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S K Chambers

Publications and source records attributed to S K Chambers.

At least 37 records · Page 2Linked to original sources
PubMed1995

The significance of urokinase- type plasminogen activator, its inhibitors, and its receptor in ascites of patients with epithelial ovarian cancer.

BACKGROUND: Strong correlations have been reported between expression of urokinase-type plasminogen activator (uPA) and poor prognosis in several human carcinomas. The clinical significance of secreted levels of uPA, its receptor (uPAR), and its inhibitors (PAI-1 and PAI-2) in the ascites of patients with epithelial ovarian cancer patients was investigated. METHODS: uPA, uPAR, PAI-1, and PAI-2 were measured in the primary ascites of 36 patients with epithelial ovarian cancer by enzyme-linked immunosorbent assay, and normalized to protein content. The relationship between levels of these factors in ascites and clinicopathologic variables, survival, and disease free interval (DFI) was studied. Because high levels of macrophage colony stimulating factor (CSF-1) in ascites is a known poor prognostic indicator for ovarian cancer, the effect of CSF-1 on secretion of PAI-2 by ovarian cancer cells was also examined in vitro. RESULTS: High uPA levels per se did not correlate with either survival or DFI. However, the ratio of uPAR normalized for uPA content correlated inversely with FIGO stage and residual disease, with a significant association between high uPAR/uPA level and prolonged survival and DFI. High PAI-1 levels (> 0.120 ng/mg) proved to be a good prognostic factor, correlating with both prolonged DFI and residual disease < or = 5 cm among Stage 3 patients. Conversely, high levels of PAI-2 (> 0.061 ng/mg) indicated a poor prognosis in Stage 3 patients, as high PAI-2 levels were associated with shorter DFI and survival. CSF-1 stimulated the secretion of PAI-2 by 2.4-fold in Bix3 ovarian carcinoma cells. Multivariate analysis revealed that the two independent prognostic factors for DFI in Stage 3 patients were PAI-1 and PAI-2; Stage 3 patients with high secreted PAI-1 and low PAI-2 levels have a median DFI that was prolonged by 30 months relative to the rest of the group. CONCLUSION: Secreted uPAR/uPA appears to measure tumor burden and predicts prolonged DFI and survival, but was not found to be an independent prognostic factor on multivariate analysis. High levels of PAI-1 in ascites were independently associated with prolonged DFI among Stage 3 patients. Therefore, secreted uPAR and PAI-1 may modulate uPA activity and lead to improved outcome. This contrasts with the finding that secreted PAI-2 is an independent factor indicating poor prognosis, which may relate in part to the actions of CSF-1. This study emphasizes the importance of uPA, its receptor, and its inhibitors in patients with epithelial ovarian cancer.

Adult↗
PubMed1995

Macrophage colony-stimulating factor mediates invasion of ovarian cancer cells through urokinase.

The macrophage colony-stimulating factor (CSF-1) is best known as a hematopoietic cytokine important to macrophage activation. Recently, the importance of CSF-1 and its receptor (encoded by the c-fms proto-oncogene) in epithelial ovarian cancer has also been recognized, with overexpression of CSF-1 denoting poor prognosis in ovarian cancer patients. During macrophage activation, CSF-1 promotes urokinase-type plasminogen activator (uPA) activity; in macrophages and in malignant cells of lung, breast, colon, and prostatic origin, uPA activity is strongly correlated with the ability to invade and, in the malignant cells, to metastasize. While there is clear evidence of CSF-1 and uPA expression in primary and metastatic ovarian cancer, the significance of their expression to invasion of these cells has not been explored. We find that all of our ovarian cancer cell lines which we have studied co-express CSF-1 and uPA transcripts and protein. Urokinase expression in these ovarian cancer cell lines correlates with the degree of tumorigenicity in nude mice, with the most virulent tumor resulting from Hey cells, a strong expressor of uPA. We studied the invasion of these primary and established ovarian cancer cells through a Matrigel (reconstituted basement membrane matrix) barrier. The ability of ovarian cancer cells to invade is strongly correlated with endogenous CSF-1 expression (Pearson's correlation, r = 0.91; P = 0.01). A total of 0.90 +/- 0.16% of Bix3 cells (very weak expressor of CSF-1) invaded through the barrier, in contrast to 6.95 +/- 0.75% of Hey cells (strong CSF-1 expressor) and 10.44 +/- 2.33% of Bixler cells (the strongest CSF-1 expressor). We studied the ability of two of the cell lines to invade human laminin and type IV collagen (Bix3, a weak invader of Matrigel, and Hey, a strong invader), to determine (a) whether our results on a Matrigel matrix may represent a relevant model for invasion in humans and (b) whether there is a potential confounding effect from the cytokines and proteases in Matrigel. On this human simple matrix, we confirm that Bix3 is a weakly invasive cell line (0.33 +/- 0.04% invasion) which contrasted to the strongly invasive Hey cell line (8.51 +/- 0.47%). Treatment of Bix3 cells with exogenous CSF-1 stimulates percentage of invasion by 2-fold and results in a similar increase in the level of uPA transcripts and cellular associated uPA antigen. Furthermore, cell surface-bound uPA increased from 74% in the absence of CSF-1 to 100% (fully saturated) in the presence of CSF-1.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

Extramammary Paget's disease of the vulva.

Fourteen patients with extramammary Paget's disease of the vulva treated at Yale-New Haven Medical Center from 1982 through 1993 were reviewed to evaluate the accuracy of methods used to delineate surgical margins and to determine if radical operations or surgical margin status was associated with likelihood of recurrence. These 14 patients underwent at total of 25 operations for extramammary Paget's disease. In 8 operations, a total of 44 separate frozen-section biopsies were performed to determine extent of disease with a mean of 5.5 biopsies per patient. Visual judgment alone was used to determine margin status in 17 operations. The ability to delineate free surgical margins on permanent sections was not different, whether judged visually or by frozen-section analysis. Frozen-section analysis was misleading in 3/8 (37.5%) cases, while visual judgment was in error in 6/17 (35%) cases. Moreover, permanent margin status was not found to be predictive of disease recurrence. Two of 5 (40%) patients with positive margins recurred after initial surgery compared with 3 of 9 (33%) patients with negative margins. Of the 14 primary operations, there were 8 wide local excisions, 3 simple vulvectomies, and 3 modified radical vulvectomies. The radicality of the operation as initial treatment did not statistically correlate with disease recurrence.

Female↗
PubMed1995

A phase II study of etoposide, cisplatin, and doxorubicin chemotherapy in mixed müllerian tumors (MMT) of the uterus.

Mixed Müllerian tumors (MMT) of the uterus are aggressive entities that result in a very poor prognosis even for patients in whom the disease is limited to the uterus. This phase II trial was undertaken in an attempt to improve overall survival as well as progression-free survival of these patients. Forty-two consecutive patients were treated with a combination chemotherapy containing etoposide 100 mg/m2 on Days 1 and 2, cisplatin 50 mg/m2 on Day 1, and doxorubicin 50 mg/m2 on Day 1, repeated every 28 days. There were 23 patients with early-stage disease (stages I and II) and 19 patients with advanced (stages III and IV) or recurrent disease. In the early-stage group, the number of cycles ranged from 2 to 9 (5.2 +/- 1.9). The median follow-up was 32 months (range 11-93). There were five recurrences: three patients died of disease at 11, 36, and 51 months, and two patients are still alive with disease at 12 and 19 months. Two-year overall survival was 92%. In the advanced disease group, the number of cycles ranged from 1 to 11 (5.9 +/- 2.4). The median follow-up for this group was 20 months (range 5-62). The median overall survival was 18 months. Two-year overall survival was 33%. Two-year progression-free survival was 20%. Four patients were evaluable for response. There were two complete responses (duration 15-33 months) and two partial responses (duration 6-10 months). The responders were patients whose adenocarcinoma component was of the papillary serous (UPSC) variety. The chemotherapy combination appears to be highly active in early-stage disease. In the advanced uterine MMT it has moderate activity, especially when associated with the UPSC component.

Aged↗
PubMed1995

Clinical stage I endometrial carcinoma: pitfalls in preoperative assessment with MR imaging. Work in progress.

PURPOSE: To identify potential pitfalls in using magnetic resonance (MR) imaging to determine the depth of myometrial invasion in patients with clinical stage I endometrial carcinoma. MATERIALS AND METHODS: Forty women with clinical stage I endometrial carcinoma underwent preoperative pelvic MR imaging. Uterine length, tumor signal intensity, appearance of the junctional zone, presence of large polypoid tumors, leiomyomata, and congenital uterine anomalies were analyzed. Univariate logistic-regression analysis was performed to identify associations between incorrect MR staging and these variables. RESULTS: MR staging of IA, IB, and IC disease was 55% accurate (22 of 40 cases); MR differentiation of deep myometrial invasion (stage IC) from superficial disease (stages IA and IB) was 78% accurate (31 of 40 cases). Older age (P = .025), presence of polypoid tumors (P = .025), and difficulty in pathologic staging (P < .005) were significantly associated with incorrect MR assessment. CONCLUSION: When present, large polypoid tumors, leiomyomata, congenital anomalies, small uteri, and indistinct zonal anatomy may make it difficult to assess myometrial invasion at MR imaging.

Aged↗
PubMed1994

Prognostic indicators for poor risk epithelial ovarian carcinoma.

BACKGROUND: The objective of this study was to identify factors that categorize patients with epithelial ovarian carcinoma into favorable and unfavorable prognostic groups at the time of initial treatment. METHODS: Data were analyzed from 51 women who were treated at Yale University, had an evaluable CA 125 half-life (t1/2), and were followed for disease recurrence for at least 2 years. RESULTS: Grade, maximum level of CA 125, and histology did not provide useful prognostic information. Stage, residual disease, minimum CA 125, and CA 125 t1/2 individually were predictive of persistent disease or recurrence within 3 years of diagnosis with sensitivities of 97, 70, 34, and 49%, respectively, and specificities of 33, 83, 100, and 83%, respectively. When these factors are combined, defining an unfavorable prognostic group as those patients having residual disease greater than 1 cm, CA 125 t1/2 greater than 12 days, or minimum CA 125 never falling below 35 U/ml, sensitivity and specificity were 96 and 65%, respectively, at 1 year of follow-up and 91 and 75%, respectively, at 3 years of follow-up. 75%, respectively, at 3 years of follow-up. CONCLUSIONS: In those patients in whom residual small volume disease after primary surgery indicates a good prognosis, minimum CA 125 and CA 125 t1/2 during chemotherapy can further categorize patients into favorable and unfavorable prognostic groups.

Antigens, Tumor-Associated, Carbohydrate↗
PubMed1994

Chemotherapy of recurrent/advanced cervical cancer: results of the Yale University PBM-PFU protocol.

Chemotherapy for cervical cancer patients with recurrent and/or advanced disease has been complicated by excessive toxicity and short duration of responses, leading to little or no improvement in survival. Modification of drug scheduling and delivery of platinum, bleomycin, methotrexate, and 5-FU has resulted in a new combination regimen with little toxicity and a survival advantage for responders. PBM (platinum 80 mg/m2 D1, bleomycin 10 mu/m2/day D3-6, methotrexate 150 mg/m2 D15, 22 with leucovorin) is alternated with PFU (platinum 100 mg/m2 D1, 5-FU 1000 mg/m2/day D2-5) q 4 weeks for 3-6 months. The platinum, bleomycin, and 5-FU were delivered by continuous infusion. Twenty-three patients with recurrent and 17 with advanced cervical cancer are evaluable; 91% of patients with recurrent disease had received prior radiation therapy. The response rate was 30.4% in those with recurrent disease, and 41.2% in those with advanced disease, with 86 and 42.9% of responders respectively achieving a CR. Survival data were analyzed for each group separately, as well as for the combined recurrent/advanced disease group (N = 40). The results and significance were not changed by the groupings. In the combined recurrent/advanced group, median duration of response was 10.5 months, mean 20.1, and the median overall survival was 11 months, mean 20.5 +/- 3.5. There was a survival advantage accrued to the responders (median, 28 months) vs the nonresponders (10 months) (P = 0.0005 by log rank test). Moreover, there was a significant difference in progression-free interval between responders vs nonresponders (P = 0.0001), as well as between responders and those with stable disease (P = 0.001). This regimen was very well tolerated and there was no significant pulmonary toxicity. Furthermore, in the subset of 23 patients who had recurrent disease, 67% achieved palliation of pain. Experience with this protocol supports the continuing use of chemotherapy in the management of cervical cancer patients.

Adult↗
PubMed1994

Post-transcriptional regulation of c-fms proto-oncogene expression by dexamethasone and of CSF-1 in human breast carcinomas in vitro.

The c-fms proto-oncogene encodes the receptor for a hematopoietic growth factor, CSF-1. Recently, the importance of c-fms and its ligand CSF-1 in malignancies of non-hematopoietic origin, such as breast, ovarian, endometrial, pulmonary, and trophoblastic cancers has been recognized. We have previously shown that glucocorticoids induce a large increase in c-fms mRNA and protein levels in breast carcinoma cell lines. In this report, we investigate the mechanism underlying such c-fms overexpression by dexamethasone. We show that dexamethasone treatment of two breast carcinoma cell lines (BT20-c-fms expressor, and SKBR3-co-expressor of both c-fms and CSF-1) does not increase the rate of c-fms gene transcription, suggesting a post-transcriptional mechanism of regulation of c-fms expression by dexamethasone. The effect of protein synthesis inhibition was studied to help determine whether there was a role for intermediary regulatory proteins in the regulation of c-fms expression. We find that several protein synthesis inhibitors interfere with dexamethasone induction of c-fms transcripts, suggesting the existence of regulatory proteins. These regulatory proteins do not appear to be constitutively expressed, as we show no effect of protein synthesis inhibition on c-fms transcript expression in resting BT20 cells. These findings suggest that the putative regulatory proteins are induced by dexamethasone. Furthermore, the addition of a protein synthesis inhibitor, pactamycin, to dexamethasone-treated BT20 cells results in a decrease in c-fms mRNA stability.(ABSTRACT TRUNCATED AT 250 WORDS)

Amidohydrolases↗
PubMed1993

Allelic loss in ovarian cancer.

Loss of heterozygosity (LOH) was examined at 86 loci distributed on every chromosomal arm in 50 human ovarian tumors. Frequent allele losses were observed on chromosomes 13q (42%), 17p (42%), 17q (45%), and Xp (41%). Deletion mapping on chromosome 17 revealed a candidate gene on the long arm distal to D17S41/S74 for ovarian cancer which is distant from the locus for early onset breast cancer. LOH on chromosome 17q was found to be concordant with LOH on chromosomes 3p, 13q, 17p and Xp suggesting that it may be an early event in neoplastic development. These findings indicate that multiple tumor-suppressor genes for ovarian cancer possibly exist on chromosomes 13q, 17, and/or Xp and provide the basis for the identification of candidate gene(s) associated with ovarian cancer. The chromosomal mechanisms resulting in allele losses in ovarian cancer include deletion, deletion/duplication, mitotic recombination and monosomy, in concordance with the developed genetic model.

Alleles↗
PubMed1993

Intravenous cisplatin, doxorubicin, and cyclophosphamide in the treatment of uterine papillary serous carcinoma (UPSC).

Thirty patients with uterine papillary serous carcinoma were treated with intravenous cisplatin, doxorubicin, and cyclophosphamide (CAP) chemotherapy, a combination with proven efficacy against ovarian carcinoma. Nineteen patients were given CAP as an adjuvant soon after surgery. Eleven patients were treated after recurrence or failure of other first-line therapy. Of the patients treated adjuvantly, 11 (58%) were alive without evidence of disease with a median follow-up of 24 months. Eight patients (42%), all with metastatic disease at diagnosis, were dead of disease (DOD) with a median survival of 14 months. In the salvage group, all patients were DOD with a median survival of 21 months from diagnosis and a median survival from initiation of CAP of 7 months. Toxicity was observed in all patients, and there was one treatment-related death from cardiotoxicity. In the salvage group there were two partial responses and one complete response (response rate = 27%). We conclude that intravenous CAP was ineffective in the treatment of metastatic or recurrent uterine papillary serious carcinoma, but deserves study as an adjuvant in patients without metastatic or with only microscopic extrauterine disease.

Aged↗
PubMed1993

Colony-stimulating factor-1 in primary ascites of ovarian cancer is a significant predictor of survival.

OBJECTIVE: Our purpose was to determine whether the concentration of colony-stimulating factor in ascites of ovarian carcinoma is a prognostic factor for survival. STUDY DESIGN: Forty-four ascites samples from patients undergoing primary surgery for ovarian carcinoma were measured for colony-stimulating factor-1 by radioimmunoassay. Retrospective analysis of clinical data allowed comparison of accepted prognostic factors to ascites colony-stimulating factor-1 concentration for impact on survival by means of life-table analysis (Kaplan-Meier) by the Wilcoxon test and the Cox regression methods. RESULTS: In patients with advanced disease (International Federation of Gynecology and Obstetrics stages III and IV, n = 37) ascites colony-stimulating factor-1 concentration levels below a critical cutoff of 8.59 ng/ml were associated with longer overall survival (p < 0.05) and were a better predictor of survival than any other prognostic factor except zero residual disease after cytoreduction. International Federation of Gynecology and Obstetrics stage, tumor histologic type, malignant cells in fluid, grade of tumor, age, and performance status at presentation were not predictive of outcome. CONCLUSION: Colony-stimulating factor-1 in ascites may be an independent indicator of prognosis in patients with epithelial ovarian cancer.

Adult↗
PubMed1993

Posttranscriptional regulation of colony-stimulating factor-1 (CSF-1) and CSF-1 receptor gene expression during inhibition of phorbol-ester-induced monocytic differentiation by dexamethasone and cyclosporin A: potential involvement of a destabilizing protein.

Colony stimulating factor-1 (CSF-1) and its receptor (encoded by the c-fms proto-oncogene) have long been recognized as playing an important role in monocytic differentiation. However, the regulation of expression of the CSF-1 and c-fms genes during inhibition of monocytic differentiation has not been fully characterized. The present studies demonstrate that dexamethasone (dex) and cyclosporin A (CsA) resulted in inhibition of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced monocytic differentiation of HL60 cells, as well as TPA induction of c-fms and CSF-1 transcripts. These agents also blocked TPA-induced adherence, alpha-naphthyl acetate esterase staining, and the development of a more differentiated morphology. Nuclear run-off analyses revealed no effect of either of these agents on transcription of either c-fms or CSF-1 genes in TPA-treated HL60 cells. Measurements of c-fms transcript half-life confirmed post-transcriptional regulation of c-fms transcript levels after the addition of dex or CsA to TPA, both of which resulted in a decrease in c-fms mRNA half-life. Others have suggested that TPA results in the stabilization of c-fms mRNA in HL60 cells through induction of a labile mRNA stabilizing protein. We observed, however, that the inhibition of protein synthesis by cycloheximide (CH) in this setting of early monocytic differentiation increased both c-fms and CSF-1 steady-state transcript levels. While CH had no effect on the transcription of c-fms and CSF-1 genes in TPA/dex- or TPA/CsA-treated HL60 cells, c-fms mRNA was stabilized after the addition of CH to TPA/dex-treated cells. Taken together, our results suggest the existence of a labile mRNA regulatory protein or proteins, whose actions include destabilization of both c-fms and CSF-1 transcripts after inhibition of TPA-induced monocytic differentiation by dex or CsA.

Cell Differentiation↗
PubMed1992

Changes in Na,K-ATPase gene expression during granulocytic differentiation of HL60 cells.

During granulocytic differentiation of HL60 cells, immediate reduction of ouabain-sensitive potassium flux is observed within the first 12 hours of addition of dimethyl sulfoxide (DMSO). We show that gene expression of the alpha 3 isoform of Na+,K(+)-ATPase, which encodes an ouabain-inhibitable Na+,K(+)-ATPase activity, significantly declines during the first 24 hours of granulocytic differentiation by DMSO of HL60 cells. The more common alpha 1 isoform decreases, but more gradually over 72 hours of DMSO induction. Loss of alpha 3 and alpha 1 messenger RNA (mRNA) are due to changes in mRNA decay; their transcription is not altered. alpha 3 mRNA half-life is 3 hours in HL60 cells; upon induction by 16 hours of DMSO, it decreases to approximately 2 hours. alpha 1 transcripts are less sensitive to DMSO induction, with their half-life being 3.5 hours in HL60 cells; upon induction, their half-life decreases to 3 hours. Experiments measuring protein stability confirm that alpha 3 protein is more labile than alpha 1. In uninduced HL60 cells, alpha 3 membrane protein comprises 30% of the total alpha isoforms, and is less stable than alpha 1, with a protein half-life of only 9 hours. Upon DMSO induction, steady-state alpha 3 protein decreases markedly within 10 hours, whereas alpha 1 protein remains stable. These results show that posttranscriptional changes during induction play a major role in the differential regulation of alpha 1 and alpha 3 isoforms of Na+,K(+)-ATPase; regulation of the latter may be important for early granulocytic differentiation, or for one of the differentiated functions of mature granulocytes.

Cell Differentiation↗
PubMed1992

NEU protein overexpression in benign, borderline, and malignant ovarian neoplasms.

In situ hybridization (ISH) analysis of 24 benign, borderline, and malignant ovarian tumor specimens revealed NEU transcript expression by epithelial elements in approximately two-thirds of the samples and high-level expression in 3 grade 3 adenocarcinomas. Immunohistochemical staining (IHC) of a total of 86 specimens (including 17 of those studied by ISH) localized NEU antigen expression to epithelial cells in 36 of 86 samples with strong membrane staining observed in 12, including 1 benign, 1 borderline serous carcinoma, 3 clear cell/endometrioid carcinomas, and 7 predominantly papillary serous carcinomas with areas of clear cell/endometrioid histology. Clinical correlation of the IHC results for the 72 Stage I-IV invasively malignant neoplasms revealed no statistically significant association of the intensity of NEU IHC staining with either relapse-free or overall survival. However, more of the patients whose tumors showed strong membrane staining for NEU antigen suffered relapses of disease by 3 and 4 years than did patients whose tumors showed weak or no membrane staining. These results suggest a role for the NEU gene product in the physiology of benign ovarian surface epithelium and the neoplastic epithelium of preinvasive borderline and some invasively malignant adenocarcinomas.

Adenocarcinoma↗
PubMed1992

Ovarian cancer staging: does it require a gynecologic oncologist?

Forty-seven patients with presumed Stages I-II invasive ovarian epithelial carcinoma were treated with intravenous 50 mg/m2 cis-platinum, for 2-18 cycles (median, 9), 50 mg/m2 doxorubicin for 2-14 cycles (median, 9), and/or 600 mg/m2 cyclophosphamide for 2-14 cycles (median, 6) after surgical staging by a gynecologic oncologist or a nononcologic surgeon. Mean follow-up is 6.8 years. Cumulative 5-year actuarial survival is 73 +/- 6%; 75 +/- 12% for Stage I and 71 +/- 8% for Stage II disease. When screened for poor prognosticators, only the specialty of the operating surgeon was identified (P < 0.05). Five-year actuarial survival and disease-free survival, respectively, for Stages I-II patients surgically staged by a gynecologic oncologist were 83 +/- 7% and 76 +/- 8%, compared to 59 +/- 11% (P < 0.05) and 39 +/- 11% (P < 0.03) for the group operated upon by a nononcologist.

Actuarial Analysis↗
PubMed1992

Endometrial sampling: When? Where? Why? With what?

Today, evaluating women with abnormal uterine bleeding generally is initiated in the office with an endometrial biopsy. The indications and contraindications for endometrial sampling along with situations which do not, per se, demand sampling are listed in Figure 1. In women younger than 40 years of age, it may be appropriate in some clinical situations to initiate hormonal therapy after an endocrine evaluation before endometrial sampling; however, with the newer sampling devices that cause minimal discomfort, a histologic evaluation can be performed easily. Furthermore, the endometrial biopsy may help to distinguish anovulatory from ovulatory bleeding and exclude a hyperplastic condition or carcinoma. If the patient does not respond to medical therapy, then hysteroscopy may identify endometrial polyps or submucosal myomas. Bleeding in postmenopausal women requires endometrial sampling. If a diagnosis of cancer can be made in the office, this will expedite treatment. For those cases in which, for technical reasons, it is impossible to do an office biopsy or in which an examination under anesthesia is necessary for evaluation, then a D&C is indicated. The refined technology of transvaginal ultrasonography and hysteroscopy in the future may influence more directly the evaluation of women with abnormal uterine bleeding. As noted, transvaginal ultrasonography may determine which women would benefit from an endometrial biopsy, both for symptomatic and asymptomatic women. Likewise, the hysteroscope, under certain circumstances, may help identify pathologic findings missed by endometrial biopsy and/or reassure the patient or physician that a negative biopsy is the result of an atrophic mucosa. Because of the increase in the use of hormonal therapy, both in postmenopausal women for replacement and in women with breast cancer as adjuvant therapy, endometrial sampling must be performed for screening. Follow-up for women with premalignant changes of the endometrium treated with hormones also would require sampling to assess response. The overwhelming arguments in favor of the accuracy of an office-based endometrial biopsy, the convenience to the patient and physician, and the cost containment have been established firmly in the literature. Office screening procedures will continue to play important roles in the diagnostic skills of the gynecologist.

Biopsy↗
PubMed1991

Adjuvant whole-abdominal radiation therapy in uterine papillary serous carcinoma.

Nine patients from 34 to 74 years of age (median, 67 years of age) with uterine papillary serous carcinoma (UPSC) were treated with whole-abdominal radiation therapy (WART) on an adjuvant basis after cytoreductive surgery. All patients were treated with megavoltage photons to an abdominopelvic field to a median dose of 2500 cGy, with continued treatment to a whole pelvic field to a median dose of 4500 cGy. Three patients received additional boost to the vaginal apex. Follow-up time ranged from 6 to 31 months (median, 25 months) after completion of WART. Six patients had recurrent disease at 5 to 20 months (median, 7.5 months). Four of these patients died of their disease during the follow-up period. Three of six patients in whom treatment failed had disease at the vaginal apex. None of these patients received boost radiation therapy to that site. In contrast, two of three patients remaining disease free were treated with additional vaginal apex irradiation. Based on these results, the authors do not routinely recommend WART for adjuvant treatment of UPSC. They do, however, recommend vaginal apex irradiation for these patients.

Adult↗