Carcinoma adrenal cortical

Another member of the FGF family, FGF-4, protects against radiation-iaduced ceU killing and enhanced the G2 arrest when overexpressed ia a human adrenal cortical carcinoma ceU line (196). This effect is again manifested as the appearance of a shoulder on the survival curve, although neither the control nor the transfected cells undergo radiation-iaduced apoptosis. No differences ia the yield or repair of either SSBs or DSBs have been observed. 

Mitotanc is indicated only for treating inoperable adrenal cortical carcinoma. Frequently (K curring sitle effects include gastrointestinal disturbances. CNS deprc.ssion. and skin toxicity. 

Transcription factor adrenal 4 binding protein (Ad4BP), also known as steroid factor-1, is a transcription factor that is positive in virtually all adrenal cortical carcinomas, being negative in renal carcinoma, hepatocellular carcinoma, and pheochromocytoma. Ad4BP is a marker of adrenocortical malignancy. ... 

Wieezorek TJ, Pinkus JL, Glickman JN, Pinkus GS. Gompari-son of thyroid transcription factor-1 and hepatocyte antigen immunohistochemical analysis in the differential diagnosis of hepatocellular carcinoma, metastatic adenocarcinoma, renal cell carcinoma, and adrenal cortical carcinoma. Am J Clin Pathol. 2002 118 911-921. 

FIGURE 10.29 A, Adrenal cortical carcinoma (H E stain). B, Immunoperoxidase stain for melan A (A103) shows granular positivity. C, Immunoperoxidase stain for synaptophysin shows prominent cytoplasmic reactivity. D, Immunoperoxidase stain for cytokeratins (CAMS.2) shows focal cytoplasmic reactivity. 

Adrenal cortical carcinomas may show evidence of NE differentiation, as manifested by immunoreactivity for synaptophysin, neurofilament proteins, and NSE (Fig. 10.29C). In contrast to pheochromocytomas, however, adrenal cortical carcinomas are typically negative for the chromogranin proteins. In one series, 60% of cortical carcinomas were positive for the... 

The differentiation of adrenal cortical carcinomas from metastatic carcinomas to the adrenal gland may be difficult. This distinction may be assisted by studies of the distribution of intermediate hlaments, particularly cytokeratins and vimentin. Normal and neoplastic adrenal cortical cells are typically vimentin-positive but exhibit considerable differences in patterns of cytokera-tin immunoreactivity depending on factors such as tissue preparation (fixed versus frozen) and the reactivities of the cytokeratin antibodies. 7258 fresh frozen tis-... 

It is indicated mainly for the treatment of inoperable adrenal cortical carcinoma. Dose. Usual, 8-10 gper day, divided into 3 or 4 equal doses. 

Adrenal cytotoxic agent used to treat adrenal cortical carcinoma. 

Adrenal cortical carcinomas are rare, highly malignant tumors which account for only 0.2% of deaths due to cancer in the United States. Their incidence has been estimated a two per milhon per year. About half of these tumors produce hormonal and metabolic syndromes that lead to their discovery. The other half are silent and are defined with the appearance of metastasis or when the primary tumor becomes large enough to produce abdominal symptoms. While adrenal cancer can occur at any age, most cases are discovered between the ages of 30-50 years (Brennan 1987 Schteingart 2000). 

Embolization Adrenal arterial emboKzation was performed in nine of our patients, four with inoperable adrenal cortical carcinoma and five with metastatic adrenal tumors. In eight patients, palliative embolization was performed either to decrease tumor bulk, suppress tumor hormonal function (n=3), or relieve pain (n=4). In four patients in whom it was possible to assess the effect of embolization, a striking reduction in size had occurred in one (Fig. 9.13), the lesion remained stable in size for 12 months in two, and the tumor continued to grow in the fourth. A reduction in the production of cortisol for 12 months was seen in two of the three patients with Cushing s syndrome (Fig. 9.13). Adrenal emboKzation resulted in the effective palliation of pain in three out of four patients and may have contributed to its amehoration in the fourth. Apart from a hypertensive episode in one patient, no serious compKcations occurred (O Keeffe et al. 1988). 

Second, the use of S-9 assumes that no mitochondrial or nuclear enzymes could have a direct involvement in mutagenesis. It is only speculative at this point not to agree necessarily with this assumption. However, there is evidence that an isomer of the insecticide DDD used in the treatment of adrenal cortical carcinoma, Mitotane, is converted to covalently binding species by mitochondria, but not by microsomes or the soluble fraction isolated from canine adrenal cortex tissue. Likewise, Bresnick has postulated that the nuclear mixed-function oxidases contribute in vivo to that activation of polycyclics that leads to mutagenesis and carcinogenesis, while the enzymes in the endoplasmic reticulum (microsomes) are more involved with the detoxification of these chemicals. Bresnick et have demonstrated with histofluorescence tech-... 

---