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Histogenesis of carcinosarcoma and establishment of leiomyosarcoma cell line (HTMMT) derived from human uterine carcinosarcoma.

A cell line designated HTMMT was established from the human uterine carcinosarcoma (composed of leiomyosarcoma and adenocarcinoma) of a 66-year-old Japanese woman. The cell line grew well and 83 serial passages were successively done within 24 months. The cell line contained spindle- or fibrous-shaped cells that revealed neoplastic and pleomorphic features, and multipled rapidly without contact inhibition. These cells were characterized as possessing myofibrils. The karyotype exhibited hyperploidy and the chromosome number was ranged from 87 to 100. The cells were transplanted into an immune-depressed hamster cheek pouch or into nude mouse skin, but produced no tumors. We supported the combination theory for the histogenesis of the carcinosarcoma.

Aged↗

Endometrial carcinosarcomas have a different prognosis and pattern of spread compared to high-risk epithelial endometrial cancer.

OBJECTIVE: The endometrial origin of uterine carcinosarcoma has recently been well established. The current study investigates whether uterine carcinosarcomas can be included in protocols on high-risk endometrial cancer, given the similarities in biologic behavior of both entities. METHODS: Pathological and surgical notes of patients diagnosed with grade 3 endometrioid, carcinosarcoma, serous and clear cell endometrial cancer subtypes were retrospectively analyzed with special attention to the spread pattern of the different subtypes. Information on site of relapse and time to recurrence was obtained. RESULTS: We traced 146 patients of which 9 patients were ineligible. Histological subtypes of the remaining 137 patients were as follows: 50 (37%) grade 3 endometrioid carcinoma, 54 (39%) serous or clear cell carcinoma (non-endometrioid carcinoma), and 33 (24%) carcinosarcomas. Distribution of early stage disease (I and II) was 67, 46, and 78% for grade 3 endometrioid, non-endometrioid, and carcinosarcoma, respectively. Although we could not trace differences in hematogenic and transperitoneal spread among the three subtypes, non-endometrioid and carcinosarcomas were more likely to spread to pelvic and paraaortic lymph nodes (P < 0.01). Using univariate analysis, both stage (P < 0.006, Wald statistic) and histological type appear to determine the outcome, whereas lymphovascular space infiltration (P < 0.25) and age (P < 0.07) were not significantly different between the three histological subtypes. Cox Regression multivariate analysis on 127 women suffering from the three histological subtypes suggested that both stage III-IV disease (P < 0.00001) and histological type (carcinosarcoma) (P < 0.003) were of prognostic significance [hazard ratio (CI 95%) were, respectively, 3.8 (2.1-7.0) and 3.2 (1.7-5.9)]. Analyzing cases limited to stage I-II endometrial cancer, 24/28 (86%) grade 3 endometrioid, 18/24 (75%) non-endometrioid, and 11/25 (44%) carcinosarcomas survived, suggesting a worse outcome for endometrial carcinosarcoma when compared to the other subtypes (P < 0.008, Log Rank). A higher incidence of pulmonary metastases explained the worse outcome for early stage carcinosarcoma (P < 0.006), whereas the incidence of liver metastasis, transperitoneal spread, or recurrences in lymph nodes or vagina were comparable between the three pathologic subtypes. CONCLUSIONS: Although endometrial carcinosarcoma originates from epithelial cancer, the intrinsic more aggressive tumor biology suggests that this subtype should not be incorporated in studies on high-risk epithelial endometrial cancer.

Adenocarcinoma, Clear Cell↗

Uterine carcinosarcomas in patients receiving tamoxifen. A report of 19 cases.

Uterine carcinosarcomas are highly aggressive neoplasms with a tendency to early extrauterine spread, high stage at diagnosis, and a poor prognosis. Tamoxifen is widely used as adjuvant therapy in the treatment of breast cancer and is known to cause endometrial proliferative lesions, including adenocarcinoma. In recent years, there have been occasional reports of uterine carcinosarcoma in patients taking tamoxifen. The aim of this study is to describe the clinicopathologic profile in 19 women taking tamoxifen who subsequently developed uterine carcinosarcoma. Nineteen patients were identified from cases of uterine carcinosarcoma diagnosed at three institutions. The case notes were examined and the pathology reviewed. The age at diagnosis of carcinosarcoma ranged from 47 to 91 years (mean 71 years). All patients were postmenopausal and received 20 mg tamoxifen daily; the duration of treatment ranged from 1 to 15 years (mean 7.1 years). The cumulative dose of tamoxifen ranged from 7.3 to 109.5 g. Ten tumors were stage I, one stage II, seven stage III, and one stage IV. Ten of the carcinosarcomas were homologous, and nine contained heterologous elements in the form of rhabdomyoblasts (six cases) or malignant cartilage (three cases). The overall prognosis was extremely poor. Fifteen patients died within 35 months of the diagnosis of carcinosarcoma (mean 12 months). Two patients are alive with very short follow-up periods, and two were lost to follow-up. The reported data support an association between tamoxifen therapy and the development of uterine carcinosarcoma. The risk is likely to be highest in those patients who have been taking tamoxifen for a prolonged period. A majority of tumors in the present study were stage I, and this suggests that uterine carcinosarcomas in patients taking tamoxifen may be diagnosed at an earlier stage than those arising de novo. However, the prognosis was still poor even with low-stage disease. Properly controlled epidemiological studies are necessary to confirm an association between tamoxifen and uterine carcinosarcoma.

Journal Article↗

Carcinosarcoma of the ovary: 19 years of prospective data from a single center.

BACKGROUND: A review of clinicopathologic features and outcome in women with carcinosarcoma of the ovary (also known as malignant mixed mesodermal tumor [MMMT]) compared with a group of women with serous adenocarcinoma (SAC) of the ovary was conducted. METHODS: Between 1984 and 2002, 1568 patients with epithelial ovarian carcinoma and 70 patients with ovarian carcinosarcoma underwent treatment at the Edinburgh Cancer Centre. Analysis was performed on 65 patients with MMMT, and 746 patients with SAC were selected as a group for comparison. Baseline variables were recorded prospectively and response to chemotherapy and progression-free and cause-specific survival between the groups were compared. RESULTS: Patients with carcinosarcoma had a mean age of 66.6 years, which is significantly older than those with SAC (62.0 years) (P < 0.001). The objective response rate to platinum-based chemotherapy was found to be significantly lower in patients with carcinosarcoma (25% vs. 60%; P = 0.02). Cause-specific survival in the carcinosarcoma group was poor and significantly shorter than that observed in the SAC group (median survival of 8.2 months vs. 20.7 months; P < 0.0001). Progression-free survival in patients with carcinosarcoma also was found to be significantly shorter compared with patients with SAC (median progression-free survival of 6.4 months vs. 12.1 months; P < 0.001). Achieving optimal debulking at the time of initial surgery was found to be a highly significant factor in patients with carcinosarcoma with regard to determining outcome (median survival of 14.8 months for patients with optimally debulked International Federation of Gynecology and Obstetrics Stage III disease vs. 3.1 months for patients with suboptimally/nondebulked Stage III disease; P < 0.001). CONCLUSIONS: Ovarian carcinosarcoma is a distinct entity with a poor prognosis. Patients with carcinosarcoma differ from those with SAC with regard to having an older mean age of onset, an inferior response to platinum-based chemotherapy, and worse progression-free and cause-specific survival. The extent of benefit from chemotherapy is unclear.

Aged↗

Effusion cytodiagnosis of carcinosarcoma derived from the female genital tract: immunohistochemical features of MMP-7 and Ki-67 and immunofluorescence double staining analyses of eight cases.

OBJECTIVE: Expression of Matrix metalloproteinase 7 (MMP-7) and Ki-67 by carcinoma components (CCs) and sarcoma components (SCs) in carcinosarcoma of the female reproductive organs has been investigated by conventional methods, but analysis with immunohistochemical staining of multiple antigens has not been reported. We report the profiles of expression of MMP-7 and Ki-67 in carcinosarcoma determined with immunohistochemical staining techniques. METHODS: We used antibodies against epithelial antigen (EA), epithelial membrane antigen (EMA), and vimentin for immunofluorescence double staining of ascitic fluid in eight cases of carcinosarcoma of female reproductive organs. We also used immunohistochemical triple staining to compare MMP-7 and Ki-67 expression between CCs and SCs in the primary site of carcinosarcoma. RESULTS: Immunofluorescence analysis revealed that all neoplastic cells in the ascitic fluid were positive for EA or EMA, indicating that these cells were CCs. Immunohistochemical analyses of the primary organ of carcinosarcoma revealed that MMP-7 was expressed on CCs in four of eight cases of carcinosarcoma, whereas MMP-7 was not expressed on SCs. The average Ki-67 labeling index (LI) in CCs and SCs was 51.8% and 28.6%, respectively. The difference in Ki-67 LI between CCs and SCs was statistically significant (t test for paired samples, P = 0.0173). CONCLUSIONS: This is the first study to examine carcinosarcoma of the female reproductive organ by immunohistochemical staining for multiple antigens, which allows analysis of mixed tumor elements. In addition, we found that expression of MMP-7 and the average Ki-67 LI differ between CCs and SCs in carcinosarcoma. The predominance of CCs as the malignant cells in the ascitic fluid may be due to cytological differences between CCs and SCs of carcinosarcoma.

Adenocarcinoma↗

Expression of p27 and p53: comparative analysis of uterine carcinosarcoma and endometrial carcinoma.

The aim of the study was to assess both p27 and p53 expression in the stromal and epithelial component of carcinosarcoma and to assess if their expression in the latter is different than in endometrial carcinoma. Immunohistochemical staining for p27 and p53 was performed on paraffin-embedded tissue blocks of 18 uterine specimens with carcinosarcoma and their expression assessed. Their expression in the epithelial element was also compared to that in 35 paraffin-embedded tissue blocks of endometrial endometrioid carcinoma. Reduced p27 expression was observed in a similarly high proportion of the stromal (77.8%) as well as of the epithelial component (66.7%) of carcinosarcoma. Although statistically not significant, the proportion of reduced p27 expression in endometrial carcinoma (85.7%) was higher than in the epithelial element of carcinosarcoma. The percentage of p53 overexpression in both elements of carcinosarcomas and in endometrial carcinomas was low and also similar (27.8 and 20.0%, respectively). Our results indicate that reduced p27 expression is common and p53 overexpression is infrequent in carcinosarcoma. Their similar rates of expression in the stromal and epithelial elements of the tumor support the contention of a monoclonal origin of carcinosarcoma. Unexpectedly, reduced p27 expression is more common in endometrial carcinoma than in the epithelial element of carcinosarcoma, in spite of the less favorable prognosticators and outcome in the latter. Further studies of p27 expression in carcinosarcoma are indicated to establish its clinical value in this aggressive malignancy.

Adult↗

Carcinosarcoma of the esophagus: a twenty-case study.

The present report reviews results from 20 carcinosarcoma patients, and compares them with 773 cases of squamous cell carcinoma of the esophagus treated surgically at the National Cancer Center Hospital from 1971 to 1988. Although there were no significant differences in age, sex, symptoms or location between the two groups, the carcinosarcoma group had morphological characteristics as follows. (1) Seventy-five percent of the carcinosarcomas were of the elevated type. (2) The tumor was large. (3) The depth of invasion was limited to the esophageal wall in 80% of the carcinosarcomas. The rate of lymph node metastasis was almost the same, at greater than 65%, in both groups. Moreover, lymph node metastasis occurred at various stages, of the depth of invasion in the carcinosarcoma group. The curative resection rate was higher for carcinosarcoma (80%) than for squamous cell carcinoma (46.5%). There was no significant difference in recurrence rate between them. Compared with the high frequency of lymph node recurrence in the squamous cell carcinoma group, the recurrence due to hematogenous metastasis was more frequent in the carcinosarcoma group. Although the three-year survival rate was higher for carcinosarcoma (62.8%) than for squamous cell carcinoma (28.1%), there was no significant difference in the five-year survival rate between them (26.7 vs. 22.4%). In conclusion, radical esophagectomy with lymph node dissection is a necessary therapy for carcinosarcoma, and careful follow-up, paying special attention to hematogenous metastasis, is required.

Adult↗

Carcinosarcoma of the prostate. Report of 21 cases.

BACKGROUND: Carcinosarcoma of the prostate is an unusual malignancy characterized by adenocarcinoma intimately admixed with sarcoma. METHODS: The authors reviewed the clinical and pathologic findings of 21 cases of carcinosarcoma of the prostate from the files of the Mayo Clinic. RESULTS: Patient age ranged from 50 to 89 years (mean, 68 years). Ten patients (48%) had a previous diagnosis of prostatic acinar adenocarcinoma 2-73 months (mean, 33 months) before the diagnosis of carcinosarcoma, 8 of whom had received androgen deprivation therapy and/or radiation therapy in the interim. The Gleason score of adenocarcinoma ranged from 7 to 10 (mean, 9; median, 9). The sarcomas consisted of osteosarcoma (13), leiomyosarcoma (5), fibrosarcoma (1), malignant fibrous histiocytoma (1), and rhabdomyosarcoma (1), and the grade of the sarcoma component ranged from 2 to 4 (mean, 4; median, 4). Adenocarcinoma was the dominant histologic pattern in 7 cases and sarcoma in 14. Immunohistochemical staining revealed cytoplasmic reactivity for prostate specific antigen or keratin in 16 of 16 cases in the adenocarcinoma component. The sarcoma component was positive for vimentin in 16 of 16 cases, actin in 8 of 16 (focal in 2), S-100 protein in 2 of 16, and desmin in 1 of 16. At the time of diagnosis of carcinosarcoma, 11 patients had metastases, including 4 with metastatic adenocarcinoma before the diagnosis of carcinosarcoma. Treatment varied, and nonsurgical therapy was ineffective. Sites of metastases included lung (10 cases), bone (7), brain (4), liver (1), and peritoneum (1). Follow-up ranged from 1 to 107 months after the diagnosis of carcinosarcoma (mean, 34 months; median, 10 months). Mean time to tumor progression was 23 months (range, 1-96 months; median, 18 months). Eighteen patients died of carcinosarcoma from 2 to 107 months (mean, 34 months; median, 9.5 months) after diagnosis. Five-year survival was 41%, and 7-year survival was 14%. Progression and survival were not affected by histologic pattern. CONCLUSIONS: Carcinosarcoma of the prostate is an aggressive malignancy, regardless of histologic type.

Aged↗

Utility of immunohistochemistry in distinguishing ovarian sertoli-stromal cell tumors from carcinosarcomas.

Poorly differentiated Sertoli-stromal cell tumors and carcinosarcomas of the ovary both show biphasic epithelial and stromal patterns and may both show heterologous stromal elements, presenting a difficult diagnosis. We studied the immunohistochemical profile of Sertoli cell differentiation in human testes and applied these findings to the ovarian tumors. Eleven Sertoli-stromal cell tumors, six carcinosarcomas of the ovary, and 11 testes (six fetal, one infant, and four adult) were studied using antibodies to cytokeratin AE1:AE3 (AE1:3), cytokeratin CAM 5.2 (CAM), epithelial membrane antigen (EMA), vimentin, desmin, muscle-specific actin (MSA), S-100 protein (S-100), CA 19-9, CA 125, carcinoembryonic antigen monoclonal (CEA-M), carcinoembryonic antigen polyclonal (CEA-P), and placental alkaline phosphatase (PLAP). In the fetal testes, immature gonadal stroma and sex cord areas stained with vimentin (six of six cases), AE1:3 (five of six cases), and CAM (six of six cases). Sertoli cells in immature gonadal stroma areas, sex cords, and seminiferous tubules of normal fetal, infant, or adult testes never showed immunoreactivity for EMA, S-100, CA 19-9, CA 125, CEA-M, CEA-P, or PLAP. All Sertoli-stromal cell tumors stained with AE1:3 and CAM in areas of Sertoli cell differentiation (11 of 11 cases) but did not stain with EMA, PLAP, CEA-P, CEA-M, CA 19-9, CA 125, or S-100 (none of 11 cases). Carcinosarcomas expressed AE1:3 and CAM in all epithelial areas (six of six cases) and most stromal areas (five of six cases). Carcinomatous areas of carcinosarcoma also showed immunoreactivity for EMA (six of six cases), CA 125 (two of six cases), PLAP (two of six cases), CEA-P (two of six cases), and CEA-M (one of six cases), while stromal areas of carcinosarcoma expressed EMA (four of six cases) and S-100 (four of six cases). Heterologous stromal elements were present in three of 11 Sertoli-stromal cell tumors (two showed skeletal muscle and one showed both skeletal muscle and cartilage differentiation) and in four of six carcinosarcomas (one skeletal muscle, one cartilage, and two cartilage and skeletal muscle). All skeletal muscle heterologous elements expressed desmin, vimentin, and MSA. The heterologous cartilage in carcinosarcoma stained with S-100 (three of three), while the one case of heterologous cartilage in Sertoli-stromal cell tumor did not. These results suggest that ovarian Sertoli-stromal cell tumor can be distinguished from carcinosarcoma by the absence of staining for EMA, PLAP, CEA, CA 125, or CA 19-9 in epithelial areas of Sertoli-stromal cell tumor.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Clinicopathological analysis of c-kit expression in carcinosarcomas and leiomyosarcomas of the uterine corpus.

OBJECTIVE: The purpose of this study was to evaluate the expression of the protooncogene, c-kit, in carcinosarcomas and leiomyosarcomas of the uterine corpus and determine the associations between c-kit expression and clinicopathologic factors, including clinical outcome. METHODS AND MATERIALS: Using a polyclonal anti-KIT-antibody, immunohistochemical staining was performed on formalin-fixed paraffin-embedded tissue blocks from 21 carcinosarcomas, 17 leiomyosarcomas, and 1 endometrial stromal sarcoma. KIT-positive tumors were defined as those tumors demonstrating immunopositivity in > or =30% of tumor cells examined. KIT-negative lesions demonstrated immunopositivity in <30% of tumor cells. Two authors independently scored the slides as positive or negative. Staining was repeated on all specimens and independently scored, and in the occasion of a mismatch, a third staining was performed. The carcinosarcomas were catalogued as to whether the sarcomatous and/or carcinomatous elements expressed c-kit. Clinical data were abstracted for those patients with uterine carcinosarcomas. The associations between clinicopathologic characteristics and c-kit expression were compared using univariate and multivariate analyses. Kaplan-Meier curves based on c-kit expression were plotted for progression-free and overall survival and compared using the log-rank test. RESULTS: Nine of 21 (43%) carcinosarcomas demonstrated immunopositivity for the KIT receptor, although staining was relatively weak. In contrast, only 1/17 (6%) leiomyosarcomas demonstrated KIT immunopositivity (P = 0.029). The solitary endometrial stromal sarcoma evaluated did not demonstrate significant KIT positivity. The majority of KIT-positive carcinosarcomas (6/9 (67%)) demonstrated KIT presence in the sarcomatous portion as compared to the carcinomatous portion (4/9 (44%)). No clinical factor had a statistically significant association with c-kit expression. The lack of c-kit expression was the only factor that was significantly associated with disease recurrence in univariate and multivariate analyses (P < 0.05), although there appeared to be a trend toward a low stage associated with kit positivity. The median progression-free interval for the KIT-negative cohort was 8 months, while it had not been reached for the KIT-positive cohort after median follow-up of 15 months (P = 0.0462). CONCLUSIONS: A significant proportion of carcinosarcomas of the uterine corpus display immunoreactivity for c-kit. Patients with KIT-positive carcinosarcomas may have an improved progression-free survival compared to KIT-negative tumors; however, further data are needed to determine whether this finding is confounded by stage.

Aged↗

Localization of the VEGF and angiopoietin genes in uterine carcinosarcoma.

OBJECTIVE: Carcinosarcoma of the uterus is a highly aggressive tumor. However, the angiogenesis in this tumor remains unclear. This is the first study to examine the characteristics of angiogenesis in this tumor at the molecular level while also comparing the findings with those of high-grade endometrial carcinoma. METHODS: The expression of vascular endothelial growth factors (VEGF) and angiopoietins (Ang) genes were examined in 35 primary uterine carcinosarcomas as well as in 12 high-grade endometrial carcinomas by in situ hybridization. RESULTS: A strong expression of VEGF-A mRNA was significantly seen in carcinosarcomas compared to high-grade endometrial carcinomas. Interestingly, in uterine carcinosarcoma, VEGF-A mRNA was more strongly expressed in the carcinoma cells than in the sarcoma cells. In addition, a decrease in the VEGF-A mRNA expression was found in the transitional areas between carcinomatous and sarcomatous elements in most carcinosarcomas evaluated. Moreover, the Ang-2 mRNA expression was significantly seen in the vasculature adjacent to the periphery of the carcinoma cells in most carcinosarcomas, in comparison to that of endometrial carcinomas. CONCLUSIONS: A high angiogenic activity in uterine carcinosarcoma was shown, in comparison to that of endometrial carcinoma. Tumor angiogenesis in uterine carcinosarcoma might be chiefly influenced by VEGF-A in the carcinoma cells, in cooperation with Ang-2 in the surrounding microvessels, however, this is not fully usually the case in sarcoma cells.

Aged↗

Defective DNA mismatch repair and XRCC2 mutation in uterine carcinosarcomas.

OBJECTIVES: A frameshift mutation in the double-strand breakage repair gene XRCC2 was identified in a mismatch repair (MMR) deficient cell line derived from a uterine carcinosarcoma. The frameshift mutation occurred in a mononucleotide run (poly-T tract), a target for strand-slippage mutation in MMR deficient tumors. We sought to determine if XRCC2 mutation is important to uterine carcinosarcoma tumorigenesis and whether the XRCC2 poly-T tract is a target for mutation in cells lacking MMR. METHODS: MSI-typing was used to assess the MMR status of 30 primary carcinosarcomas. The entire XRCC2 coding region was sequenced in all tumors. Single strand conformational variant (SSCV) analysis was used to screen for poly-T tract mutation in 50 endometrioid adenocarcinomas with defective MMR. RESULTS: Seven of 30 (23.3%) primary carcinosarcomas had an MSI-H phenotype. No XRCC2 coding mutations were identified in the 30 carcinosarcomas, and only one of the fifty MSI-H endometrioid adenocarcinomas had an XRCC2 poly-T tract mutation. CONCLUSIONS: Despite the high frequency of mismatch repair deficiency in carcinosarcomas, no XRCC2 poly-T tract frameshift mutations were identified in these tumors. The fact that only one of 50 additional MSI-H tumors had a frameshift mutation suggests that the XRCC2 poly-T tract is not a frequent target for defective MMR. The absence of coding sequence mutations in primary carcinosarcomas suggests that XRCC2 defects are unlikely to play a significant role in carcinosarcoma tumorigenesis.

Base Pair Mismatch↗

An immunohistological comparison of primary lung carcinosarcoma and sarcoma.

We wished to assess the antigenic expression of primary lung tumors diagnosed as either carcinosarcoma or sarcoma in order to determine whether this information would be useful in distinguishing the two. We therefore immunohistochemically analyzed six pulmonary carcinosarcomas and five primary lung sarcomas for the presence of carcinoembryonic antigen (CEA), S100 protein, cytokeratin and vimentin using commercially available monoclonal and polyclonal antibodies on formalin fixed tissues. Six of six carcinosarcomas stained positively for cytokeratin while none of the sarcomas stained. In three carcinosarcomas both the carcinomatous and sarcomatous areas were positive while in three only the carcinomatous areas were positive. CEA staining was present in five carcinosarcomas and absent in all the sarcomas. CEA positivity was strong and not confined to those tumors with obvious gland formation. Staining for S100 protein was positive in two carcinosarcomas but only in those areas showing chondroid differentiation. Immunohistochemical staining for vimentin using two different monoclonal antibodies gave inconsistent results. We conclude that in differentiating between a carcinosarcoma and a sarcoma of the lung, immunohistochemical staining for both cytokeratin and CEA are useful with cytokeratin marginally preferable. The data indicate that carcinosarcoma of the lung, like that of the upper aerodigestive tract, expresses antigens suggesting both epithelial and mesenchymal differentiation.

Antigens, Neoplasm↗

Pulmonary carcinosarcoma: diagnostic problems and determinants of the prognosis.

OBJECTIVE: Bronchopulmonary carcinosarcoma is a very rare tumor and the prognosis of patients with carcinosarcoma is assessed as unfavourable. The problems concerning diagnosis, therapy, and prognosis after resection treatment are discussed with reference to our seven cases and with consideration of the pertinent literature. METHODS: The retrospective data of seven patients with pulmonary carcinosarcoma were analysed. All were staged postoperatively according to the international TNM staging system. The diagnosis was verified by immunohistochemical investigation. The prognosis of the patients with carcinosarcoma was compared with the prognosis of patients with non-small cell carcinoma of the lung. RESULTS: Whether lung resection is the treatment of choice for these patients is of no relevance, because in most cases the preoperative diagnosis is incomplete, as only one component of the tumor, namely the epithelial one, is found in the biopsy specimen. The complete and correct diagnosis in five of the seven cases was not made before the resection had been performed and in the remaining two patients it was only made when tumor recurrence or metastases occurred. The prognosis of patients with carcinosarcoma of the lung is assessed to be comparable to that of patients with other pulmonary carcinoma: in this study survival times ranged from only 3 months (T2N3) to 4 years 6 months (T3N1). The causes of death of the patients with carcinosarcoma were local recurrence in four patients and metastases at distant sites in two. Two recurrent tumors as well as the metastases consisted only of the sarcoma component of the primary tumor histologically. CONCLUSION: One may suggest that the prognosis of carcinosarcoma might be determined by the sarcoma component of the tumor. Therefore the generally accepted therapies of soft tissue sarcomas should be adopted for the follow-up treatment of patients with pulmonary carcinosarcoma.

Adult↗

Carcinosarcoma of the colon: report of a rare tumor.

Carcinosarcoma is a rare tumor that shows both epithelial and stromal malignant differentiation. Most reported cases of carcinosarcoma affect the female genital tract (and are called malignant mixed müllerian tumors), but there are also some isolated reports of cases affecting the lung and the head and neck area. Carcinosarcomas only rarely affect the gastrointestinal tract, mainly the esophagus. To the best of our knowledge, only eight cases of carcinosarcoma of the colon have been reported to date. For some lesions, the term 'sarcomatoid carcinoma' is preferred to 'carcinosarcoma', as both stromal and epithelial cells have shown cytokeratin expression on immunohistochemistry. The expression 'carcinosarcoma' should be applied only to those lesions, the stromal elements of which do not express epithelial markers. We report a new case of carcinosarcoma affecting the left colon. The most unique feature of this tumor is that it shows chondro-and osteosarcomatous differentiation, a feature that has been described previously in only one colonic carcinosarcoma. We discuss the histopathological and immunohistochemical features of this lesion as well as its possible histogenesis.

Aged↗

Evaluation of the relationship between adenosarcoma and carcinosarcoma and a hypothesis of the histogenesis of uterine sarcomas.

The terminology of uterine sarcomas is confusing and has been inconsistently applied. The relationships among the various types of uterine sarcomas are unknown. To elucidate the relationship between carcinosarcoma (malignant mullerian mixed tumor) and adenosarcoma, a series of 26 consecutive endometrial carcinosarcomas was evaluated for the presence of an adenosarcoma-like component. Four of 26 carcinosarcomas (15%) had an adenosarcoma-like component. The clinical and pathologic features of these tumors were otherwise similar to ordinary endometrial carcinosarcomas. A histogenetic schema for uterine sarcomas is proposed, interrelating endometrial stromal sarcomas, adenosarcomas with and without sarcomatous overgrowth, and poorly differentiated sarcoma not otherwise specified. Although most carcinosarcomas are accepted as being metaplastic or sarcomatoid carcinomas, it is suggested that the carcinomatous component of 8% to 16% of carcinosarcomas arise within, or in the endometrium adjacent to, an adenosarcoma. This latter group is then integrated into the histogenetic schema. Observations based on our data and the limited data in the literature that support this hypothesis include: 13% of endometrial carcinosarcomas have gross and microscopic features of collision tumors, 13% have an adenosarcoma-like component, 16% have a low-grade stroma, and approximately 8% are biclonal indicative of a collision tumor. The most parsimonious interpretation of these data indicates that approximately 8% to 16% of endometrial carcinosarcomas arise because of malignant transformation of the epithelial component within, or in the endometrium adjacent to an adenosarcoma.

Adenosarcoma↗