1029 Background: Pac/bev is superior to pac alone as first-line therapy for MBC. Ixa/bev has greater preclinical activity than pac/bev in human tumor models. The primary objective of this trial was to evaluate objective response rates (ORR) of ixa/bev given weekly or every 3 weeks relative to pac/bev as 1st line therapy for women with advanced breast cancer. Methods: Women with measurable disease and no prior chemotherapy for advanced breast cancer (locally advanced or MBC) were randomized in a 3:3:2 ratio to Arm A (ixa 16 mg/m2 IV on days 1, 8 & 15 q28 days/ bev 10 mg/kg IV q 2 wks), Arm B (ixa 40 mg/m2 IV q3 wks / bev 15 mg/kg IV q 3 wks) or Arm C (pac 90 mg/m2 IV, schedule/bev as in Arm A). Treatment was continued until disease progression or unacceptable toxicity. Results: Key efficacy and safety results from a pre-planned analysis of all randomized subjects after at least 24 weeks of follow-up are presented. Baseline characteristics were balanced between arms except for liver metastasis. Conclusions: The combination of ixa/bev weekly or q 3 wks demonstrated encouraging clinical activity and safety comparable to 1st line pac/bev in E2100. Final PFS will be provided when data is mature. These results support ongoing clinical trials of ixa given weekly or q 3wk in 1st line MBC, and in combination with bev. [Table: see text] [Table: see text]

Abstract Abstract #4120 Background: Trastuzumab (T) combined with docetaxel (D) is approved for the first-line treatment of HER2+ advanced BC (ABC). Sunitinib (SU) is an oral, multitargeted tyrosine kinase inhibitor of VEGFRs, PDGFRs, KIT, RET, and FLT3 with single-agent activity in pts with previously treated ABC. The tolerability and preliminary antitumor activity of SU combined with D and T was investigated in this exploratory study as a first-line regimen for ABC. Materials and methods: A target of 25 female pts (≥18 yrs, ECOG PS 0 or 1) with unresectable, locally recurrent or metastatic HER2+ BC are being enrolled. Starting doses for the 3 treatments are listed in the table below. The primary objective is safety. Secondary endpoints are PK and preliminary tumor activity according to RECIST. After discontinuation of D, responsive pts (PR or SD) can continue SU and T until PD. Results: As of May 2008, 18 pts were enrolled; 11 pts continue on study therapy and 7 have discontinued (5 due to PD; 1 due to pt decision; 1 due to G3 fatigue). Of the 18 pts enrolled, 16 are evaluable for safety and 11 for activity. Pts completed 75/96/98 cycles of D/SU/T, respectively, with a median of 5 cycles/pt for each drug (range: 1-13/1-12/1-13). The planned dose of SU (37.5 mg/d) was reduced to 25 mg/d in 6/16 pts due to G4 neutropenia (1); G3 febrile neutropenia (1); G3 fatigue (1); G2 hyperbilirubinemia (1); G2 hypertension (1); and G2 diarrhea (1). D was reduced in 4 pts due to febrile neutropenia (2) and G4 neutropenia (2). T was given q3w in 12 pts and wkly in 4 pts. T dosing was delayed by ≥4 days in 6 pts, 4 due to D dose delay and 2 due to AEs when D was already discontinued (G2 neutropenia and G3 fatigue). Overall, the most frequent AEs were fatigue (68.8%) and neutropenia (43.8%), consistent with the most common toxicities of D. No GI perforation or bleeding were reported. The most frequently reported severe AEs were neutropenia (1 G3 and 6 G4) and febrile neutropenia (5 G3). G-CSF was administered to 8 pts. Of the 11 pts evaluable for antitumor activity, 1 showed a confirmed CR, 7 a confirmed PR, 2 had PD and 1 was not evaluable. Conclusions: The combination of SU 37.5 mg/d (Schedule 2/1) with D 75 mg/m2 q3w and T wkly/3-wkly, given as first-line treatment to HER2+ pts with ABC, shows manageable toxicities. The use of G-CSF appears beneficial. Preliminary antitumor activity is encouraging. Enrollment is ongoing. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 4120.

Bevacizumab (Avastin®, Genentech, CA) was granted accelerated approval by the FDA for metastatic breast cancer in 2008. This occurred after the initial clinical trial, E2100, demonstrated an improvement in progression-free survival (PFS) and overall survival (OS) with the addition of bevacizumab to a standard chemotherapy. Unfortunately, the approval was rescinded in 2011 when two subsequent trials, AVADO and RIBBON-1, failed to show survival benefit. We compare and analyze the landmark trials E2100, AVADO and RIBBON-1, and suggest that the present-day clinical trial model may not be suited for the investigation of targeted therapies such as bevacizumab. The existing clinical trial model does not allow for modification of chemotherapeutic doses in a manner that maximizes the effect of biologic response modifiers and does not account for its “chemosensitizing” effect. The E2100, AVADO, and RIBBON-1 trials differed in the type and dose of chemotherapy, the dose and frequency of bevacizumab, and in the trial design, making it difficult to effectively compare and evaluate the results. The efficacy of combining bevacizumab with a maximum tolerated dose (MTD) of chemotherapy is also discussed in view of the observation that increased tumor response did not translate to an increase in survival. We suggest that even though angiogenesis inhibitors are non-toxic as monotherapies, they increase the toxicity of standard chemotherapy, and consequently a re-design of the now classic clinical trial model should be considered. Modifying the existing clinical trial model will lead to a more accurate evaluation of the safety and efficacy of bevacizumab and other biological agents in treating metastatic cancer.

Abstract Background: T + D is a standard 1st-line treatment (tx) for HER2+ ABC (locally recurrent or metastatic BC). SU is an oral, multitargeted tyrosine kinase inhibitor of VEGFRs, PDGFRs, KIT, RET, and FLT3 with single-agent activity in previously treated ABC. In this study, a SU/D/T combination was investigated as 1st-line tx for pts with HER2+ ABC.Materials and methods: Female pts (≥18 yrs, ECOG PS ≤1) with HER2+ ABC were enrolled. Starting doses were D: 75 mg/m2, q3w, iv, day 1; T q1w: 4 mg/kg, day 1, followed by 2 mg/kg q1w, iv or q3w: 8 mg/kg, day 1, followed by 6 mg/kg q3w, iv; SU: 37.5 mg/d, Schedule 2/1, po, day 2. The primary objective was safety. Antitumor activity and pharmacokinetics were secondary endpoints. On discontinuation of D, responsive pts (PR or SD) could continue SU + T until disease progression.Results: As of Mar 2009, 25 pts were enrolled. 1 pt did not receive tx, 1 pt received a dose of D/T (pt died from multiorgan failure after T administration), and 23 pts received ≥1 dose of SU/D/T; data from the latter group are reported. 12 pts (52%) were chemo-naïve. 5 pts continue on study tx; 18 have discontinued (8 due to PD, 2 due to pt decision, 7 due to AEs, 1 due to global deterioration). Pts received 201/128/211 cycles of SU/D/T, respectively, with a median of 9/6/10 cycles/pt (range: 1–18/1–12/1–18). The 37.5 mg/d SU dose was reduced to 25 mg/d in 14/23 pts and interrupted in 17/23 pts. AEs led to SU dose reductions/interruptions in 17 pts, most frequently grade (G) 3/4 neutropenia (n=8) and G3 febrile neutropenia, G3 fatigue, and G3 diarrhea (each n=2). In 23 evaluable pts, the most frequent non-hematologic G3 AEs were fatigue/asthenia (26%), diarrhea (13%), and stomatitis, vomiting, and dyspnea (each 9%). G4 AEs were transaminase increase, accidental overdose of SU, and intestinal perforation (each n=1). 1 cardiac AE was reported (G3 supraventricular tachycardia) and transient G1/2 LVEF decline was seen in 2 pts (9%). G3/4 neutropenia was reported in 20 pts (91%); 5 pts (22%) had febrile neutropenia. 2 pts (9%) had G3 anemia and 1 pt (4%) had G3 thrombocytopenia. G-CSF was administered to 11 pts without complications. Preliminary median steady-state levels of SU and its metabolite: 40.6 and 15.6 ng/mL, respectively; end D infusion: 993 ng/mL; T levels: <20 µg/mL. In 19 evaluable pts, ORR was 79% (1 CR [5%], 14 confirmed PRs [74%], 2 SD [11%]). Preliminary median PFS was 10.5 months (95% CI: 8.1–13.6) and median DR was 9.0 months (95% CI: 7.3–12.3).Conclusions: The combination of SU/D/T, given as 1st-line tx to HER2+ pts with ABC, is feasible. AEs were manageable through dose delay/reduction, and no new, unexpected AEs occurred. SU and D levels were consistent with known single-agent levels; evaluation of T levels is ongoing. Preliminary evidence of antitumor activity is encouraging and warrants further evaluation. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 6088.

Metastasis is the most life threatening aspect of breast cancer. It is a multi-step process involving invasion and migration of primary tumor cells with a subsequent colonization of these cells at a secondary location. The aim of the present study was to investigate the role of thioredoxin (Trx1) in the invasion and migration of breast cancer cells and to assess the strength of the association between high levels of Trx1 and thioredoxin reductase (TrxR1) expression with breast cancer patient survival. Our results indicate that the expression of both Trx1 and TrxR1 are statistically significantly increased in breast cancer patient cells compared with paired normal breast tissue from the same patient. Over-expression of Trx1 in MDA-MB-231 breast cancer cell lines enhanced cell invasion in in vitro assays while expression of a redox inactive mutant form of Trx1 (designated 1SS) or the antisense mRNA inhibited cell invasion. Addition of exogenous Trx1 also enhanced cell invasion, while addition of a specific monoclonal antibody that inhibits Trx1 redox function decreased cell invasion. Over-expression of intracellular Trx1 did not increase cell migration but expression of intracellular 1SS inhibited migration. Addition of exogenous Trx1 enhanced cell migration while 1SS had no effect. Treatment with auranofin inhibited TrxR activity, cell migration and clonogenic activity of MDA-MB-231 cells, while increasing reactive oxygen species (ROS) levels. Analysis of 25 independent cohorts with 5910 patients showed that Trx1 and TrxR1 were both associated with a poor patient prognosis in terms of overall survival, distant metastasis free survival and disease free survival. Therefore, targeting the Trx system with auranofin or other specific inhibitors may provide improved breast cancer patient outcomes through inhibition of cancer invasion and migration.

535 Background: Anthracycline-based sequential chemotherapy significantly improves efficacy outcomes compared to CMF alone. Methods: 806 eligible patients with operable breast cancer were enrolled into a randomized study (ratio 1:1:1:1) of sequential chemotherapy. In a 2×2-type design patients were allocated to first receive 4 cycles of AT (doxorubicin, A 60 mg/m2 iv + paclitaxel, T 200 mg/m2 as 3 h inf q 3wks) or EV (epirubicin, E 75 mg/m2 iv + vinorelbine, V 25 mg/m2 iv D1,8 q3wks) followed either by 4 monthly cycles of iv CMF or 6 cycles of q3w T alone (100 mg/m2 as 1h inf D1,8). Tamoxifen was recommended for 5 yr after chemotherapy in patients with HR+ tumors. Patients with tumors > 2 cm in diameter were allowed to start primary chemotherapy with 4 cycles of either AT or EV followed by surgery and postoperative systemic treatment as detailed above. Aim of the study was to test the role of T vs V when combined with an anthracycline during the first 4 cycles of the regimen as well as the role of CMF vs T during the last 4 cycles. Results: At a median follow-up of approximately 48 months, the 5 year freedom from progression (FFP) and overall survival (OS) for the main endpoints were as in the Table : The four treatment sequences were fairly well tolerated, with only 1 treatment-related death after EV. Type and severity of hematological toxicities were similar in all treatment arms. The incidence of reversible G2–3 neurotoxicity was 21.9% after AT, 5.3% after EV and 29.1% after sequential T. Chemical phlebitis was more frequent after EV (6.5%) then after AT (0.3). Conclusions: The results indicate that vinorelbine-epirubicin and classical CMF when appropriately used in a sequential modality for high-risk breast cancer are as valid and less neurotoxic an option of adjuvant therapy than the more widely used taxane-containing adjuvant regimens. Supported in part by Bristol-Myers Squibb, Pierre Fabre and Pharmacia. [Table: see text] [Table: see text]

The authors performed a randomized trial comprising patients with metastatic breast carcinoma (MBC). They used a noninferiority design to evaluate whether the results of sequential administration of epirubicin and paclitaxel were not markedly worse than the concomitant administration in terms of objective response rates (ORRs). Toxicity profile, quality of life (QOL), and pharmacoeconomic evaluations were evaluated as well.

The aim of the study was to evaluate cardiac safety of two different schedules of Epirubicin and Paclitaxel in advanced breast cancer patients enrolled into a multicenter randomized phase III trial. Patients received Epirubicin 90 mg m −2 plus Paclitaxel 200 mg m −2 (3-h infusion) on day 1 every 3 weeks for eight courses (arm A), or Epirubicin 120 mg m −2 on day 1 every 3 weeks for four courses followed by four courses of Paclitaxel 250 mg m −2 on day 1 every 3 weeks (arm B). Left ventricular ejection fraction was evaluated by bidimesional echocardiography at baseline, after four and eight courses of chemotherapy and every 4 months during follow-up. Baseline median left ventricular ejection fraction was 60% in arm A and 65% in arm B; after four courses, figures were 57 and 60%, respectively. After eight courses, the median left ventricular ejection fraction in arm A declined to 50% while no further reduction was detected in arm B by adding four courses of high-dose Paclitaxel. Seven episodes of congestive heart failure were observed during treatment in arm A. Present monitoring demonstrated that the risk of congestive heart failure or impairment in the cardiac function correlated only with the cumulative dose of Epirubicin; no impact on cardiotoxicity can be attributed to high-dose Paclitaxel.

PURPOSE:To compare the efficacy of chemotherapy versus that of tamoxifen plus ovarian suppression in pre-/perimenopausal estrogen receptor-positive patients with early breast cancer. PATIENTS AND METHODS:Patients were randomly assigned to receive either six cycles of a standard regimen of cyclophosphamide 100 mg/m(2) orally days 1 to 14, methotrexate 40 mg/m(2) intravenously (IV) days 1 and 8, and fluorouracil 600 mg/m(2) IV days 1 and 8 (CMF), with all drugs restarted on day 29, or 5 years of tamoxifen, 30 mg/d, plus ovarian suppression with surgical oophorectomy, ovarian irradiation, or monthly goserelin 3.6-mg injections. Disease-free survival was the main study end point. Overall survival and toxicity were additional end points. RESULTS:Between 1989 and 1997, 120 patients were assigned to CMF and 124 to tamoxifen and ovarian suppression (oophorectomy, n = 6; ovarian irradiation, n = 31; and goserelin injections, n = 87). At the time of analysis (median follow-up time, 76 months; range, 9 to 121 months), 82 patients had relapsed and 39 had died. No difference between groups had emerged with respect to either disease-free or overall survival. Treatments were comparable even in respect to age, tumor size, and nodal status, although a nonsignificant trend favored patients with poorly differentiated tumors treated with CMF. Leukopenia, nausea, vomiting, stomatitis, and alopecia were significantly more common in patients treated with CMF. There were few patients who developed benign gynecologic changes in either group, and numbers were comparable. CONCLUSION:The combination of tamoxifen with ovarian suppression seems to be safe and to yield comparable results relative to standard CMF.

A multicentric randomized trial was performed in premenopausal women with node-positive, estrogen-receptor-negative breast tumors to assess the potential superiority of alternating adjuvant chemotherapy over 'standard' CMF chemotherapy. Between January 1989 and June 1992, 107 patients were entered into the study and randomly allocated to receive either cyclophosphamide 100 mg/m2 per as on days 1-14, methotrexate 40 mg/m2 and 5-fluorouracil 600 mg/m2 intravenously (i.v.) on days 1, 8 (CMF), every 4 weeks for a total of 6 cycles, or the following regimens: CMF as previously; epidoxorubicin 75 mg/m2 i.v. on day 1 and vincristine 0.75 mg/m2 i.v. on days 1, 8 (EV); mitomycin-C 10 mg/m2 i.v. on day 1 and vindesine 2 mg/m2 i.v. on days 1, 8 (MVs). The three regimens were given every 4 weeks for a total of 6 cycles according to the following schedule: CMF, EV, MVs, CMF, EV, MVs. At a median follow up of 48 months (range 30-72), 40 patients have relapsed and 17 have died overall. More patients in the triple-combination arm have relapsed and more have died, the latter difference tending toward statistical significance (p = 0.06). There was no statistical difference in the site of relapse between the two groups. Total duration of adjuvant therapy was similar in the two arms (312 chemotherapy cycles in the triple arm and 308 in the CMF arm). Treatment toxicity was also comparable, although more patients in the triple-combination arm were still regularly menstruating 6 months after the completion of chemotherapy. This study failed to show any advantage ensuing from the use of alternating chemotherapy in patients with early breast cancer.

Annals of the New York Academy of SciencesVolume 698, Issue 1 p. 318-328 Endocrine Therapy of Breast Cancer The Experience of the Italian Cooperative Group for Chemohormonal Therapy of Early Breast Cancer (GROCTA) FRANCESCO BOCCARDO, Corresponding Author FRANCESCO BOCCARDO Div. di Oncologia Medica II, Istituto Nazionale per la Ricerca sul Cancro, Viale Benedetto XV, 10, 16132 Genova, Italy.Francesco Boccardo, M.D., Div. di Oncologia Medica II, Istituto Nazionale per la Ricerca sul Cancro, Viale Benedetto XV, 10, 16132 Genova, Italy.Search for more papers by this authorDOMENICO AMOROSO, DOMENICO AMOROSO Div. di Oncologia Medica II, Istituto Nazionale per la Ricerca sul Cancro, Viale Benedetto XV, 10, 16132 Genova, Italy.Search for more papers by this authorALESSANDRA RUBAGOTTI, ALESSANDRA RUBAGOTTI Div. di Oncologia Medica II, Istituto Nazionale per la Ricerca sul Cancro, Viale Benedetto XV, 10, 16132 Genova, Italy.Search for more papers by this authorPIERO SISMONDI, PIERO SISMONDI Cattedra di Ginecologja Oncologica, Università di Torino, Italy.Search for more papers by this authorCORRADO DE SANCTIS, CORRADO DE SANCTIS Cattedra di Ginecologja Oncologica, Università di Torino, Italy.Search for more papers by this authorMARIO CAPPELLINI, MARIO CAPPELLINI Unità Operativa Radioterapia, Policlinico Careggi, Firenze, Italy.Search for more papers by this authorPAOLO PACINI, PAOLO PACINI Unità Operativa Radioterapia, Policlinico Careggi, Firenze, Italy.Search for more papers by this authorLUIGI CASTAGNETTA, LUIGI CASTAGNETTA Biochimica degli Ormoni, Università di Palermo, Italy.Search for more papers by this authorADELE TRAINA, ADELE TRAINA Biochimica degli Ormoni, Università di Palermo, Italy.Search for more papers by this authorANTONIO FARRIS, ANTONIO FARRIS Cattedra di Oncologia Clinica, Università di Sassari, Italy.Search for more papers by this authorSTEFANO IACOBELLI, STEFANO IACOBELLI Cattedra di Oncologia Medica, Università di Chieti, Italy.Search for more papers by this authorGIORGIO MUSTACCHI, GIORGIO MUSTACCHI Centra Oncologico, Trieste, Italy.Search for more papers by this authorITALO NENCI, ITALO NENCI Istituto Anatomia Patologica, Università di Ferrara, Italy.Search for more papers by this authorADRIANO PIFFANELLI, ADRIANO PIFFANELLI Istituto di Radiologia, Università di Ferrara, Italy.Search for more papers by this authorEUGENIO VILLA, EUGENIO VILLA Radio-Chemioterapia, Istituto Scientifico S. Raflaele, Milano, Italy.Search for more papers by this authorDANIELA ALDRIGHETTI, DANIELA ALDRIGHETTI Radio-Chemioterapia, Istituto Scientifico S. Raflaele, Milano, Italy.Search for more papers by this authorLUIGI GALLO, LUIGI GALLO Oncologia Medica, Ospedali Galliera, Genova Italy.Search for more papers by this authorMARIO MESITI, MARIO MESITI Cattedra di Oncologia, Università di Messina, Italy.Search for more papers by this authorGIUSEPPE SCHIEPPATI, GIUSEPPE SCHIEPPATI Medicina I, Ospedale Generale Provinciale, Saronno (VA), Italy.Search for more papers by this authorOTHER PARTICIPANTS IN THE GROCTA TRIALS, OTHER PARTICIPANTS IN THE GROCTA TRIALS Div. di Oncologia Medica II, Istituto Nazionale per la Ricerca sul Cancro, Viale Benedetto XV, 10, 16132 Genova, Italy.Search for more papers by this author FRANCESCO BOCCARDO, Corresponding Author FRANCESCO BOCCARDO Div. di Oncologia Medica II, Istituto Nazionale per la Ricerca sul Cancro, Viale Benedetto XV, 10, 16132 Genova, Italy.Francesco Boccardo, M.D., Div. di Oncologia Medica II, Istituto Nazionale per la Ricerca sul Cancro, Viale Benedetto XV, 10, 16132 Genova, Italy.Search for more papers by this authorDOMENICO AMOROSO, DOMENICO AMOROSO Div. di Oncologia Medica II, Istituto Nazionale per la Ricerca sul Cancro, Viale Benedetto XV, 10, 16132 Genova, Italy.Search for more papers by this authorALESSANDRA RUBAGOTTI, ALESSANDRA RUBAGOTTI Div. di Oncologia Medica II, Istituto Nazionale per la Ricerca sul Cancro, Viale Benedetto XV, 10, 16132 Genova, Italy.Search for more papers by this authorPIERO SISMONDI, PIERO SISMONDI Cattedra di Ginecologja Oncologica, Università di Torino, Italy.Search for more papers by this authorCORRADO DE SANCTIS, CORRADO DE SANCTIS Cattedra di Ginecologja Oncologica, Università di Torino, Italy.Search for more papers by this authorMARIO CAPPELLINI, MARIO CAPPELLINI Unità Operativa Radioterapia, Policlinico Careggi, Firenze, Italy.Search for more papers by this authorPAOLO PACINI, PAOLO PACINI Unità Operativa Radioterapia, Policlinico Careggi, Firenze, Italy.Search for more papers by this authorLUIGI CASTAGNETTA, LUIGI CASTAGNETTA Biochimica degli Ormoni, Università di Palermo, Italy.Search for more papers by this authorADELE TRAINA, ADELE TRAINA Biochimica degli Ormoni, Università di Palermo, Italy.Search for more papers by this authorANTONIO FARRIS, ANTONIO FARRIS Cattedra di Oncologia Clinica, Università di Sassari, Italy.Search for more papers by this authorSTEFANO IACOBELLI, STEFANO IACOBELLI Cattedra di Oncologia Medica, Università di Chieti, Italy.Search for more papers by this authorGIORGIO MUSTACCHI, GIORGIO MUSTACCHI Centra Oncologico, Trieste, Italy.Search for more papers by this authorITALO NENCI, ITALO NENCI Istituto Anatomia Patologica, Università di Ferrara, Italy.Search for more papers by this authorADRIANO PIFFANELLI, ADRIANO PIFFANELLI Istituto di Radiologia, Università di Ferrara, Italy.Search for more papers by this authorEUGENIO VILLA, EUGENIO VILLA Radio-Chemioterapia, Istituto Scientifico S. Raflaele, Milano, Italy.Search for more papers by this authorDANIELA ALDRIGHETTI, DANIELA ALDRIGHETTI Radio-Chemioterapia, Istituto Scientifico S. Raflaele, Milano, Italy.Search for more papers by this authorLUIGI GALLO, LUIGI GALLO Oncologia Medica, Ospedali Galliera, Genova Italy.Search for more papers by this authorMARIO MESITI, MARIO MESITI Cattedra di Oncologia, Università di Messina, Italy.Search for more papers by this authorGIUSEPPE SCHIEPPATI, GIUSEPPE SCHIEPPATI Medicina I, Ospedale Generale Provinciale, Saronno (VA), Italy.Search for more papers by this authorOTHER PARTICIPANTS IN THE GROCTA TRIALS, OTHER PARTICIPANTS IN THE GROCTA TRIALS Div. di Oncologia Medica II, Istituto Nazionale per la Ricerca sul Cancro, Viale Benedetto XV, 10, 16132 Genova, Italy.Search for more papers by this author First published: November 1993 https://doi.org/10.1111/j.1749-6632.1993.tb17222.xCitations: 7 See Appendix. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume698, Issue1Breast Cancer: From Biology to Therapy–Pisa Symposia in OncologyNovember 1993Pages 318-328 RelatedInformation

From January 1981 to December 1987, 264 patients affected with small breast cancers were treated with quadrantectomy plus axillary dissection and radiation therapy on the breast remnant (QUART). Mean age of the patients was 53 years; 124 of them were less than or equal to 50 years old (46.9%); 85 had axillary nodal metastases (32.2%), and 58 presented a primary tumor with pathologic size (greater than 2 cm) (22.9%). Overall actuarial survival at 3 and 7 years, according to the Kaplan and Meyer method, was 95.5% and 85.3%, respectively; NED survival was 85.9% and 77.4%. Twenty patients died (19 of cancer). Local relapses were 6 (2.3% on the whole and 13.3% on the whole of recurrences observed at follow-up). Local relapses were central in the quadrantectomy scar in 4/6 patients. Histology and site of the primary lesion were not correlated with a major risk of local failure. Isolated recurrences in the breast did not worsen survival. Nodal failures were 5 (1.9% on the whole of cases; 11.1% on the whole of failures). Our study confirms the role of QUART as an effective and reliable method in the treatment of small breast carcinomas.