Disease relevance of Adrenal Cortex Neoplasms

• Suramin in adrenocortical cancer: limited efficacy and serious toxicity [1].
• Interestingly allelic loss at 17p13 and 11p15 have been observed in sporadic adrenocortical cancer and somatic PRKAR1A mutations in secreting adrenocortical adenomas [2].
• In an attempt to understand the mechanism behind the invasion and metastasis in adrenocortical cancer we performed mRNA in situ hybridization on 30 tumors for three matrix metalloproteinases (MMPs): gelatinase A, membrane type 1 matrix metalloproteinase (MT1-MMP), and collagenase-3 [3].
• A human non-functioning adrenocortical cancer tissue showed an unresponsiveness in adenylate cyclase to ACTH although ACTH and CT activated adenylate cyclase in a non-functioning adrenal adenoma tissue [4].

High impact information on Adrenal Cortex Neoplasms

• High frequency of germline p53 mutations in childhood adrenocortical cancer [5].
• Functional studies showed that the activating Ser45 beta-catenin mutation found in the adrenocortical cancer H295R cell line leads to constitutive activation of T-cell factor-dependent transcription [6].
• These properties provide the first evidence that expression of cAMP-regulated AKR1B1 is decreased in adrenocortical cancer [7].
• We recently reported the loss of cAMP-responsive element-binding protein (CREB) expression in the adrenocortical cancer cell line H295R [8].
• In preliminary studies we demonstrated that the CYP11B1 (11beta-hydroxylase) promoter could direct specific expression of a suicide gene in adrenocortical cancer cells, providing a potentially specific therapeutic option for adrenocortical cancer [9].

Chemical compound and disease context of Adrenal Cortex Neoplasms

• Low-dose monitored mitotane treatment achieves the therapeutic range with manageable side effects in patients with adrenocortical cancer [10].
• We describe a patient with a metastasized adrenocortical cancer who exhibited excessive production of both glucocorticoids and mineralocorticoids combined with suppressed androgen production [11].
• BACKGROUND: To evaluate the efficacy of streptozocin and o.p'DDD (SO) in adrenocortical cancer (ACC) patients since other chemotherapeutic regimens have limited effects [12].
• Suramin, a sulfonated drug, has been used successfully in the treatment of inoperable adrenocortical cancer [13].
• Adrenocortical tumours (ACTs) may be responsible for excess steroid production and, in the case of adrenocortical cancers, for morbidity or mortality due to tumour growth [14].

Biological context of Adrenal Cortex Neoplasms

• The adrenocortical cancer cells expressed mutant p53, and no evidence for induction of apoptosis by these drugs was found [11].
• After finding prolonged bleeding times in 2 patients treated with mitotane, we prospectively studied 7 patients with adrenocortical cancer on mitotane therapy [15].
• Moreover, this study points towards a role for ER beta as an important mediator of the repressive effects exerted by antiestrogens on H295R cells; however, further studies are needed to clarify its role in the control of adrenocortical cell proliferation and on the potential benefits of antiestrogens for treatment of adrenocortical cancer [16].
• The aim of the present study was to demonstrate the expression of the AR gene in normal and neoplastic adrenocortical human tissues and in the human adrenocortical cancer cell line, NCI-H295, and then to evaluate the effect of dihydrotestosterone (DHT) on human adrenocortical cell growth [17].

Anatomical context of Adrenal Cortex Neoplasms

• We have previously found that the androgen receptor gene is expressed both in normal and adenomatous human adrenal cortex and in the NCI-H295 human adrenocortical cancer cell line [18].
• Two adrenocortical cancer cytosols were found to contain the binder with a relative low affinity (Kd 5 X 10(-9) M) for estradiol [19].

Gene context of Adrenal Cortex Neoplasms

• The putative role of OSM as an immunotherapeutic agent in human adrenocortical cancer remains to be elucidated [20].
• Alterations of CRE binding proteins with loss of CREB expression and compensatory overexpression of CREMtau is observed in the human adrenocortical cancer cell line H295R [21].
• The present investigation was performed in order to study the properties of abnormal membrane function related to ACTH receptor-adenylate cyclase system interaction in human ACTH-unresponsive adrenocortical cancer [22].
• After surgery, MMP-8 and MMP-9 levels decreased significantly in patients with adrenocortical cancers, whereas the decrease of these MMPs in patients with benign tumors, although noticeable, was not statistically significant [23].
• Adrenocortical cancers, like other cancers, typically have telomerase activity [24].

Analytical, diagnostic and therapeutic context of Adrenal Cortex Neoplasms

• Feasibility of the association of mitotane with etoposide, adriamycin and cisplatin combination chemotherapy in advanced adrenocortical cancer patients. Report on 7 cases [25].
• BACKGROUND: Suramin inhibits growth of neural crest-derived cells and is used to treat adrenocortical cancer and neuroblastoma in clinical trials [26].

References