[Endometrial carcinoma].
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Antineoplastic Agents, Hormonal↗
Biomedical subjects
Satoru Nagase
Publications and source records attributed to Satoru Nagase.
Progesterone receptor isoforms as a prognostic marker in human endometrial carcinoma.
The possible role of specific progesterone receptor (PR) isoforms (PRA and PRB) as predictive factors in endometrial carcinoma is unclear. The present study was undertaken to evaluate the clinical significance of intratumoral PR isoform status in patients with endometrioid endometrial carcinoma. We studied 103 cases of endometrioid endometrial carcinoma using immunohistochemistry. We correlated the findings with various clinicopathological parameters of the patients. PRA and PRB immunoreactivity was detected in 51/103 (48.5%) and 79/103 (76.7%) of carcinoma cases, respectively. A significant positive correlation was detected between the status of PRB immunoreactivity and the amount of PRB mRNA by real-time reverse transcription-polymerase chain reaction (P = 0.012). PR isoform expression was significantly lower in the cases with higher histological grade (P = 0.0001 and P = 0.002, for PRA and PRB, respectively). Cases that were negative for either one or both PR isoforms were significantly associated with shorter disease-free and overall survival of the patients. The absence of either one or both of these two PR isoforms was detected in all nine patients who died (100.0%), whereas the absence of these immunoreactivities was detected only in 43 of 94 (45.7%) patients who had lived during the same period. In addition, multivariate analysis demonstrated that an absence of PRA immunoreactivity was an independent risk factor in disease-free survival of the patients (P = 0.0258). The results of our study demonstrated that loss or absence of PR isoform expression determined by immunohistochemistry could become an important prognostic indicator in patients with endometrioid endometrial carcinoma.
Adenocarcinoma↗
Phase I trial of concurrent chemoradiation with weekly nedaplatin in patients with squamous cell carcinoma of the uterine cervix.
OBJECTIVE: This phase I clinical trial for cervical carcinoma had three objectives: to evaluate the toxicity of a concurrent chemoradiation regimen featuring weekly nedaplatin; to determine the recommended dose of nedaplatin for a phase II concurrent chemoradiation trial; and to evaluate the formula for predicting area under the curve data for nedaplatin through pharmacokinetic studies. PATIENTS AND METHODS: Twelve patients with locally advanced squamous cell carcinoma of the uterine cervix were enrolled. Nedaplatin was administered once a week for 6 weeks. The starting dose of nedaplatin was 25 mg/m(2)/week, with increments of 5 mg/m(2)/week planned for each dose level. Three cases were enrolled at each of the dose levels. Radiation therapy was delivered with both external beam teletherapy and intracavitary brachytherapy with HDR-RALS. Volunteering patients underwent pharmacokinetics studies during the second course. RESULTS: Nedaplatin at a dose of 25, 30, and 35 mg/m(2) was safely administered for three cases at each dose level. At a dose of 40 mg/m(2), however, all three cases had Grade 3 neutropenia. Observed area under the curve value and predicted value was closely correlated, with differences between the two area under the curve values within 25%. All 12 cases achieved a clinical complete response, as evaluated with RECIST. CONCLUSIONS: Our recommended dose for a phase II trial of concurrent chemoradiation with weekly nedaplatin is 35 mg/m(2). The formula can predict unbound concentration of nedaplatin based on area under the curve within 25% error.
Adult↗
Lactation and risk of endometrial cancer in Japan: a case-control study.
The incidence of endometrial cancer is rapidly increasing in Japan. Although the risk factors in European populations have been well described, there are few epidemiologic studies regarding risk factors for endometrial cancer in Japanese women. This hospital-based case-control study among Japanese women was carried out from 1998 to 2000. The cases were selected from women with endometrial cancer (n =155), and the controls selected from women attending the university gynecological outpatient clinic for cervical cancer screening (n = 96). Subjects were interviewed to ascertain breast feeding practices, contraceptive usage, as well as potential risk factors for endometrial cancer. We observed a lower risk of endometrial cancer associated with oral contraceptive (OC) and a higher risk associated with higher body mass index (BMI), and older ages at first and last delivery. Gravidity reduced odds ratio (OR) for endometrial cancer to 0.34 (95% confidence interval [CI] 0.13-0.92). Compared with parous women who had never breastfed, the multivariate OR for women with a history of breastfeeding was 0.37 (95% CI, 0.17-0.82). Additionally, a greater lapse of time since breastfeeding increased OR for endometrial cancer by over three times. In conclusion, the present study has indicated that breastfeeding reduces the risk of endometrial cancer in Japanese women.
Adult↗
Two somatic biallelic lesions within and near SMAD4 in a human breast cancer cell line.
Loss of chromosome arm 18q is a common event in human pancreatic, colon, and breast cancers and is often interpreted as representing loss of one or more tumor-suppressor genes. In this article, we describe two novel biallelic deletions at chromosome band 18q21.1 in a recently characterized human breast cancer cell line, HCC-1428. One lesion deletes a fragment of approximately 300 kb between SMAD4 and DCC that encodes no known genes. The second lesion is an in-frame SMAD4 deletion (amino acids 49-51) that affects the level of SMAD4 protein but not the SMAD4 message. This change accelerates 26S proteasome-mediated degradation of both endogenous and exogenous mutant SMAD4. Examination of normal DNA from the same patient demonstrated that both lesions are somatic and associated with loss of both normal alleles. These data support the concept that two independent tumor-suppressor loci exist at chromosome segment 18q21.1, one at SMAD4 and the other potentially at an enhancer of DCC or an unrelated novel gene.
Alleles↗