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At least 109 records · Page 6Linked to original sources
PubMed1977

[Mullerian adenosarcoma and uterine adenofibroma].

Description of a case of a mixed Mullerian tumour of the body of the uterus, with histologically benign epithelial and connective components, developing in a 72-year-old woman. A cervical recurrence and perineal metastasis were solely leiomyomatous in terms of their structure and were associated with peritoneal carcinomatosis and pulmonary involvement. Death occurred three years after subtotal hysterectomy and five years after the first clinical manifestations.

Adenofibroma↗
PubMed1996

Endometrioid ciliated-cell tumors of the ovary: a report of five cases.

Five patients with ovarian endometrioid tumors composed predominantly of ciliated cells are reported; two patients had bilateral neoplasms. Two unilateral, predominantly cystic ciliated-cell tumors from women in their 40s were associated with endometriosis: one was borderline and arose in an endometriotic cyst; the other was borderline with foci of carcinoma and was associated with ipsilateral ovarian and peritoneal endometriosis. Five predominantly adenofibromatous tumors in the three other women, all postmenopausal, were not associated with endometriosis. One woman with a borderline ciliated-cell adenofibroma had had a prior contralateral adnexectomy, another with a borderline ciliated-cell adenofibroma had a contralateral ciliated-cell adenofibroma, and the third woman had a ciliated-cell adenocarcinoma and a contralateral borderline ciliated-cell adenofibroma. In two of the latter three patients the fallopian tubes contained foci of ciliated-cell hyperplasia. All five ciliated-cell malignant tumors were stage I, were treated by operation alone, and had not recurred 21 to 64 (mean 39) months postoperatively. Ciliated-cell tumors of the ovary should be distinguished from serous and mixed serous and endometrioid cancers because of different pathological and possibly different clinical features. Criteria for separating endometrioid ciliated-cell tumors into benign, borderline, and malignant categories are presented; whether any of these neoplasms behaves in a clinically aggressive fashion has yet to be determined.

Adenofibroma↗
PubMed1975

Carcinogenicity of the antineoplastic agent, 5-(3,3-dimethyl-1-triazeno)-imidazole-4-carboxamide, and its metabolites in rats.

Chronic oral administration of the antineoplastic agent, 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (NSC-45388, DTIC), induced predominantly thymic and mammary tumors as demonstrated previously. Male and female Sprague-Dawley and female Buffalo rats were susceptible to the carcinogenicity of DTIC. A 50% incidence of mammary adenocarcinomas was induced in males within 18 weeks. Type of tumor and tumor incidence were dose dependent. Single and multiple intraperitoneal injections of DTIC did not alter organ specificity. DTIC-induced thymic lymphosarcomas and mammary adenocarcinomas were transplantable. Tissue distribution studies revealed no correlation between uptake of DTIC by a given tissue and its susceptibility to carcinogenicity. Metabolites of DTIC were tested for carcinogenic activity. Animals administered 5-diazoimidazole-4-carboxamide orally, intraperitoneally, or intragastrically developed low incidences of thymic, stomach, bladder, or mammary tumors. A low incidence of mammary tumors developed in rats fed 2-azahypoxanthine. A variety of tumors, including several ependymoblastomas, were induced in rats that received 5-aminoimidazole-4-carboxamide orally. 5-(3-Methyl-1-triazeno)imidazole-4-carboxamide (MTIC), when fed or given in single or multiple intraperitoneal injections, induced a high incidence of mammary adenofibromas and a low incidence of uterine leiomyosarcomas. Control rats had low incidences of mammary adenocarcinomas and adenofibromas after 52 weeks. These data show that the carcinogenic properties of DTIC resemble those of carcinogenic N-nitroso compounds, hydrazine, azo, and azoxy-alkanes and aryltriazenes and thus suggest similar mechanism(s) of action. These data also indicate that MTIC is involved in the induction of mammary adenofibromas and uterine leiomyosarcomas by DTIC.

Adenofibroma↗
PubMed2000

A clinicopathologic analysis of atypical proliferative (borderline) tumors and well-differentiated endometrioid adenocarcinomas of the ovary.

Atypical proliferative (borderline) endometrioid tumors (APTs) and well-differentiated endometrioid carcinomas of the ovary constitute a spectrum of morphologically diverse proliferative tumors. There is currently no agreement on the criteria for distinguishing them. We report the clinicopathologic features of 56 proliferative endometrioid tumors focusing on the criteria for invasion, the clinical significance of microinvasion and cytologic atypia, and prognosis. Endometriomas, adenofibromas, adenosarcomas and moderately to poorly differentiated carcinomas were excluded, as were patients with concurrent endometrioid carcinoma of the endometrium. The tumors were classified as atypical proliferative tumor (APT) (33 tumors), APT with intraepithelial carcinoma (high-grade cytology in a tumor lacking stromal invasion) (three tumors), APT with microinvasion (invasion <5 mm) (five tumors), and invasive carcinoma (invasion > or = 5 mm) ( 15 tumors). All tumors were confined to the ovary (stage I). In 50 patients, the tumor involved one ovary, and in three patients, the tumors were bilateral. The predominant growth pattern was adenofibromatous in 29 tumors and glandular or papillary in 27 tumors. In 8 (24%) of 41 APTs, areas of benign adenofibroma were identified, and in 13 (87%) of 15 carcinomas, areas of associated APT were identified. Stromal invasion was manifested by confluent glandular growth in all 15 invasive carcinomas and all tumors with microinvasion. Destructive infiltrative growth was also present in 2 (13%) of 15 carcinomas. Confluent glandular growth was the most common manifestation of stromal invasion and therefore served as the best criterion for the diagnosis of carcinoma. Squamous differentiation was observed in 24 tumors, and mucinous differentiation was seen in 20 tumors and was most often seen in APTs. Endometriosis was present in 14 patients with APTs and one patient with carcinoma. Four patients had hyperplasia or atypical hyperplasia of the endometrium. One patient with an APT had a concurrent peritoneal serous neoplasm. Twenty-one patients had available clinical follow-up. Twenty (95%) of 21 patients, including six with invasive carcinoma, two with microinvasion, one with intraepithelial carcinoma, and 11 with APT were alive with no evidence of disease with a mean follow-up of 47 months. One patient with carcinoma had recurrent tumor after 46 months and was alive 40 months after resection of the recurrent tumor. In this large series of proliferative endometrioid tumors, all were stage I and only one patient had a recurrence. Most carcinomas contained evidence of a precursor APT, and in some APTs, an associated benign adenofibroma was identified. Microinvasion or intraepithelial carcinoma occurred in 19% of APTs. This finding likely reflects the various stages of endometrioid carcinogenesis in the ovary. For clinical management, we suggest that these tumors be divided into two categories-APTs and well-differentiated carcinoma-because based on the available data, cytologic atypia and microinvasion appear not to affect the prognosis.

Adolescent↗
PubMedDate not supplied

[Mixed mesodermal tumors of the uterus. Clinico-pathologic characteristics of 23 patients].

The clinical and pathological features, histogenesis and treatment of 23 cases of mixed mesodermal tumours of the uterus (15 benign and 8 malignant) in woman aged from 27 to 78 years (mean 51.25) are reviewed. The tumours manifested by non-specific symptoms, most often uterine bleeding, arising suspicion of malignancy in only two cases. Unlike malignant mixed mesodermal tumours, differentiation of adenofibromas from low-grade adenosarcomas was often very difficult, and needed careful pathohistological analysis of extirpated tissues, including all available histochemical, immunohistochemical and EM procedures. Two cases of adenofibromas recurred as adenosarcomas after four months and five years respectively. Poor prognosis of malignant variants of mixed mesodermal tumours and their difficult differentiation from adenofibromas require close collaboration of pathologists and gynaecologists, implicating hysterectomy as proposed treatment and permanent clinical monitoring.

Adult↗
PubMed1991

Lineage-restricted clonality in biphasic solid tumors.

Cytogenetic analysis of two pulmonary chondroid hamartomas and nine breast adenofibromas revealed clonal chromosome aberrations in both hamartomas and in four breast tumors. To determine lineage of the cells with chromosome aberrations, a combined immunohistochemical/cytogenetic approach was developed that enabled simultaneous ascertainment of cytogenetic aberrations and immunohistochemical features in individual cells. Immunohistochemical/cytogenetic evaluation of one hamartoma and two adenofibromas demonstrated that neoplastic proliferation, in each case, was confined to the mesenchymal (stromal) component, whereas epithelial cells appeared to be reactive. Cytogenetically abnormal short-term cultures of the remaining hamartoma and another of the breast adenofibromas were composed entirely of mesenchymal elements, indicating mesenchymal clonality in those tumors as well. Our findings support redesignation of pulmonary chondroid hamartomas as 'pulmonary chondromas' and suggest that carcinomas developing within fibroadenomas arise from reactive epithelial proliferation. Combined immunohistochemical/cytogenetic analysis might be useful in the development of novel therapeutic approaches that selectively target neoplastic populations within solid tumors.

Adenocarcinoma↗
PubMedDate not supplied

[Giant fibroadenoma of the breast. Its clinical picture and differential diagnosis. A report of a clinical case].

An 18-year-old girl came to our Institute with a large tumefaction at the right breast, that during the last year had risen slowly but continuously. She underwent some clinical and instrumental exams that allow us to diagnose a giant adenofibroma or cystosarcoma phyllodes without excluding either of them. Then she undergoes a subcutaneous mastectomy with an application of a prosthesis. From the histologic point of view it is a giant adenofibroma. Giant adenofibroma is a rare breast pathology, always benign. Nowadays we have some difficulties distinguishing it from cystosarcoma phyllodes, which has both a benign and malignant form. It is important to distinguish the two pathologies before operation as they have a different therapeutic approach and a different follow-up. Cystosarcoma phyllodes can in fact relapse and when malignant can cause metastasis.

Adolescent↗