col... Computed Tomogr... Magnetic Resona... Pharmacodynamic... Positron Emissi... Telaglenastat H...	18 Years -	National Cancer Institute (NCI)
Epacadostat and Pembrolizumab Before Surgery in Treating Participants With Stage II-III Esophageal or Gastroesophageal Cancer	NCT03592407	Esophageal Squa... Esophageal Aden... Gastroesophagea...	Epacadostat Laboratory Biom... Pembrolizumab Pharmacodynamic...	18 Years -	City of Hope Medical Center
Ibrutinib and Ixazomib Citrate in Treating Newly Diagnosed, Relapsed or Refractory Waldenstrom Macroglobulinemia	NCT03506373	Recurrent Walde... Refractory Wald... Waldenstrom Mac...	Ibrutinib Ixazomib Citrat... Laboratory Biom... Pharmacodynamic... Pharmacokinetic...	18 Years -	Mayo Clinic
Utomilumab, Cetuximab, and Irinotecan Hydrochloride in Treating Patients With Metastatic Colorectal Cancer	NCT03290937	Metastatic Colo... Stage IV Colore... Stage IVA Color... Stage IVB Color... Stage IVC Color...	Cetuximab Irinotecan Hydr... Pharmacodynamic... Utomilumab	16 Years -	M.D. Anderson Cancer Center

Spots Global Cancer Trial Database for pharmacodynamic study