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- Ahlman, Håkan, 1947, et al.
(författare)
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Cytotoxic treatment of adrenocortical carcinoma.
- 2001
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Ingår i: World journal of surgery. - : Springer Science and Business Media LLC. - 0364-2313 .- 1432-2323. ; 25:7, s. 927-33
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Tidskriftsartikel (refereegranskat)abstract
- Adrenocortical carcinoma (ACC) is a rare, aggressive tumor that is often detected in an advanced stage. Medical treatment with the adrenotoxic drug mitotane has been used for decades, but critical prospective trials on its role in residual disease or as an adjuvant agent after surgical resection are still lacking. The concept of a critical threshold plasma level of the drug must be confirmed in controlled studies. Because individual responsiveness cannot be predicted, the use mitotane is still advised for nonresectable disease. In case of cortisol or other steroid overproduction, several drugs (e.g., ketoconazole or aminoglutethimide) may be used. Chemotherapy with single agents (e.g., doxorubicin or cisplatin) have been disappointing, with low response rates (< 30%) and a short response duration. Part of this refractoriness may be explained by the fact that ACC tumors express the multidrug-resistance gene MDR-1. Chemotherapy with multiple agents has been tested in smaller series and has resulted in significant side effects. The best results were achieved by the combination of etoposide, doxorubicin, and cisplatin associated with mitotane, achieving a response rate of 54%, including individual complete responses. To be able to make progress in treating advanced ACC disease, adjuvant multicenter trials must be encouraged. When mitotane-based therapies are used, monitored drug levels are mandatory.
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| 3. |
- Khorram-Manesh, Amir, 1958, et al.
(författare)
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Mortality associated with pheochromocytoma in a large Swedish cohort
- 2004
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Ingår i: European journal of surgical oncology. - 0748-7983. ; 30:5, s. 556-9
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The aim of the present study was to report the risk of death in a national cohort of patients with aPC (adrenal PC) and their risk of developing a second tumour. METHODS: Using the National Cancer Registry, 481 patients (222 men and 259 women) with aPC in Sweden (1958-1997) were identified. Autopsy-based diagnoses were excluded. As control group the entire Swedish population was used and the risk of death in patients after diagnosis of aPC was compared with the normal risk taking age, sex and calendar year into account. The risk for a second tumour disease after diagnosis of aPC was also calculated. RESULTS: Patients with aPC had an increased tumour-related mortality after diagnosis of aPC. For both men and women this mortality was four times higher than for controls. Liver/biliary tract and CNS tumours in men; and malignant melanoma and uterine cervical cancer in women were significantly over-represented in the cohort of patients with aPC. CONCLUSION: Patients with aPC run an increased risk of developing additional cancers. Surveillance strategies may thus be necessary for these patients.
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| 4. |
- Khorram-Manesh, Amir, 1958, et al.
(författare)
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N-cadherin expression in adrenal tumors: upregulation in malignant pheochromocytoma and downregulation in adrenocortical carcinoma.
- 2002
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Ingår i: Endocrine pathology. - 1046-3976. ; 13:2, s. 99-110
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Tidskriftsartikel (refereegranskat)abstract
- Cell adhesion molecules (CAMs) are important regulators of tumor growth. The aim of the present study was to evaluate the expression pattern of CAMs in adrenal tumors regarding origin (cortex vs medulla) and biologic behavior (benign vs malignant). Eighty seven adrenal tumors were investigated by immunocytochemistry (ICC) using monoclonal antibodies against N-cadherin (NCAD), E-cadherin (ECAD), neural cell adhesion molecule (NCAM), and CD44. Western blotting was performed on 30 tumors using the same antibodies. Markers for proliferation (Ki-67) and catecholamine synthesis (tyrosine hydroxylase) were also analyzed in tumors by ICC. NCAD was expressed in 12/27 benign pheochromocytomas (BPCs) (12 familial cases), 8/8 malignant pheochromocytomas (MPCs), 28/30 adrenocortical adenomas, and 9/22 adrenocortical carcinomas. ECAD was expressed in 0/27 BPCs, 0/8 MPCs, 0/30 adrenocortical adenomas, and 2/22 adrenocortical carcinomas. NCAM was expressed in 26/27 BPCs, 7/8 MPCs, 21/30 adrenocortical adenomas, and 17/22 adrenocortical carcinomas. CD44 was expressed in 23/27 BPCs, 6/8 MPCs, 7/30 adrenocortical adenomas, and 4/22 adrenocortical carcinomas. Both cortical and medullary adrenal tumors expressed NCAD, NCAM, and CD44 but were devoid of ECAD. The expression of CD44 and NCAM did not correlate with the malignant potential of tumors. NCAD was upregulated in MPCs, but downregulated in adrenocortical carcinoma. Thus, NCAD appears to be involved in the development of both cortical and medullary adrenal tumors.
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