RESUMO
We report a case of a patient with unresectable gastric cancer who showed complete response(CR)to S-1 and paclitaxel (PTX)combination therapy. The patient(a 67-year-old woman)was diagnosed with unresectable advanced gastric cancer with metastases in the Virchow's lymph nodes and para-aortic lymph nodes. Systemic chemotherapy with 70mg/m2 S-1 (days 1-14)and 70mg/m2 PTX(day 1)was administered every 3 weeks. At the end of 7 courses of chemotherapy, the primary lesion and swollen lymph nodes became markedly smaller. After 7 courses, an additional 39 courses were administered over 2.5 years. No notable adverse events were seen, and the patient's performance status(PS)was 0. CR was monitored by imaging studies. No cancer cells were detected on cytological examination of the primary lesion. Monotherapy with 70mg/m2 S-1(days 1-28, 2-week drug holiday)has been administered for the past 3 years. The patient is currently treated as an outpatient and maintains CR and a PS of 0.
Assuntos
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Neoplasias Gástricas/tratamento farmacológico , Idoso , Combinação de Medicamentos , Feminino , Humanos , Metástase Linfática , Estadiamento de Neoplasias , Ácido Oxônico/administração & dosagem , Paclitaxel/administração & dosagem , Indução de Remissão , Neoplasias Gástricas/patologia , Tegafur/administração & dosagemRESUMO
In this study, we used 7 informative microsatellite markers at 8p22, 23.1, and 23.2 in Japanese patients to compare frequency of loss of heterozygosity (LOH) in 53 lesions of high-grade prostatic intraepithelial neoplasia (HGPIN), 38 cases (38 lesions) of incidental prostate cancer (IPC), 31 cases (41 lesions) of latent prostate cancer (LPC), and 102 cases (168 lesions) of clinical prostate cancer (CPC). The frequency of LOH at 8p22-23.2 with at least 1 marker was 0%, 33%, 57%, and 51% in the HGPIN, IPC, LPC, and CPC cases, respectively. No statistically significant difference was found at 8p22-23.2 between the types of prostate cancer. However, the frequency of 8p22 deletion was significantly higher in CPC and LPC cases than in IPC cases (P = 0.0003) or lesions (P = 0.0017). The frequency of LOH at 8p22 and 8p23.1 loci in high-grade tumors was significantly higher than in low-grade tumors in both the LPCs/IPCs and CPCs (P < 0.05). Allelic loss at 8p22 was significantly more frequent in CPC than in IPC (P = 0.002) and in pT4 CPC than in earlier-stage CPC (P = 0.038). These findings suggest that deletion of 8p is an important event in both the initiation and metastasis of prostate cancer. The extremely high frequency of LOH at 8p22-23.1 in high-grade tumors suggests the existence of a novel putative tumor-suppressor gene associated with the progression of prostate cancer. These results should be useful in identifying the target gene of deletion at 8p.
Assuntos
Alelos , Cromossomos Humanos Par 8 , Neoplasia Prostática Intraepitelial/genética , Sequência de Bases , Primers do DNA , Humanos , Perda de Heterozigosidade , Masculino , Reação em Cadeia da Polimerase , Neoplasia Prostática Intraepitelial/patologiaRESUMO
BACKGROUND: Loss of heterozygosity (LOH) at 13q is one of the most common chromosomal alterations in high-stage prostate cancer, yet little is known about genetic changes in earlier-stage prostate cancer. METHODS: We used five microsatellite markers at 13q14, 21, and 33 to compare LOH frequencies in 51 lesions of high-grade prostatic intraepithelial neoplasia (HGPIN), 21 cases of incidental prostate cancers (IPCs), 31 cases of latent prostate cancers (LPCs), and 102 cases of clinical prostate cancers (CPCs). RESULTS: The frequency of LOH at 13q with at least 1 marker was 0%, 38%, 56%, and 49% in HGPIN, IPCs, LPCs, and CPCs, respectively. No statistically significant difference was found between the types of prostate cancer. Allelic loss at 13q14 was significantly more frequent in pT4 tumors than in earlier-stage tumors (P=0.011). CONCLUSIONS: Allelic loss at 13q is not only an important event in the metastasis of prostate cancer, but also associated with the initiation of the tumor.