Breast Cancer (MD Anderson Solid Tumor Oncology Series)

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Another phenomenon became apparent with prolonged paclitaxel treatment in some cases, beyond 20 courses. Among a series of 52 patients experiencing continued response of visceral, osseous, and soft-tissue metastases during paclitaxel treatment, 6 experienced disease progression in the central nervous system in the absence of other evidence of treatment failure.

This manifested as both parenchymal brain metastases and leptomeningeal disease. Thus, the central nervous system does appear to be a sanctuary site in many women receiving paclitaxel for the management of metastatic breast cancer. Our next phase II clinical and pharmacologic trial was motivated by in vitro data showing less resistance to paclitaxel in p-glycoprotein-overexpressing MCF-7 breast cancer cells with longer drug exposure time.

In this study, we evaluated the possibility of schedule-dependent activity by administering paclitaxel via a hour continuous infusion specifically to patients with disease that had demonstrated clinical resistance to short taxane exposure. Because early data had suggested that the omission of steroid and H1- and H2-receptor antagonist premedication was not associated with significant hypersensitivity-like reactions with this dose and schedule,[11] these drugs were not given in our study. With cycles administered, seven partial responses were noted in 26 evaluable patients Despite the omission of standard premedication, no cases of hypersensitivity-like reactions occurred.

This suggests that the slower rate of exposure to paclitaxel--and possibly to the polyoxyethylated castor oil Cremophor EL formulation--may not precipitate mast-cell degranulation and other cellular phenomena associated with hypersensitivity reactions. Serum paclitaxel concentrations were assayed in 23 patients by high-performance liquid chromatography at 24, 48, 72, and 96 hours of the infusion. The median steady-state paclitaxel concentration Css was. For 11 patients experiencing grade 4 neutropenia, median Css was. Median Css and absolute neutrophil count ANC nadirs were.

No relationship between steady-state level and tumor response was noted with this limited sample size. To further define the significance of infusion duration for paclitaxel, a recently completed multi-institution trial led by the M. Anderson Cancer Center randomized patients with refractory metastatic breast cancer to receive paclitaxel via either a 3- or hour infusion schedule.

It is noteworthy that there are greater pharmacologic differences between the 3- and hour infusion schedules than between the 3- and hour schedules, and many preclinical data suggest the importance of paclitaxel exposure duration in breast carcinoma cells. Thus, this trial should provide the most definitive information about the impact of paclitaxel infusion duration on efficacy and toxicity. Seidman AD: The emerging role of paclitaxel in breast cancer therapy.

Clin Cancer Res , J Natl Cancer Inst , J Clin Oncol , Seidman AD, Portenoy R, Yao T-J, et al: Quality of life in phase II trials: A study of methodology and predictive value in patients with advanced breast cancer treated with paclitaxel plus granulocyte colony-stimulating factor. Proc Am Assoc Cancer Res , Cancer Chemother Pharmacol , Br J Cancer , Klaassen U, Wilke I-L, Strumberg D, et al: Phase I study with a weekly 1-h infusion of paclitaxel, in heavily pretreated patients with metastatic breast and ovarian cancer.

Eur J Cancer 32A, Breast Cancer Res Treat 41 3 , Schmid FA, Sirotnak FM, Otter GM, et al: New folate analogs of the deazaaminoptefin series: Markedly increased antitumor activity of the ethyl analog compared to the parent compound and methotrexate against some human tumor xenografts in nude mice. Cancer Treat Rep , Ann Oncol , Proc Am Soc Clin Oncol , Baselga J, Norton L, Masui R, et al: Antitumor effects of doxorubicin in combination with anti-epidermal growth factor receptor monoclonal antibodies.

Tsimberidou, D. The costs of publication of this article were defrayed in part by the payment of page charges.

Why I came to MD Anderson for breast cancer treatment

This article must therefore be hereby marked advertisement in accordance with 18 U. Section solely to indicate this fact. NOTE: We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail. We do not retain these email addresses. Skip to main content. Personalized Medicine and Imaging. Denis L. Wheler , Ralph G. Zinner , Aung Naing , Apostolia M.

Tsimberidou , Vijaykumar Holla , Marylin M. University of Chicago, Chicago, Texas. DOI: Abstract Purpose: This study aimed to assess MET amplification among different cancers, association with clinical factors and genetic aberrations and targeted therapy response modifications. Treatment and evaluation Patients referred to the Phase I Clinic who met inclusion criteria were enrolled in clinical trials judged to be clinically appropriate.

Statistical analysis Statistical analysis was verified by our statistician K. View this table: View inline View popup. Table 1. Table 2. Pathologic and molecular characteristics of patients MET -amplified patients presented with more metastatic sites, compared with nonamplified patients median 3 vs. Figure 1. Table 3. Responses of patients on phase I protocols by MET status. Table 4. Characteristics of patients with MET amplification. Discussion MET amplification was detected in 2. Disclosure of Potential Conflicts of Interest G.

Authors' Contributions Conception and design: D. Hong Development of methodology: D. Hong Acquisition of data provided animals, acquired and managed patients, provided facilities, etc. Hong Analysis and interpretation of data e.

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Hong Administrative, technical, or material support i. Hong Study supervision: D. Jardim, J. Wheler, D. References 1. Targeting MET in cancer: rationale and progress.

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Nat Rev Cancer ; 12 : 89 — Appleman LJ. MET signaling pathway: a rational target for cancer therapy. J Clin Oncol ; 29 : — 8. Autocrine activation of the MET receptor tyrosine kinase in acute myeloid leukemia. Nat Med ; 18 : — Expression and mutational analysis of MET in human solid cancers. Genes Chromosomes Cancer ; 47 : — BMC Cancer ; 11 : Int J Cancer ; : — MET amplification identifies a small and aggressive subgroup of esophagogastric adenocarcinoma with evidence of responsiveness to crizotinib. J Clin Oncol ; 29 : — Cancer Lett ; : 1 — Gene amplification in gastric and esophageal adenocarcinomas.

Cancer Res ; 50 : — Assessing the significance of chromosomal aberrations in cancer: methodology and application to glioma. Exp Lung Res ; 39 : — Clinical significance of c-met oncogene alterations in human colorectal cancer.

click here Oncology ; 56 : — PloS ONE ; 9 : e Increased MET gene copy number negatively affects survival of surgically resected non-small-cell lung cancer patients. J Clin Oncol ; 27 : — Cancer Discov ; 3 : — MET increased gene copy number and primary resistance to gefitinib therapy in non-small-cell lung cancer patients.

Ann Oncol ; 20 : — Br J Cancer ; : — 9. Peters S , Adjei AA. MET: a promising anticancer therapeutic target. Nat Rev Clin Oncol ; 9 : — Blumenschein GR Jr. Targeting the hepatocyte growth factor-cMET axis in cancer therapy.

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J Clin Oncol ; 30 : — Varella-Garcia M. Stratification of non-small cell lung cancer patients for therapy with epidermal growth factor receptor inhibitors: the EGFR fluorescence in situ hybridization assay. Diagn Pathol ; 1 : Cancer Lett ; : — Eur J Cancer ; 45 : — New guidelines to evaluate the response to treatment in solid tumors. J Natl Cancer Inst ; 92 : — J Clin Oncol ; 31 : — 6.

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