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- B1750宫腔肿瘤
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comeonyuyu 离线
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I think Drs. Ma and Zhao are right about it. We do need lot more information and photos to have a full picture of this complicated case before we can render a "right" opinion about it. Also, please do not use "auto correction" function when you edit the photos using photoshop or other photo-editting software. Auto correction will make color very black/dark looking and lose the originality.
- 不坠青云之志，长怀赤子之心
What a misleading case and mismatch between history and pathologic photos. Much information is missing in this case:
(1) Gross and histopathology of endometrial biopsy - How bulky was the endometrial tumor? Can you estimate it from the specimen size and/or from the microscopic sections? Was all biopsied/curetted tissue submitted for microscopic evaluation? Was there myometrial invasion or angiolymphatic invasion in the biopsy? Uterine endometrioid adenocarcinoma (or type 1 endometrial cancer) is certainly much more common than either serous adenocarcinoma or clear cell carcinoma (type 2 endometrial cancer). The fact that hysterectomy specimen did not show any residual endometrial cancer (assuming this was concluded after a thorough examination of uterus) suggests the cancer was very superficial and could have been entire curetted out. To be certain that this was a grade 2 endometioid adenocarcinoma and not a secous adenocarcinoma, please review and show us the histopathology of endometrial biopsy/curettage. Rarely, combined endometrioid and serous adenocarcinoma of endometrium occurs in the same uterus, and the biologic behavior is dominated by the serous component no matter how small it is. And, please see if you can find out the BMI (biomass index) of the patient. Type 1 EM cancer is associated with estrogenic stimulation, hence more common in younger obese (high BMI) women. Type 2 EM cancer, on the other hand, tends to occur in older and non-obese women.
(2) Gross and histopathology of "omental metastasis" - Is this multifocal and bulky (what was the maximal size of tumor deposits)? Or is it just microscopic in small volume? If it is microscopic, are we sure it is not just endosalpingiosis surrounded by fibrosis? Comparing the histopathology of omental disease with the endometrial cancer (1) is essential to determine cancer histognesis/classification and primary origin. It is much more common to see uterine serous and clear cell carcinomas to spread to omentum at the time of initial surgery than with a superficial endometrioid adenocarcinoma of endometrium. If the omental disease is very bulky and there is no similar disease in either ovary or uterus, one has to consider the possibility of primary serous carcinoma of peritoneum.
(3) Ovarian lesion - No actual size of the involved ovary was given. I assume that it is not very bulky since you described it as 正常或稍大. If so, this is the least of the patient's problem because I do not believe the ovarian lesion is either endometrioid or serous adenocarcinoma. From the photos I would still consider it an unclassified sex cord stromal tumor, unless more and better photos show otherwise.
聞道有先後,術業有專攻
宫腔活检我们报的是中分化宫内膜样癌.手术切除标本未见宫腔内肿块,镜下未见癌细胞. Do not understand this. You mean the all endometrioid ca was taken out by biopsy.
the same tumors or differnet tumors can be present in ovary and uterus. Of cause it can be metastatic from ov to uterus or uterus to ov.
Above are my two related papers. They are for your reference.
I will guess it is a sertoli-form endometrioid carcinoma if i do not know IHC. However you must do some IHC for this case. The guess can often be wrong.
Sertoli-form endometrioid ca is just a variant of endometrioid carcinoma, showing some morphologic features of sertoli cell tumor.
同时大网膜转移灶表现为浆乳癌. Are you sure it is serous carinoma in omentum?
Good weekend, cz
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Am J Surg Pathol. 2007 Sep;31(9):1378-86.
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Diagnostic utility of WT1 immunostaining in ovarian sertoli cell tumor.
Department of Pathology, Magee-Womens Hospital, University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA. zhaoc@upmc.edu
WT1, the Wilms tumor gene product, can be expressed in various tumors from different anatomic sites, including some types of ovarian tumors. Regarding the latter, most studies have focused on surface epithelial-stromal tumors in which serous carcinomas are usually positive and endometrioid carcinomas are negative. Very few studies have specifically investigated this marker in ovarian sex cord-stromal tumors; however, limited data in the literature suggest that WT1 may be frequently expressed in sex cord-stromal tumors. As pure Sertoli cell tumor can be in the histologic differential diagnosis of endometrioid tumors (particularly borderline tumor and carcinoma) and carcinoid, immunostaining for WT1 might be of diagnostic value. Immunohistochemical staining for WT1 was performed in 108 ovarian tumors: pure Sertoli cell tumor (n=26), endometrioid borderline tumor (n=25), classic well-differentiated endometrioid carcinoma (n=23), sertoliform endometrioid carcinoma (n=12), and carcinoid (n=22). Additionally, inhibin and calretinin immunostaining were performed in all cases of Sertoli cell tumor for purposes of comparing expression with WT1. Extent of immunostaining was scored on a 0 to 4+ semiquantitative scale, and immunohistochemical composite scores based on a combination of extent and intensity of immunostaining were calculated in positive cases (possible range, 1 to 12). Nuclear expression of WT1 was present in 96% of Sertoli cell tumors, 16% of endometrioid borderline tumors, 13% of classic well-differentiated endometrioid carcinomas, 25% of sertoliform endometrioid carcinomas, and 0% of carcinoids. In Sertoli cell tumors, expression was diffuse (>50% of positive cells) in all positive cases. When positive in the non-Sertoli cell tumors, the extent of expression tended to be focal to patchy (50% or less positive cells). In Sertoli cell tumors, inhibin and calretinin were expressed in 96% and 54% of cases, respectively. The extent of expression of inhibin tended to be diffuse, similar to WT1; however, the extent of immunostaining for calretinin tended to be focal to patchy. The immunohistochemical composite scores for WT1, inhibin, and calretinin were 11.2, 7.6, and 4.8, respectively. Coordinate patterns for the extent of expression of WT1, inhibin, and calretinin in pure Sertoli cell tumor showed that all 3 markers were positive in 54% of cases; however, 42% were positive for WT1 and inhibin but negative for calretinin. In cases positive for both WT1 and inhibin, expression of both markers was diffuse in 84% of cases, but WT1 was diffuse while inhibin was focal to patchy in 16% of cases. We conclude that ovarian Sertoli cell tumor should be added to the growing list of WT1-positive tumors. This marker is useful for the distinction of Sertoli cell tumor from endometrioid tumors and carcinoid. The diagnostic utility of WT1 in Sertoli cell tumor is similar to inhibin but better than that of calretinin.
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Am J Surg Pathol. 2007 Feb;31(2):255-66.
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Comparative analysis of alternative and traditional immunohistochemical markers for the distinction of ovarian sertoli cell tumor from endometrioid tumors and carcinoid tumor: A study of 160 cases.
Department of Gynecologic and Breast Pathology, Armed Forces Institute of Pathology, Washington, DC, USA. chengquanzhao@yahoo.com
The main neoplasms in the differential diagnosis for primary ovarian tumors with a tubule-rich pattern are pure Sertoli cell tumor, endometrioid tumors (including borderline tumor, well-differentiated carcinoma, and the sertoliform variant of endometrioid carcinoma), and carcinoid tumor. Because traditional immunohistochemical markers [pan-cytokeratin (pan-CK), low molecular weight cytokeratin (CK8/18), epithelial membrane antigen (EMA), inhibin, calretinin, CD99, chromogranin, and synaptophysin] can occasionally have diagnostic limitations, the goal of this study was to determine whether or not any alternative markers [cytokeratin 7 (CK7), estrogen receptor (ER), progesterone receptor (PR), CD10, and CD56] have better diagnostic utility when compared with traditional markers for this differential diagnosis. Immunohistochemical stains for alternative, as well as traditional, markers were performed on the following primary ovarian tumors: pure Sertoli cell tumor (n = 40), endometrioid borderline tumor (n = 38), sertoliform endometrioid carcinoma (n = 13), well-differentiated endometrioid carcinoma (n = 27), and carcinoid tumor (n = 42). Extent and intensity of immunostaining were semiquantitatively scored. In addition, immunohistochemical composite scores (ICSs) in positive cases were calculated on the basis of the combination of extent and intensity scores. Cytokeratin 7 (CK7) was positive in 97% of endometrioid tumors, 13% of Sertoli cell tumors, and 24% of carcinoid tumors. The differences in the mean ICSs for endometrioid tumors versus Sertoli cell tumor or carcinoid tumor were statistically significant (P values ranging from <0.001 to 0.018). ER and PR were positive in 87% and 86% of endometrioid tumors, 8% and 13% of Sertoli cell tumors, and 2% each of carcinoid tumors, respectively. The differences in the mean ICSs for endometrioid tumors versus Sertoli cell tumor were statistically significant (P values ranging from <0.001 to 0.012). Among the epithelial markers, EMA seemed to be the most discriminatory but only slightly better than CK7, ER, or PR. Pan-CK and CK8/18 were not helpful. CD10 showed overlapping patterns of expression in all categories of tumors. Among the sex cord markers, CD10 was markedly less useful than inhibin or calretinin; CD99 was not discriminatory. CD56 showed overlapping patterns of expression in all categories of tumors. Among the neuroendocrine markers, CD56 was less useful than chromogranin or synaptophysin. When traditional immunohistochemical markers are problematic for the differential diagnosis of ovarian Sertoli cell tumor versus endometrioid tumors versus carcinoid tumor, adding CK7, ER, and/or PR to a panel of markers can be helpful. Endometrioid tumors more frequently express CK7, ER, and PR and show a greater extent of immunostaining in contrast to Sertoli cell tumor and carcinoid tumor. Compared with traditional epithelial markers, CK7, ER, and PR are nearly as advantageous as EMA. Inhibin is the most discriminatory sex cord marker, and CD10 is not helpful in the differential diagnosis. Chromogranin and synaptophysin are excellent discriminatory markers for carcinoid tumor, and CD56 is neither sufficiently sensitive nor specific enough for this differential diagnosis to warrant its use in routine practice.
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本帖最后由 于 2009-07-11 08:38:00 编辑
If it is ovarian tumor, the differential dx includes sertoli cell tumor and sertoli-form endometrioid carcinoma. The immunostains can help you to distinguish these two very easily.
EMA, CK7, Inhibin, calretinin, WT1, ER
Sertoli cell tumor: positive for Inhibin, calretinin, negative for WT1, EMA, ER, ck7
endometrioid ca: positive for ema, ck7, er, negative for inhibin, calretinin.
You can do EMA, CK7, inhibin, wt1.
EMA pos in all endometrioid ca and negative in all sertoli cell tumor.
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