Cytotoxic and antiproliferative activity of the CMF regimen administered in association with tamoxifen as primary chemotherapy in breast cancer patients.

Bottini, Alberto; Berruti, Alfredo; Bersiga, Alessandra; Brunelli, Antonio; Brizzi, Maria Pia; Marco, Bernini; Cirillo, Fernando; Tampellini, Marco; Bolsi, G; Aguggini, Sergio; Betri, Enrico; Filippini, L; Bertoli, Ada; Alquati, P; Dogliotti, Luigi

doi:10.3892/ijo.13.2.385

Cited by 5 publications

(6 citation statements)

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“…Model runs applying only nCS drugs showed no such decline in the PI (not shown). This drop is consistent with empirical results showing a decline in Ki67 expression (an assay for PI) by more than 50% in breast cancer patients who attained a complete response to treatment (Bottini et al, 1998;Colleoni et al, 1999). In addition, di!erent drug regimes have di!erent a!ects on the proliferating fraction.…”

Section: Timecourse Of Tumor Growthsupporting

confidence: 78%

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Modeling Multi-drug Chemotherapy: Tailoring Treatment to Individuals

Gardner

2002

Journal of Theoretical Biology

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Section: Timecourse Of Tumor Growthsupporting

confidence: 78%

“…CS drugs, by selectively killing clones with the highest proliferative fractions, may result in the evolution of slower tumor growth (Bottini et al, 1998;Colleoni et al, 1999). nCS drugs, in contrast, may favor clones with high proliferative fractions, because those are the clones with the greatest regrowth between drug applications.…”

Section: Introductionmentioning

confidence: 99%

Modeling Multi-drug Chemotherapy: Tailoring Treatment to Individuals

Gardner

2002

Journal of Theoretical Biology

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“…In a phase II study conducted by our group with CMF (cyclophosphamide, methotrexate, 5-flurouracil) administered in association with tamoxifen in the patient subset with ER+ primary tumors, we observed that reduction in proliferation activity was mainly confined to ER+ neoplasms (Bottini et al 1998, Bottini et al 2001. Whether this phenomenon was linked or not to the tamoxifen administration was uncertain, since this study was unable to separate the effect of chemotherapy from that of tamoxifen.…”

Section: Discussionmentioning

confidence: 96%

Cytotoxic and antiproliferative activity of the single agent epirubicin versus epirubicin plus tamoxifen as primary chemotherapy in human breast cancer: a single-institution phase III trial

Bottini

Berruti²,

Brizzi³

et al. 2005

Endocrine Related Cancer

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This study was designed to address whether simultaneous primary chemo-hormonal therapy provides additional activity compared with chemotherapy alone in breast cancer patients with operable or locally advanced disease. Between January 1997 and January 2002, 211 consecutive patients with T2-4, N0-1, M0 breast cancer were randomized to receive either epirubicin alone (EPI) or epirubicin plus tamoxifen (EPI-TAM). Ki67 expression was evaluated immunohistochemically in tumor specimens obtained before chemotherapy by incision biopsy and at definitive surgery. Tumor shrinkage of >50% was obtained in 76% of patients randomized in the EPI arm and 81.9% of patients randomized in the EPI-TAM arm (not significant). The corresponding rates of clinical and pathological complete response were 20.2 and 21.9% (not significant), and 4.8 and 6.7% (not significant), respectively. Pathologically complete response was more frequently observed in estrogen receptor (ER)-negative (ER -) tumors (P=0.04) and correlated with elevated baseline Ki67 expression (P<0.01). Both EPI and EPI-TAM treatments resulted in a significant reduction in Ki67 expression, either in overall patients (P=0.000) or in patients with ER+ breast cancer (P=0.000). The reduction in Ki67 immunostaining in the EPI-TAM arm was greater than in the EPI arm, leading to a lower Ki67 expression at post-operative residual histology (P=0.0041). The addition of tamoxifen to epirubicin chemotherapy did not improve the response rate but led to a significantly higher reduction in the Ki67 expression. Baseline elevated Ki67 expression and the ER -status were both associated with a greater chance of obtaining a pathological complete response at residual histology.

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“…Clinical studies have revealed higher resistance to fluoropyrimidine therapy of tumors expressing p53 mutants (Benhattar et al, 1996;Cabelguenne et al, 2000;Zheng et al, 1999). In several cases such effects of p53 mutants were attributed to dominant-negative suppression of the wild type p53 activity that resulted in abrogation of p53-induced apoptosis (Bunz et al, 1999), and an increase in activity of the MDR1 gene (Bottini et al, 2000). Clearly, induction of dUTPase by certain p53 mutants can additionally contribute to resistance to 5-FU therapy.…”

Section: Resultsmentioning

confidence: 99%