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Biomedical subjects

W Zoli

Publications and source records attributed to W Zoli.

At least 37 records · Page 2Linked to original sources
PubMed1998

Chromosomal alterations, biological features and in vitro chemosensitivity of SCLC-R1, a new cell line from human metastatic small cell lung carcinoma.

A new human cancer cell line was established from a metastatic lesion of a small cell lung carcinoma (SCLC-R1) and maintained in continuous culture with a doubling time of 62 h. The SCLC-R1 line, whose ultrastructural features are presented, showed a diploid DNA content, a translocation involving chromosome 16 [t(16;?)(q24;?)] and noticeable deletions in the FHIT (fragile histidine triad) region in the short arm of chromosome 3 [del(3)(p14)] and in the telomeric region of the short arm of chromosome 12 [del(12)(p13)]. The involvement of 12p in metastatic small cell lung cancer is reported here for the first time. No amplification or rearrangements were evident in the c-myc, L-myc, N-myc, int-2, c-erbB-2, H-ras, K-ras, c-mos, and hst-1 genes by Southern blot analysis. Wild-type p53, RB, K-ras and H-ras genes were evident by polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) analysis. The neuron specific enolase (NSE) level was much higher in the cell line's cytosol than in the patient's serum and the cell line also had high expression of chromogranin A and cytokeratin 19. SCLC-R1 cells were sensitive to cisplatin, carboplatin and doxorubicin. The clinical history of the patient from whom the cell line was derived is reported. The characteristics of this new cell line indicate it to be a useful experimental model to investigate lung cancer biology and anticancer drug response.

Aged↗
PubMed1998

Modulating effect of lonidamine on response to doxorubicin in metastatic breast cancer patients: results from a multicenter prospective randomized trial.

Previous results from our preclinical studies have shown that lonidamine (LND) can positively modulate the antiproliferative activity of doxorubicin (DOX) on breast cancer cell lines. To evaluate the effect of LND in a clinical setting, a multicenter randomized trial was carried out on patients with advanced breast cancer. From September 1991 to July 1993, 181 patients were enrolled in the trial and received an initial treatment of DOX at 75 mg/m2 for 3 cycles. The 137 patients who reached complete remission, partial remission, or stable disease were randomized to receive either DOX alone (75 mg/m2 day 1) (arm A) or DOX plus LND (600 mg orally/day) (arm B). The patients enrolled in the two arms were fairly homogeneous in terms of major clinical characteristics. Toxicity was similar in both arms except for myalgia: WHO grade > or=2 was observed in 57% of arm B patients. Overall response rate to DOX + LND was 50% and to DOX alone 38% in evaluable patients, and 48% vs 37% in all registered patients, as determined by an intention-to-treat analysis. The differences did not reach statistical significance. Conversely, in agreement with previous findings, we observed a significant difference in response rate in the subgroup of patients with liver metastases, regardless of the extent of hepatic involvement (DOX + LND 68% vs DOX 33%, p=0.03). This observation makes LND an important tool in association with anthracyclines in the treatment of this subgroup of patients.

Adult↗
PubMed1997

Establishment and characterization of two new cell lines derived from human metastatic breast carcinomas.

Two human cancer cell lines (MA 2 and MA 3) were established from pleural effusions of infiltrating ductal carcinomas of the breast. The lines were maintained in continuous monolayer culture with doubling times of 70 (MA 2) and 78 (MA 3) hr for more than two years and possessed extensively rearranged abnormal karyo-types with modal chromosome number of 83 (MA 2) and 81 (MA 3) and DNA index values of 1.65 and 1.77, respectively. No amplifications or rearrangements were evident in the c-myc, int-2, c-erb B2, c-Ha-ras, or hst 1 genes in MA 2 and MA 3 cell lines. The clinical histories of the patients from whom the cell lines were derived are reported and compared with the results observed in the cell lines in vitro. The presence of CEA, CA 15-3, and MCA tumor markers observed in the primary tumor tissues was retained by the established cell lines. While the primary tumor tissues were ER+/PgR borderline+ (MA 2) and ER-/PgR+ (MA 3), the MA 2 line was ER+/PgR- and the MA 3 line remained ER-/PgR+. The MDR P-glycoprotein was not expressed either in primary tumor tissues or in the respective cell lines. High expression of cytokeratins 7, 18, and 19 was evident by immunohistochemical analysis in each cell line. whereas cytokeratins 8 and 17 were poorly or not at all expressed. The treatment history of the patients from whom the cell lines were derived involved CMF followed six months later by novantrone and cisplatin plus VP 16 (MA 2) and FEC followed four years later by CMF (MA 3). The chemosensitivity pattern assay of the cell lines indicated that the MA 2 line was sensitive to doxorubicin, cisplatin, and vinblastine, whereas the MA 3 line was sensitive to doxorubicin and cisplatin. The characteristics of these cell lines indicate them to be a good experimental model to investigate breast cancer biology and anticancer drug response.

Adult↗
PubMed1997

Saporin 6 and lonidamine in primary cell cultures from human breast carcinomas: a synergistic effect.

Lonidamine (LND) is a potential chemotherapeutic agent which can positively modulate the efficacy of several antineoplastic agents. The ribosome-inactivating protein Saporin 6 (SO 6), which acts as a rRNA N-glycosidase and a DNA nuclease, has recently attracted interest as a novel potential anticancer and antiviral agent. Synergism between LND and SO 6 was previously demonstrated by us in the human metastatic MAST breast cancer cell line in vitro. In the present study, the antiproliferative effect of the drugs, either alone or in combination, was investigated in vitro at various concentrations in 17 primary cell cultures established from patients carrying infiltrating ductal carcinomas of the breast. Results indicate a strong synergistic effect in 11/17 cases, when LND was administered as a second drug. This is in agreement with previous results in the MAST cell line. Synergism was evident at SO 6 concentrations between 3.3 x 10(-10) and 1.7 x 10(-9) M.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1997

Doxorubicin and paclitaxel (sequential combination) in the treatment of advanced breast cancer.

Based on preclinical data, we designed a phase I/II clinical trial to determine the efficacy and toxicity of doxorubicin followed by paclitaxel in the treatment of advanced breast cancer (either untreated or relapsed after adjuvant therapy). In the phase I dose-finding study, 19 enrolled patients received bolus doxorubicin (50 mg/m2) and, after a 16-hour interval, a three-hour infusion of paclitaxel in escalating doses from 130 to 250 mg/m2, increased by 30-mg/m2 increments for each dose-level group. The first dose level group (paclitaxel 130 mg/m2) included three patients. The other dose level groups included four patients. Treatment was repeated every three weeks for a maximum of eight cycles. The paclitaxel dose was escalated to 250 mg/m2 without reaching the maximum tolerated dose. In the 128 cycles assessable for toxicity, there were no relevant clinical signs or symptoms of cardiotoxicity. This absence of significant cardiotoxicity required confirmation in a phase II trial. Since a maximum tolerated dose of paclitaxel had not been reached during the first study and an increasing risk of neutropenia and peripheral neurotoxicity was feared if doses continued to escalate, a phase II confirmatory study was begun to evaluate treatment with fixed doses of doxorubicin (50 mg/m2) and paclitaxel (220 mg/m2), using the same schedule and interval as in phase I. The 13 patients enrolled in phase II received a total of 95 cycles of therapy; in 10 cycles (three patients) dose reductions were necessary because of toxicity. However, no significant clinical cardiotoxicity was observed in 12 of the 13 patients. One patient experienced an asymptomatic, transient decrease in left ventricular ejection fraction at a cumulative doxorubicin dose of 400 mg/m2. Overall clinical responses included 10 complete remissions (31.3%) and 15 partial remissions (46.9%) for an objective response rate of 78.1%. At 16 months' median follow-up, the median time to progression for all patients is nine months. The high response rate obtained in the phase I/II studies and, in particular, the absence of significant cardiotoxicity require confirmation in further clinical trials. To date, two confirmatory phase II trials are ongoing in our institutions.

Antibiotics, Antineoplastic↗
PubMed1997

Paclitaxel plus doxorubicin in breast cancer: an Italian experience.

Based on preclinical data, phase I/II clinical trials were performed at Istituto Oncologico Romagnolo (IOR) Operative Units (Medical Oncology Departments of Forlì, Rimini, and Ravenna, Italy) to determine the efficacy and toxicity of sequential administration of doxorubicin followed by paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ) in the treatment of patients with advanced breast cancer that either had been previously untreated or that had relapsed after adjuvant therapy. In the phase I trial, 19 patients received bolus doxorubicin (50 mg/m2) followed after a 16-hour interval by paclitaxel (given at dose levels ranging from 130 to 250 mg/m2) by 3-hour infusion every 3 weeks, for a maximum of eight cycles. Paclitaxel doses were escalated in 30-mg/m2 increments if the maximum tolerated dose had not been reached in the previous dose level. Analysis of the 128 cycles assessable for toxicity demonstrated neutropenia (<500/microL) in 26 courses (20.3%), with no significant clinical events. No relevant clinical cardiotoxicity was observed. The paclitaxel maximum tolerated dose was not reached at the 250-mg/m2 dose level (no grade 3 or 4 extramedullary toxicity). In the IOR phase II trial, 13 patients were treated with fixed doses of both drugs (doxorubicin 50 mg/m2 and paclitaxel 220 mg/m2). Grade 4 neutropenia occurred in 39 of the 95 cycles, but was complicated by fever in only eight cycles (8.4%); three cycles required granulocyte colony-stimulating factor support. Peripheral neurotoxicity was the most common extramedullary side effect noted. Overall clinical responses in the IOR trials included 10 complete responses (31.3%) and 15 partial responses (46.9%), with an objective response rate of 78.1%. Comparison of these results with those obtained from a phase I trial using the opposite drug sequence showed comparable overall response rates, but IOR's sequence was associated with a higher complete response rate, as well as less frequent and less severe nonhematologic toxicity.

Adult↗
PubMed1996

A new cell line from human infiltrating ductal carcinoma of the breast: establishment and characterization.

We established a novel cancer cell line (MAST) from the ascitic fluid of a metastatic infiltrating ductal carcinoma of the breast. The epithelial and neoplastic nature of the MAST cells was confirmed by ultrastructural analysis. The cell line was maintained as a monolayer with a doubling time of about 68 h, and it possessed an abnormal karyotype with a modal chromosome number of 60, a trisomy of chromosome 18 and other unidentified rearranged chromosomes. Among the markers consistently found in MAST metaphases, we noted a t(14; 14) and a very large subtelocentric, a large satellited acrocentric and a very large submetacentric chromosome with striking fluorescent bands. Immunoenzymatic assay demonstrated that the MAST cell line was positive for estrogen and progesterone receptors. The in vitro drug-sensitivity assay showed a marked resistance of the cell line to 5-fluorouracil and 4-hydroperoxycyclophosphamide and a moderate resistance to etoposide and 4'-epidoxorubicin. The molecular analysis showed a four-to sixfold amplification of the c-myc gene and no amplification or rearrangement of the int-2, c-erbB-2, c-Ha-ras, c-mos and hst-1 genes.

Adult↗
PubMed1996

A Phase I/II study of paclitaxel and doxorubicin in the treatment of advanced breast cancer.

We designed a clinical study in which fixed doses of doxorubicin were infused by intravenous bolus 16 hours before escalating doses of paclitaxel (Taxol; Bristol-Myers Squibb Company, princeton, NJ) for the treatment of patients with advanced breast cancer, an interval selected to allow systemic clearance of doxorubicin before administration of paclitaxel in an outpatient setting. Courses of fixed-dose doxorubicin 50 mg/m2 by intravenous bolus and paclitaxel (doses escalated from 130 mg/m2 to 250 mg/m2 via dose escalation of 30 mg/m2) were repeated every 21 days, to a maximum of eight cycles. Maximum tolerated dose was reached if two or more of six patients at a given dose level were affected by the following events: absolute neutrophil count less than 500/microliter for > or = 7 days, absolute neutrophil count less than 100/microliter for > or = 3 days, insufficient hematopoietic recovery with absolute neutrophil count less than 1,500/microliter on day 21, febrile neutropenia, grade 4 thrombocytopenia, any World Health Organization grade 3 nonhematologic toxicity for more than 7 days. There were 19 patients enrolled; the patients received a total of 128 treatment courses. Grade 4 neutropenia was the main side effect, occurring in 20% of courses but generally not associated with clinical events. No relevant clinical cardiac toxicity or alteration of left ventricular ejection fraction was observed. Other toxicities included complete alopecia, mild peripheral neuropathy, and mild myalgia. There was a reduction of one dose level for moderate myalgia in one patient (190 mg/m2 level). Complete alopecia was always present. Maximum tolerated dose was not reached at paclitaxel 250 mg/m2. Ultimately, the introduction of this combination in the adjuvant setting is warranted.

Adult↗
PubMed1996

A phase I/II study of sequential doxorubicin and paclitaxel in the treatment of advanced breast cancer.

Based on preclinical data, we designed a phase I/II clinical trial to determine the efficacy and toxicity of doxorubicin followed by paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ) in the treatment of patients with advanced breast cancer (either untreated or relapsed after adjuvant therapy). In the phase I study, 19 enrolled patients received bolus doxorubicin (50 mg/m2) and, after a 16-hour interval, escalating doses of paclitaxel (from 130 to 250 mg/m2 in 30-mg/ m2 increments) by 3-hour infusion every 3 weeks for a maximum of eight cycles. Paclitaxel doses were increased if the maximum tolerated dose (MTD; defined by dose-limiting toxicities) had not been reached. Analysis of the 128 cycles assessable for toxicity demonstrated neutropenia (< 500/microL) in 20% of cycles with no significant clinical events. No relevant clinical cardiotoxicity was observed. Other toxicities included mild peripheral neuropathy and mild myalgia/arthralgia (In 37.5% and 30.4% of cycles, respectively). The maximum tolerated paclitaxel dose was not reached at the 250 mg/m2 dose level. In the second phase, 13 patients were treated with fixed doses of both drugs (doxorubicin 50 mg/m2 and paclitaxel 220 mg/m2, the dose level immediately preceding the highest paclitaxel dose used in phase I). Grade 4 neutropenia occurred in 36 of the 87 cycles but was complicated by fever in only eight cycles (9%); three patients needed granulocyte colony-stimulating factor. Peripheral neuropathy (grades 1 and 2 in 41.3% and 5.7% of cycles, respectively) and a myalgic syndrome (grades 1 and 2 in 24.1% and 17.2% of cycles, respectively) were observed. No significant clinical cardiotoxicity was observed in 12 of the 13 patients. One patient experienced a decrease in left ventricular ejection fraction (from 60% to 43%) at a cumulative doxorubicin dose of 400 mg/m2. Antitumor efficacy was evaluated in both phase I and phase II. Overall clinical responses included 10 complete (31.3%) and 15 partial (46.9%) responses, for an objective response rate of 78.1%. Six patients (18.8%) had stable disease. The median durations of objective and complete response were 9 and 7 months, respectively. The 78.9% objective response rate in the phase I trial (31.6% complete and 47.3% partial responses) suggests a dose response relationship: at paclitaxel dose > or = 190 mg/m2, all patients had an objective response (six complete and nine partial responses). These results confirm that doxorubicin followed by paclitaxel is active and should be tested as adjuvant treatment and in patients treated previously with anthracyclines.

Adult↗
PubMed1996

The sequential administration of combined doxorubicin and paclitaxel in the treatment of advanced breast cancer.

In phase I and II studies we administered fixed doses of doxorubicin by intravenous bolus 16 hours before escalating doses of paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ) for the treatment of patients with advanced breast cancer who had received no prior treatment or who had relapsed after adjuvant therapy. Nineteen patients were entered in the study from April 1994 to February 1995. The median age of participants was 54 years; the median disease-free interval was 328 days. Eleven patients had undergone prior adjuvant chemotherapy, seven had undergone prior hormonal therapy, and six had undergone chest radiotherapy. A total of 128 courses of fixed-dose doxorubicin 50 mg/m2 by intravenous bolus and paclitaxel (doses escalated from 130 to 250 mg/m2, through dose escalations of 30 mg/m2 if maximum tolerated dose was not reached) were repeated every 21 days for a median of seven cycles per patient. Toxicities encountered in this trial included grade 4 neutropenia (20% of courses) and grade 4 thrombocytopenia (3% of courses). No grade 3 or 4 nonhematologic toxicities were observed (World Health Organization grade I peripheral neuropathies and mild myalgias in 37.5% and 30% of courses, respectively). No cardiac toxicity was observed. Responses included six complete responses (31.6%), nine partial responses (47.2%), and three stable disease (15.8%), for an overall response rate of 78.8%. Median duration of overall and complete response was 8+ months and 7+ months, respectively. At dose levels > or = 190 mg/m2, all patients had achieved a response (six complete responses and six partial responses). A phase II trial using fixed doses of doxorubicin (50 mg/m2) and paclitaxel (220 mg/m2) is ongoing. Preliminary data on 71 courses report no cardiac toxicity. Treatment with paclitaxel has been well tolerated at each dose level. The maximum tolerated dose was not reached at 250 mg/m2. No cardiac toxicity was reported. The dosing sequence of doxorubicin followed by paclitaxel is a highly active regimen and needs to be tested in anthracycline patients and in an adjuvant setting.

Adult↗
PubMed1995

In vitro activity of taxol and taxotere in comparison with doxorubicin and cisplatin on primary cell cultures of human breast cancers.

The in vitro activities of taxol and taxotere in comparison with cisplatin and doxorubicin were assessed in 30 primary tumor cultures from human breast cancers. Both taxanes were much more potent than cisplatin and doxorubicin. Taxotere was 3.1; 296, and 9.6-fold more cytotoxic than taxol, cisplatin, and doxorubicin respectively. The cytotoxic activity observed in our experiments confirms the potential clinical relevance of the two taxanes in the management of breast cancer.

Antineoplastic Agents, Phytogenic↗
PubMed1993

Cell kinetics and prognosis in gastric cancer.

METHODS: The potential proliferative activity of primary gastric cancer was determined using the in vitro tritiated thymidine labeling index (LI) technique. RESULTS: The proliferative rate had a wide range (0.1-28.4%) with a median value of 9.3%. The cell kinetics of the primary tumor were not related to clinicopathologic features, such as the patient's age and sex or the tumor's histologic type and stage. The contribution of cell kinetics to prognosis was investigated in a series of 28 patients (median follow-up, 34 months). The 3-year survival rate was 50% for patients with slowly proliferating tumors compared with only 13% for those with rapidly proliferating tumors. Moreover, in patients with high-LI tumors, the risk of death was more than sixfold greater than for those with low-LI tumors. CONCLUSIONS: These data suggest that cell kinetic studies might be an important discriminant to predict prognosis in gastric cancer.

Adult↗
PubMed1993

Establishment and characterization of a new cell line from primary human breast carcinoma.

A new cell line (BRC-230) was established from surgical material of primary ductal infiltrating breast carcinoma. The epithelial nature of this cell line was confirmed by ultrastructural analysis and demonstrated the retention of structural properties characteristic of the original tumor. The BRC-230 cell line induced tumor in athymic Cr1:nu/nu(CD-1)BR nude mice, it possessed an abnormal karyotype with a modal chromosome number between 60-61 with eight recurrent marker chromosomes, and it presented a doubling time of 30.5 hr. Scatchard analysis demonstrated that both primary tumor and BRC-230 cells were estrogen and progesterone receptor negative. Immunoenzymatic and radioimmunoassays showed a production of marker antigens (CEA, TPA, CA125, CA15-3, CA19-9) which was similar in the patient's serum and BRC-230 cells. The in vitro drug sensitivity assay of the cell line and of the parental tumor tissue showed overlapping results to all tested antiblastic drugs. BRC-230 cells were resistant to 4-Idroperoxy-cyclophosphamide, Idarubicinol, Mitoxantrone, Etoposide, 4'Epidoxorubicin, and Doxorubicin, showing a multiple drug resistance phenotype. Amplification or rearrangement of Her-2neu, Ha-ras, and C-myc genes was observed neither in the original tumor nor in BRC-230 cells; the mdr-1 gene was also present in a single copy. We conclude from these studies that the BRC-230 cell line maintains the same characteristics as the original tumor and may provide us with a good model to study in vitro the biology of drug resistance of breast cancer.

Aged↗
PubMed1992

In vitro potentiation by lonidamine of the cytotoxic effect of adriamycin on primary and established breast cancer cell lines.

Lonidamine is a new potential chemotherapeutic agent, relatively non-toxic, that can positively modulate the efficacy of several antineoplastic drugs. We evaluated the response of two established human breast cancer cell lines (MCF-7 and BRC-230) and of 20 primary breast cancer cell lines to lonidamine, either alone or in combination with adriamycin, the drug most widely used in the management of breast cancer. Different schedules were tested by varying either concentration of the drugs (LND: 10-150 micrograms/ml; ADM: 0.10-0.15 micrograms/ml), or time of exposure (1-96 hours), or sequence of administration (ADM-->LND; LND-->ADM; ADM+LND). Our results indicate slight sensitivity of the cell lines to lonidamine when used alone, whereas an increase of efficacy was noted when lonidamine was added for at least 24 hours after a 4 hour exposure to adriamycin. Such efficacy was significantly greater than that expected from an additive effect between the two drugs. We conclude that lonidamine, when given according to an appropriate schedule, enhances, in vitro, the efficacy of adriamycin. A correct employment of lonidamine in the management of breast cancer might therefore potentiate the therapeutic effect of adriamycin.

Antineoplastic Agents↗
PubMed1991

An efficient method for culturing human breast epithelium: analysis of results.

We have examined the possibility of obtaining primary cultures from breast tissue utilizing a method especially developed for breast epithelium. The number of specimens able to grow in culture was very high: 82.8%, 64.3%, 75.0% and 77.8%, respectively, for primary breast cancer, skin recurrences, inflammatory breast cancer and normal breast tissue. In our experience, growth was not related to menopausal status or histopathologic type, whereas for skin recurrences, a prior pharmacologic treatment (chemotherapy) of the patient enhanced the growth capacity of the tissue. This culture method could help to study the basic biology of breast epithelia and to improve the chemotherapy approach of breast cancer patients.

Breast Neoplasms↗
PubMed1991

Cell kinetics and hormonal features in relation to pathological stage in breast cancer.

Proliferative activity (expressed as 3H-thymidine labeling index, 3H-TdR LI) was evaluated on a series of 281 primary tumors recruited in two years in 6 different institutions from central Italy. 3H-TdR LI proved to be low in intraductal, or well and moderately differentiated, or hormone receptor positive tumors. Conversely, no relation was observed between 3H-TdR LI and menopause, tumor size, or lymph node involvement. An inverse relation was observed between 3H-TdR LI and hormone receptor content. Specific patterns of 3H-TdR LI value and ER content association were observed as a function of menopause, lymph nodal status, and degree of lymph nodal involvement.

Breast Neoplasms↗
PubMed1990

Preliminary correlations of clinical outcome with in vitro chemosensitivity of second passage human breast cancer cells.

These studies describe the clinical correlations of 63 in vitro chemosensitivity assays on breast cancer cells after short-term monolayer culture. Forty-five of the assays were single agent correlations. Based on cut-off values determined empirically, the test accurately predicted resistance for 36 of 41 patients (88%) who did not respond to the drug. It also predicted sensitivity with a high degree of accuracy: 21 of 22 patients (95%) who responded to the drug tested had a sensitive assay. In five cases, two biopsies were evaluated from the same patient. Whenever assays were performed before and after treatment with a given drug, tumor cells from the second biopsy were more resistant in vitro if the patient failed on therapy. If the patient did not fail, but stopped therapy for other reasons, or if there was no intervening therapy with the tested drug, the two biopsies remained similar in drug sensitivity. These results suggest that in vitro chemosensitivity assays which accurately predict both sensitivity and resistance can be obtained with breast cancer cells after short-term culture and that further prospective trials are warranted.

Antineoplastic Agents↗
PubMed1988

Radioligand-labeled binding assay and immunochemical assay for estrogen receptor in 115 human breast cancers.

The aim of this study was to evaluate the results obtained from a new enzyme immunoassay (Abbott-ER-EIA) for the determination of estrogen receptor levels in tumor cytosols in comparison with the currently used DCC method. One hundred and fifteen consecutive primary breast cancer specimens were examined; 66 of the women were postmenopausal and 49 were premenopausal. A good correlation (r = 0.88, p less than 0.001 and a slope of 1.3) was found between ER-EIA and the steroid binding assay (DCC). When these data were analyzed according to menopausal status, no differences were observed for the slopes and correlation coefficients in pre' and postmenopausal groups. The ER-EIA appears to produce results comparable to those obtained with the conventional DCC method for the determination of ER in breast tumor cytosols.

Breast Neoplasms↗