[Trastuzumab for treatment of advanced breast cancers].
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Antibodies, Monoclonal↗
Biomedical subjects
N Katsumata
Publications and source records attributed to N Katsumata.
Endothelial vasodilator function is preserved at the spastic/inflammatory coronary lesions in pigs.
BACKGROUND: The question of whether or not endothelial vasodilator function in the spastic coronary artery is preserved is still controversial. We recently developed a porcine model in which long-term and local treatment with interleukin-1beta (IL-1beta) from the adventitial site causes coronary arteriosclerotic changes and vasospastic responses to autacoids. The aim of this study was to examine the endothelial vasodilator function in our new porcine model of the spasm both in vivo and in vitro. METHODS AND RESULTS: A segment of the porcine coronary artery was aseptically wrapped with cotton mesh that held absorbed IL-1beta-bound microbeads. Two weeks after the procedure, intracoronary administration of serotonin caused coronary vasospasm at the IL-1beta-treated site (n = 10). Coronary vasodilatation to bradykinin, substance P, or an increase in coronary blood flow was preserved at the spastic site. Vasodilator responses to 3-morpholinosydnonimine (an NO donor) and nitroglycerin also were comparable between the 2 sites. The vasoconstricting response to N(G)-monomethyl-L-arginine and the extent of the augmentation of the serotonin-induced vasoconstriction were comparable between the 2 sites. Organ chamber experiments showed that endothelium-dependent relaxations to bradykinin, the calcium ionophore A23187, and even the vasospastic agonist serotonin were preserved at the spastic site, whereas contractions to serotonin were augmented at the spastic site regardless of the presence or absence of the endothelium (n = 6). Endothelium-independent relaxations to sodium nitroprusside were also preserved at the spastic site. CONCLUSIONS: These results indicate that endothelial vasodilator function is preserved at the spastic site and that the spasm is caused primarily by smooth muscle hypercontraction in our porcine model.
Animals↗
Phase II study of KRN8602, 3'-deamino-3'-morpholino-13-deoxo-10-hydroxycarminomycin hydrochloride, MX2 x HCl in patients with metastatic breast cancer.
PURPOSE: KRN8602 (3'-deamino-3'-morpholino-13-deoxo-10-hydroxycarminomycin hydrochloride, MX2 x HCl) is a newly developed anthracycline that has been found to be effective against multidrug-resistant tumor cells in vitro and in vivo. In order to clinically confirm these promising preclinical observations, we performed a phase II trial of KRN8602 in patients with anthracycline-resistant metastatic breast cancer. METHODS: Of 41 patients registered with metastatic breast cancer, 37 were eligible and were given at least two cycles of KRN8602 15 mg/m2 per day at 3-4 week intervals by intravenous bolus injection on days 1, 2, and 3. RESULTS: Of the 37 patients, 6 (16.2%, with a 95% confidence interval of 4.3-28.1%) had a partial response (PR). No complete responses (CRs) were observed. The difference between response rates according to prior history of anthracycline administration was not significant. Myelosuppression was moderately severe, with grade 3 or 4 leukopenia occurring in 65%. Severe nausea/vomiting was observed in 44% of the patients. CONCLUSIONS: The results indicate that KRN8602 has modest activity in refractory metastatic breast cancer and is associated with relatively severe toxicity. Furthermore, the preclinical finding that KRN8602 overcomes anthracycline resistance was not reliably reproduced in this clinical phase II trial.
Adult↗
Rho-kinase-mediated pathway induces enhanced myosin light chain phosphorylations in a swine model of coronary artery spasm.
OBJECTIVE: We recently demonstrated in our swine model of coronary artery spasm that enhanced myosin light chain (MLC) phosphorylations (both MLC mono- and diphosphorylations) play a central role in the pathogenesis of the spasm. However, the molecular mechanism for and the phosphorylation sites for the enhanced MLC phosphorylations were unknown. In the present study, we addressed these points using hydroxyfasudil, a novel inhibitor of protein kinases, which we found preferentially inhibits Rho-kinase. METHODS: The specificity of the inhibitory effects of hydroxyfasudil on Rho-kinase, MLCK, MRCK beta and PKC were examined by kinase assay in vitro. The left porcine coronary artery was chronically treated with interleukin-1 beta (IL-1 beta, 2.5 micrograms). Two weeks after the operation, coronary artery vasomotion was examined both in vivo and in vitro. MLC phosphorylations were examined by Western blot analysis and the sites for the phosphorylations by anti-phosphorylated MLC antibodies that identified the monophosphorylation site as Ser19 and diphophorylation sites as Ser19/Thr18 of MLC. RESULTS: Inhibitory effects of hydroxyfasudil was at least 100 times more potent for Rho-kinase as compared with other protein kinases tested. Intracoronary serotonin (10 micrograms/kg) caused coronary hyperconstriction at the IL-1 beta-treated site in vivo, which was dose-dependently inhibited by hydroxyfasudil (p < 0.01). The coronary segment taken from the spastic site also showed hypercontractions to serotonin in vitro, which were again dose-dependently inhibited by hydroxyfasudil (p < 0.01). Western blot analysis showed that MLC monophosphorylation was significantly greater in the spastic segment than in the control segment, while MLC diphosphorylation was noted only at the spastic segment (p < 0.01). The sites for the mono- and diphosphorylated MLC were identified as the monophosphorylated site Ser19 and diphosphorylated sites Ser19/Thr18 of MLC, respectively. Both types of MLC phosphorylations at the spastic segment were markedly inhibited by hydroxyfasudil (p < 0.01). CONCLUSION: These results indicate that hydroxyfasudil-sensitive Rho-kinase-mediated pathway appears to mediate the enhanced MLC phosphorylations (on Ser19 and Ser19/Thr18 residues) and plays a central role in the pathogenesis of coronary artery spasm.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
Investigation of fading responses induced by non-depolarising muscle relaxants in the evoked EMG of the gastrocnemius muscle of the cat.
BACKGROUND: During partial neuromuscular blockade indirect repetitive nerve stimulation causes fade in the response of the muscle. We studied the intensity of the fade induced by intravenous administration of three steroidal muscle relaxants, and investigated the mechanism of fade by comparing with results obtained during partial blockade with animal toxins and vesamicol. METHODS: In 60 cats, we measured the fade in the compound action potentials of the gastrocnemius muscle evoked by repetitive sciatic nerve stimulation at 100 Hz during partial neuromuscular blockade with rocuronium, vecuronium, pancuronium, alpha-bungarotoxin, mu-conotoxin and vesamicol, respectively. RESULTS: Profound fade was induced by all three non-depolarising muscle relaxants (rocuronium=vecuronium<pancuronium) and by vesamicol, in contrast to alpha-bungarotoxin and mu-conotoxin which induced no fading. CONCLUSION: Our results suggest that non-depolarising muscle relaxant-induced fade is caused by an inhibitory effect on acetylcholine release. Pancuronium seems to have a higher potency of presynaptic inhibition of acetylcholine release than both rocuronium and vecuronium.
Acetylcholine↗
Dose escalation and pharmacokinetic study of a humanized anti-HER2 monoclonal antibody in patients with HER2/neu-overexpressing metastatic breast cancer.
We conducted a phase I pharmacokinetic dose escalation study of a recombinant humanized anti-p185HER2 monoclonal antibody (MKC-454) in 18 patients with metastatic breast cancer refractory to chemotherapy. Three or six patients at each dose level received 1, 2, 4 and 8 mg kg(-1) of MKC-454 as 90-min intravenous infusions. The first dose was followed in 3 weeks by nine weekly doses. Target trough serum concentration has been set at 10 microg ml(-1) based on in vitro observations. The mean value of minimum trough serum concentrations at each dose level were 3.58 +/- 0.63, 6.53 +/- 5.26, 40.2 +/- 7.12 and 87.9 +/- 23.5 microg ml(-1) respectively. At 2 mg kg(-1), although minimum trough serum concentrations were lower than the target trough concentration with a wide range of variation, trough concentrations increased and exceeded the target concentration, as administrations were repeated weekly. Finally 2 mg kg(-1) was considered to be sufficient to achieve the target trough concentration by the weekly dosing regimen. One patient receiving 1 mg kg(-1) had grade 3 fever, one at the 1 mg kg(-1) level had severe fatigue defined as grade 3, and one at 8 mg kg(-1) had severe bone pain of grade 3. No antibodies against MKC-454 were detected in any patients. Objective tumour responses were observed in two patients; one receiving 4 mg kg(-1) had a partial response in lung metastases and the other receiving 8 mg kg(-1) had a complete response in soft tissue metastases. These results indicate that MKC-454 is well tolerated and effective in patients with refractory metastatic breast cancers overexpressing the HER2 proto-oncogene. Further evaluation of this agent with 2-4 mg kg(-1) weekly intravenous infusion is warranted.
Antibodies, Monoclonal↗
Augmentation of vecuronium-induced neuromuscular block during sevoflurane anaesthesia: comparison with balanced anaesthesia using propofol or midazolam.
We have quantified the potentiating effects of 1.7% sevoflurane (n = 12) on vecuronium-induced neuromuscular block and compared the results with those obtained during balanced anaesthesia with propofol (n = 12) or midazolam (n = 12) in 36 patients. Neuromuscular function was monitored using an accelerograph and the train-of-four responses of the adductor pollicis muscle to ulnar nerve stimulation. Vecuronium 0.1 mg kg-1 was administered as an intubating dose, and maintenance doses of 0.02 mg kg-1 were administered on three occasions when T1/T0 had recovered to 25%. Thereafter, spontaneous recovery was monitored until complete. Times to 25% recovery of T1/T0 (DUR25) after an intubating dose of vecuronium did not differ between groups (mean 44.2 (SD 18.7) min for sevoflurane, 38.3 (7.5) min for propofol and 35.5 (9.5) min for midazolam). DUR25 values after each maintenance dose were 29.8 (9.5) min, 30.3 (10.4) min and 31.6 (10.7) min during sevoflurane anaesthesia, and were significantly longer than values for propofol (21.7 (6.0) min, 21.5 (5.8) min and 21.9 (5.8) min) and midazolam (20.0 (5.9) min, 19.3 (7.7) min and 19.8 (8.0) min) (P < 0.05) in each case). Recovery index25-75% and interval from T1/T0 = 25% to T4/T1 = 0.7 after the final dose of vecuronium were significantly prolonged by sevoflurane (28.3 (13.2) min and 42.7 (16.4) min) compared with propofol (17.6 (6.1) min and 26.6 (9.8) min) or midazolam (16.3 (9.4) min and 26.0 (10.2) min) (P < 0.05 in each case).
Adult↗
When and how to combine growth hormone with a luteinizing hormone-releasing hormone analogue.
The effect of combined treatment with growth hormone (GH) and a luteinizing hormone-releasing hormone (LHRH) analogue, or GH alone, on pubertal height gain was assessed in an uncontrolled study in 15 boys and 10 girls with GH deficiency (GHD). Seven boys and six girls were treated with GH alone (group 1), and eight boys and four girls were treated with a combination of GH and an LHRH analogue during puberty (group 2). Mean ages (+/- SD) at the start of GH treatment and at the onset of puberty were significantly lower in group 2 (8.0 +/- 3.3 years and 11.2 +/- 0.8 years, respectively, in boys, and 6.3 +/- 1.6 years and 10.8 +/- 0.7 years in girls) than in group 1 (12.8 +/- 1.9 years and 13.7 +/- 1.4 years in boys, and 11.2 +/- 1.0 years and 12.5 +/- 1.2 years in girls). Height at the onset of puberty was less in group 2 than in group 1, but the difference was significant only for the boys. Combination treatment was started at a mean age of 11.7 +/- 1.2 years in boys and 11.5 +/- 1.0 years in girls. The duration of the combination treatment was 5.1 +/- 1.5 years in boys and 2.3 +/- 0.7 years in girls. The duration of the period between the onset of puberty and the end of GH treatment was significantly longer in group 2 (6.8 +/- 1.2 years in boys and 5.5 +/- 1.0 years in girls) than in group 1 (4.3 +/- 1.6 years in boys and 3.6 +/- 1.4 years in girls). The pubertal height gain was also significantly greater in group 2 (36.7 +/- 6.5 cm in boys and 29.0 +/- 8.3 cm in girls) than in group 1 (21.9 +/- 4.1 cm in boys and 18.6 +/- 4.1 cm in girls). Final height was significantly greater in group 2 than in group 1 in boys. Although there was no significant difference in final height between groups in the girls, the change in height SDS from the start of GH treatment until final height was significantly greater in group 2 (2.7 +/- 1.6 in boys and 4.5 +/- 0.5 SD in girls) than in group 1 (1.0 +/- 0.8 in boys and 1.8 +/- 0.9 SD in girls), in both boys and girls. In conclusion, it appears that combination of an LHRH analogue and GH may increase the pubertal height gain and the final height of children with GHD. The improvement is attributed to the prolongation of the treatment period, permitting slow bone maturation, and to the maintenance of height velocity. This combination treatment appears to be more effective in boys than girls. To fully assess this therapeutic approach, prospective controlled studies are needed.
Adolescent↗
A novel compound heterozygous mutation in the steroidogenic acute regulatory protein gene in a patient with congenital lipoid adrenal hyperplasia.
Congenital lipoid adrenal hyperplasia (CLAH) is an autosomal recessive disorder characterized by impaired synthesis of all adrenal and gonadal steroid hormones. Recently, it was reported that mutations in the steroidogenic acute regulatory protein (StAR) gene cause CLAH. In the present study, we have analyzed the StAR gene of a Japanese patient with CLAH. PCR amplification and subsequent nucleotide sequencing of the StAR gene and those of her parents revealed that the patient has a compound heterozygous mutation of this gene. In one allele, an undescribed G to C transversion in codon 217, which occurred at the last base of exon 5 and thus altered the splice donor site sequence, apparently resulted in a substitution of Arg to Thr (AGG to ACG: R217T), and in the other allele, a C to T transition in codon 218 caused a substitution of Ala to Val (GCG to GTG: A218V), which has been previously shown to abolish StAR activity. In vitro expression analysis of an allelic minigene that consists of exons 4-6 of the R217T mutant StAR gene showed that the G to C transversion in the splice donor site of exon 5 caused by the R217T mutation disrupts normal splicing, resulting in the complete skipping of exon 5, which alters the translation reading frame of exon 6, introduces a stop codon at amino acid position 174, and thus impairs the activity. A functional expression study of the R217T replacement mutant revealed that the mutant has no steroidogenesis-enhancing activity if the transcript of the R217T mutant allele is ever spliced normally and translated into the protein. From the genetic analysis of 50 healthy subjects, the novel R217T mutation was unlikely to be due to polymorphism. Together, these results indicate that this patient is a compound heterozygote for the mutation in the StAR gene (T217R and A218V) and that these mutations inactivate the StAR function and give rise to clinically manifest CLAH.
Adrenal Hyperplasia, Congenital↗
Selective amplification of exons 3 and 8 of the human growth hormone receptor (hGHR) gene based on newly identified intron sequences.
The gene for human growth hormone receptor (hGHR) consists of at least 10 exons, and the corresponding protein is encoded in exons 2-10 which span at least 87 kbp of chromosome 5. Failure to amplify exons 3 and 8 of the hGHR gene from Japanese subjects with the previously reported primers prompted us to determine intron sequences flanking exon 3 and those flanking exon 8 of the hGHR gene, and novel intron sequences flanking exons 3 and 8 of the hGHR gene were identified. We designed new oligonucleotide primers based on these sequences, and successfully amplified DNA fragments encompassing exon 3 and those encompassing exon 8 of the hGHR gene. Since all of the 50 Japanese and the two Caucasians had the very same intron sequences which were different from the previously reported ones, it is more likely that the previously reported sequences were simply wrong than that there exist polymorphic differences in the intron sequences among different ethnic populations.
Asian People↗
Histology according to the Revised European-American Lymphoma Classification significantly predicts the prognosis of ocular adnexal lymphoma.
Lymphoid infiltrates in the ocular adnexa are mostly low-grade B-cell lymphoma, but their clinicopathologic characteristics and prognostic factors have not been extensively analyzed according to the Revised European-American Lymphoma (REAL) Classification. We reviewed histopathologic sections from 77 patients with primary ocular adnexal lymphoid infiltrates, and conducted univariate and multivariate analyses of possible prognostic factors. Fifty-seven of the 77 patients were confirmed to have malignant lymphoma. Histopathologic sections from 44 of the 57 patients were reclassified into the following categories; marginal zone lymphoma (MZL) in 35, mantle cell lymphoma (MCL) in two, diffuse large cell lymphoma (DLCL) in six, and lymphoplasmacytoid lymphoma (LPL) in one. In the remaining 13 patients, biopsied specimens were inadequate for further subclassification. The cause-specific survival rates of the 57 patients with primary ocular adnexal lymphoma at 5, 10, and 15 years were 90.1%, 84.8% and 84.8%, respectively. The univariate analysis showed that the clinical stage, serum lactate dehydrogenase (LDH) value and histopathologic subtype were significant. The 5-year cause-specific survival rate of the 35 patients with MZL was 100%, whereas that of the eight patients with non-MZL (DLCL and MCL) was 25% (p<0.0001). The multivariate analysis revealed that the histologic subtype (p=0.010) and serum LDH value (p=0.015) were independent significant predictors of survival. We conclude that malignant lymphomas occurring in the ocular adnexa histologically consist mostly of MZL. The histologic subtype according to the REAL Classification significantly predicts the prognosis of ocular adnexal lymphoma.
Adult↗
[Effect of non-depolarizing muscle relaxants on autonomic nervous system activity--assessment by heart rate variability analysis].
We investigated the effect of d-tubocurarine (d-Tc), pancuronium (PAN), vecuronium (VEC), and rocuronium (ROC) on the autonomic nervous system in cats by measuring changes in the invasive mean arterial pressure (MAP), heart rate (HR), and heart rate variability following four administrations of each drug at 2.ED95. Heart rate variability analysis was used to assess the effects of the drugs on sympathetic and parasympathetic nervous system function using low-frequency (0.04-0.22 Hz) component (LF) and high-frequency (0.22-0.60 Hz) component (HF). Comparisons of the HR, MAP, LF, HF, and LF/HF ratio before and after drug administration were made for each drug. The administration of d-Tc caused a significant decrease in MAP and a significant increase in HR accompanied by increase in LF, HF, and LF/HF ratio. The increases in the LF, HF and LF/HF ratio appeared to be related to the mean abrupt enhancement of sympathetic and parasympathetic nervous system function caused by changes in circulatory dynamics. PAN caused a significant increase in HR, and a significant decrease in the HF, which we thought were related to suppression of cardiac parasympathetic function. Neither VEC nor ROC produced a significant change in any of the parameters and were considered to have no significant effect on the autonomic nervous system.
Animals↗
A novel frameshift mutation 840delA and a novel polymorphism D203A in the steroidogenic acute regulatory protein gene in a Japanese patient with congenital lipoid adrenal hyperplasia. Mutations in brief no. 117. Online.
Congenital lipoid adrenal hyperplasia (CLAH) is an autosomalrecessive disorder characterized by impaired production of all steroids including glucocorticoids, mineralocorticoids and sexsteriods. It has recently been reported that mutations in the steriodogenic acute regulatory protein (StAR) gene cause CLAH. We analyzed the StAR gene in a Japanese patient with CLAH. The patient was revealed to be a compound heterozygote bearing a nonsense mutation Q258X, changing codon 258 (CAG) encoding Gln to the stop codon TAG, and a novel framshift mutation 840delA resulting from deletion of one of the three adenosines normally present in codon 238 (AAA), thus leading to a frameshift after codon 237 (Thr) in the StAR gene. The patient was also revealed to be homozygous for a novel missense point mutation D203A, changing codon 203 (GAC) encoding Asp to GCC encoding Ala in the StAR gene. To elucidate the significance of the D203A mutation, we analyzed the StAR gene sequence in twenty normal subjects, and found that all of them were homozygous for the D203A mutation, indicating that the D203A mutation is an innocent polymorphism. In conclusion, we have identified a novel frameshift mutation 840delA which seems to cause 840delA and the first polymorphism D203A in the human StAR gene.
Adrenal Hyperplasia, Congenital↗
Novel frameshift mutation 840delA and a novel polymorphism D203A in the steroidogenic acute regulatory protein gene in a Japanese patient with congenital lipoid adrenal hyperplasia.
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Adrenal Hyperplasia, Congenital↗
A phase I trial of docetaxel and 5-day continuous infusion of 5-fluorouracil in patients with advanced or recurrent breast cancer.
To determine the maximum-tolerated doses (MTDs), the dose-limiting toxicities (DLTs) and the recommended doses for further trials of docetaxel in combination with a 5-day continuous infusion of 5-fluorouracil (5-FU) in advanced or recurrent breast cancer patients who had been treated previously with at least one chemotherapeutic regimen, patients were treated with docetaxel as a 1-h infusion on day 1 followed by 5-FU as a continuous infusion on days 1 through 5 every 3-4 weeks. Three or six patients were assessed at the following escalating dose levels of docetaxel/5-FU per day: 40/150, 40/300, 50/300, 50/500 and 60/500 mg m(-2). Nineteen patients entered this trial, of whom 18 could be assessed for adverse event and therapeutic efficacy. The DLTs were neutropenia and diarrhoea. The MTDs were 60 mg m(-2) of docetaxel on day 1 and 500 mg m(-2) per day of 5-day continuous infusion of 5-FU. One of 18 patients achieved a complete response and eight achieved partial response (over all response rate: 50%). The recommended doses of docetaxel and 5-day continuous infusion of 5-FU for a phase II trial are 50 mg m(-2) and 500 mg m(-2) per day every 3 or 4 weeks.
Adult↗
Cerebral metastasis in patients with uterine cervical cancer.
We report on eight patients who developed brain metastases following uterine cervical cancer. The mean interval between diagnosis of the primary cancer and diagnosis of the brain metastasis was 28.4 months (range: 6.1-61.8 months). Nausea and vomiting due to increased intracranial pressure were the most frequent symptoms. Surgical excision of the brain lesions, followed by postoperative radiotherapy, was performed in three patients. The other five patients received only cranial radiotherapy. When the metastatic brain lesions were detected, other distant metastatic lesions were confirmed at the same time in five patients. The median survival time after diagnosis of the brain metastases was only 3.0 months.
Adenocarcinoma↗
Clinicopathological factors predicting retroperitoneal lymph node metastasis and survival in endometrial cancer.
BACKGROUND: By clarifying the significance of clinicopathological factors for retroperitoneal lymph node metastasis and survival of patients with endometrial cancer, we suggest ideas for optimal treatment of this disease. METHODS: A retrospective study was conducted in 310 women with endometrial cancer who underwent surgery with retroperitoneal lymphadenectomy. To evaluate retroperitoneal lymph node metastasis, age-adjusted and multivariable analyses were carried out for six clinicopathological factors including pathological grade, myometrial invasion, cervical invasion, peritoneal cytology, lymphatic permeation and vascular invasion. To evaluate survival, besides the above factors, a positive rate of metastasis of dissected retroperitoneal lymph nodes was included. RESULTS: In 40 patients (13%) with nodal metastasis, the average positive rate of metastasis of dissected retroperitoneal lymph nodes was 22%. For retroperitoneal lymph node metastasis, the odds ratio of deep myometrial invasion, cervical invasion and severe lymphatic permeation were 5.97, 2.72 and 12.01, respectively. For survival, the hazard ratios of the positive rates of metastasis of dissected retroperitoneal lymph nodes (both 25% and < 25%), positive peritoneal cytology and poor pathological grade were 7.10, 3.24, 3.82 and 3.27, respectively, and 5-year survival rates for them were 0, 50, 72 and 77%, respectively. CONCLUSIONS: For retroperitoneal lymph node metastasis, lymphatic permeation, deep myometrial invasion and cervical invasion were the independent prognostic factors. For survival, retroperitoneal lymph metastasis, poor pathological grades and positive peritoneal cytology were the independent prognostic factors. The positive rate of metastasis of dissected retroperitoneal lymph metastasis plays an important role in predicting survival of endometrial cancer. Lymph node biopsy is insufficient in treatment of this disease.
Adenocarcinoma↗
Clinical characteristics of patients with metastatic breast cancer with complete remission following systemic treatment.
BACKGROUND: Patients with metastatic breast cancer (MBC) have variable clinical courses. The purpose was to describe the clinical characteristics of MBC patients with complete remissions (CR) following systemic treatment. METHODS: We analyzed 315 consecutive MBC patients treated with several types of systemic treatments at the National Cancer Center Hospital between January 1988 and December 1993. RESULTS: The median survival time (MST) and median progression-free survival were 28.0 and 17.1 months, respectively. Forty patients were defined as 'first-CR' following initial or second-line systemic treatment and the majority of them had a good performance status, low number of metastatic sites and low incidence of liver involvement. Nine of 40 patients with first-CR continued progression-free 5 years after beginning systemic treatments. The major sites of metastasis were the lung and bone and there were no cases with liver metastasis. Five patients received standard doxorubicin-containing combination chemotherapy with or without tamoxifen. Two of these nine patients remain progression free in first-CR. Three of them remained in first-CR after 5 years and died of progressive breast cancer and two others died of unrelated causes. Two patients relapsed after obtaining a first-CR for at least 5 years and remain alive with active metastatic disease. The MST and median progression-free survival of nine patients were 10.6 and 9.0 years, respectively. These nine patients represented 22.5% of all first-CR patients and 3.2% of the total patients. CONCLUSIONS: Although MBC is commonly recognized to be an incurable disease, a small percentage of patients clearly are alive and progression free for prolonged periods after initiation of systemic treatments.
Adult↗