Imatinib Mesylate, Gemcitabine, and Capecitabine in Treating Patients With Advanced Solid Tumors

Summary

RATIONALE: Imatinib mesylate may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Drugs used in chemotherapy, such as gemcitabine and capecitabine, work in different ways to stop the growth of tumor cells, either by killing the cells or by stopping them from dividing. Giving imatinib mesylate together with gemcitabine and capecitabine may kill more tumor cells.

PURPOSE: This phase I trial is studying the side effects and best dose of gemcitabine and capecitabine when given together with imatinib mesylate in treating patients with advanced solid tumors.

Conditions

• Unspecified Adult Solid Tumor, Protocol Specific

Interventions

DRUG

capecitabine

Dose level Capecitabine -1 400 mg/m2 bid 0 500 mg/m2 bid 1. 500 mg/m2 bid 2. 600 mg/m2 bid 3. 600 mg/m2 bid 4. 725 mg/m2 bid 5. 725 mg/m2 bid 6. 850 mg/m2 bid 7. 850 mg/m2 bid

DRUG

gemcitabine hydrochloride

Dose level Gemcitabine -1 400 mg/m2 0 450 mg/m2 1. 550 mg/m2 2. 550 mg/m2 3. 675 mg/m2 4. 675 mg/m2 5. 825 mg/m2 6. 825 mg/m2 7. 1000 mg/m2

DRUG

imatinib mesylate

Dose level Imatinib -1 400 mg/d 0 400 mg/d 1. 400 mg/d 2. 400 mg/d 3. 400 mg/d 4. 400 mg/d 5. 400 mg/d 6. 400 mg/d 7. 400 mg/d

GENETIC

mutation analysis

C-kit mutations will be assessed on existing paraffin-embedded blocks by Polymerase Chain Reaction and direct sequencing of both juxtamembrane domains (exons 9 and 11) and the tyrosine kinase domain (exons 13 and 17). Every ABI sequence will be compared to a NCBI Human KIT gene nucleotide sequence and will be blast using a NCBI Standard Nucleotide Blast Search to determine the presence of mutation within a particular exon.

GENETIC

nucleic acid sequencing

C-kit mutations will be assessed on existing paraffin-embedded blocks by Polymerase Chain Reaction and direct sequencing of both juxtamembrane domains (exons 9 and 11) and the tyrosine kinase domain (exons 13 and 17). Every ABI sequence will be compared to a NCBI Human KIT gene nucleotide sequence and will be blast using a NCBI Standard Nucleotide Blast Search to determine the presence of mutation within a particular exon.

GENETIC

polymerase chain reaction

C-kit mutations will be assessed on existing paraffin-embedded blocks by Polymerase Chain Reaction and direct sequencing of both juxtamembrane domains (exons 9 and 11) and the tyrosine kinase domain (exons 13 and 17). Every ABI sequence will be compared to a NCBI Human KIT gene nucleotide sequence and will be blast using a NCBI Standard Nucleotide Blast Search to determine the presence of mutation within a particular exon.

Sponsors & Collaborators

• National Cancer Institute (NCI)

  collaborator NIH

• University of Nebraska

  lead OTHER

Principal Investigators

• Ralph Hauke, MD · University of Nebraska

• Elizabeth C. Reed, MD · University of Nebraska

Study Design

Allocation

NA

Purpose

TREATMENT

Masking

NONE

Model

SINGLE_GROUP

Eligibility

Min Age

19 Years

Max Age

120 Years

Sex

ALL

Healthy Volunteers

No

Timeline & Regulatory

Start

2006-08-15

Primary Completion

2009-01-30

Completion

2011-03-29

Countries

• United States

Study Locations