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Cortical Carcinoma (cortical + carcinoma)

Distribution by Scientific Domains
Medical Sciences100%

Kinds of Cortical Carcinoma

  • adrenal cortical carcinoma
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    Selected Abstracts

    Incidental Detection of Inferior Vena Caval Dissection by Intraoperative High Frequency Vascular Duplex Ultrasonography

    ECHOCARDIOGRAPHY, Issue 3 2007
    Sarinya Puwanant M.D.
    Inferior vena caval (IVC) dissection has been rarely reported. This could be due to less susceptibility of the venous structure to dissect or under recognition of this entity. We first report a case of IVC dissection detected by high frequency surface ultrasonography following tumor thrombectomy of adrenal cortical carcinoma. This report described the value of intraoperative surface echocardiography and reviewed previous literatures with regard to IVC dissection. [source]

    Adrenocortical carcinoma with delayed cutaneous metastasis

    JOURNAL OF CUTANEOUS PATHOLOGY, Issue 7 2008
    Elizabeth K. Satter
    Adrenal cortical carcinoma (ACC) is an uncommon and aggressive malignancy. Patients often have metastatic disease at initial presentation, with the most common sites being the liver, local lymph nodes, lungs, peritoneum and bone. Despite a high frequency of metastases, there are only isolated reports of ACC that have metastasized to the skin. Herein, we report a case of an 82-year-old woman who presented with a cyst-like lesion on her back, which on biopsy proved to be ACC metastatic from a primary tumor diagnosed 30 years previously. [source]

    Hereditary Breast Cancer: Part I. Diagnosing Hereditary Breast Cancer Syndromes

    THE BREAST JOURNAL, Issue 1 2008
    Henry T. Lynch MD
    Abstract:, Hereditary breast cancer (HBC) accounts for as much as 10% of the total BC burden. Most of these cases will be found to be due to a BRCA germline mutation. An estimated additional 15,20% of those affected with BC will have one or more first- and/or second-degree relatives with BC. Therefore, when these numbers are combined, familial BC risk accounts for approximately 20,25% of the total BC burden. However, because of the often limited information on family history in the etiologic assessment of BC, this may be an underestimate. Confounding factors include its phenotypic and genotypic heterogeneity, given the association of HBC with a plethora of differing cancer syndromes. Its most common occurrence is its association with ovarian cancer in the so-called hereditary breast-ovarian cancer syndrome due to BRCA1 and BRCA2 mutations. More rarely, it occurs in the Li-Fraumeni syndrome, caused by a p53 germline mutation, in which markedly early-onset BC is found in association with brain tumors, sarcomas, leukemia, lymphoma, malignant melanoma, and adrenal cortical carcinoma. Importantly, the age-adjusted incidence of BC in women in the United States fell sharply, by 6.7%, in 2003, when compared with the rate identified in 2002. We postulate that increasing knowledge about the genetics of BC may have partially contributed to the identification of high-risk patients who thereby may have benefited significantly from early diagnosis. [source]

    Proliferative activity and genetic changes in adrenal cortical tumors examined by flow cytometry, fluorescence in situ hybridization and immunohistochemistry

    INTERNATIONAL JOURNAL OF UROLOGY, Issue 2 2005
    KOUSUKE TAKEHARA
    Abstract Background: To determine differences in biological features among different adrenal tumors, we investigated the DNA ploidy, numerical chromosomal aberration and proliferative activity in human adrenal cortical neoplasms. Methods: Our study included six adrenal cortical adenomas with Cushing syndrome, 12 adenomas with hyperaldosteronism, three non-functioning adenomas and three adrenal cortical carcinomas. Isolated nuclei from frozen samples were used for fluorescence in situ hybridization (FISH) analysis, and formalin-fixed, paraffin-embedded tissues from the same materials were analyzed using flow cytometry (FCM) for DNA ploidy. Sections from paraffin blocks were stained immunohistochemically with antibodies against Ki-67 and p53. For FISH analysis, we used an ,-centromeric enumeration probe for chromosome 17. Results: The mean Ki-67 labeling index (LI) of adrenal cortical carcinomas was markedly higher than that of adrenal cortical adenomas (209.4 vs 8.7). In functional adrenal cortical adenomas, the LI was significantly lower in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004), although FCM results indicated that tetraploid patterns were more frequently observed in the former type. Tumor size was significantly smaller in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004). Chromosome 17 showed disomy in all adrenal cortical adenomas, whereas chromosome 17 abnormalities were found in two of three adrenal cortical carcinomas. Only the latter two cases strongly expressed p53 protein. Conclusions: Our study characterized various biological features of benign and malignant adrenal cortical tumors. The use of a combination of markers might provide additional information to assist our understanding of the clinical behavior of an individual adrenal cortical tumor. [source]

    Immunohistochemical localization of somatostatin receptor subtypes in benign and malignant adrenal tumours

    CLINICAL ENDOCRINOLOGY, Issue 6 2008
    Nicole Unger
    Summary Background, Somatostatin mediates its action through five receptor subtypes (sst1,5) that are widely distributed in various endocrine tissues and tumours. Because of the inhibitory effects of somatostatin, long-acting analogues have been synthesized. In contrast to their well-established use in neuroendocrine and pituitary tumours, little is known about their potential use in adrenal tumours. Objective, We examined somatostatin receptor protein expression in adrenal tumours of various aetiologies. Immunostaining was performed with specific polyclonal antibodies for sst1,5. Design, Seven benign and eight malignant pheochromocytomas (PHEOs), eight aldosterone-secreting adenomas (APAs), nine cortisol-secreting adenomas (CPAs), seven nonfunctioning adrenal tumours (NFAs) and 25 adrenal carcinomas (CAs) as well as eight normal adrenal glands were investigated. Measurements, Staining pattern, distribution and subcellular localization of the somatostatin receptor subtypes were evaluated. Results, In the majority of normal cortices the expression of sst1,5 was limited to the reticular zone. The medulla was predominantly positive for sst3. Most cortical adenomas were positive for all five subtypes. However, in the majority of these tumours, less than 30% of cells were positively stained. A high expression of sst4 was found in CPAs but only very few cortical carcinomas exhibited sst immunostaining. All benign PHEOs were positive for sst3. The majority presented with more than 60% of tumour cells stained. By contrast, only six out of eight malignant PHEOs were positive for sst3. Conclusions, Somatostatin receptor subtypes are expressed in PHEOs as well as in tumours of the adrenal cortex with tumour-specific distribution patterns. This may offer new diagnostic and therapeutic possibilities. [source]