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At least 163 records · Page 9Linked to original sources
PubMed1997

Ribonucleic acid expression of the CLA-1 gene, a human homolog to mouse high density lipoprotein receptor SR-BI, in human adrenal tumors and cultured adrenal cells.

Human CLA-1 is homologous to the mouse SR-BI gene, which was recently identified as a high density lipoprotein receptor involved in selective cholesterol uptake in rodent adrenal cells. We screened 42 normal and pathological adrenal samples by Northern blotting and found abundant expression of CLA-1 messenger ribonucleic acid (mRNA) in normal adult and fetal adrenals, adrenocortical adenomas, and hyperplasias. Adrenocortical carcinomas and the adrenals adjacent to Cushing's adenomas contained less CLA-1 mRNA than normal adrenals. CLA-1 mRNA was also highly expressed in a Leydig cell tumor, but much less in liver, kidney, and pheochromocytomas. The accumulation of CLA-1 mRNA in primary cultures of normal adrenocortical cells was up-regulated by ACTH in a dose- and time-dependent manner. Both dibutyryl cAMP and staurosporine increased the basal expression of CLA-1 mRNA. Although there was no additive effect of ACTH and dibutyryl cAMP, staurosporine slightly enhanced the stimulatory effect of ACTH on the expression of CLA-1 mRNA. The abundant expression of CLA-1 mRNA and its regulation by the physiological hormone ACTH in human adrenal cells suggest that CLA-1 has a role in adrenal steroidogenesis, probably as a lipoprotein receptor mediating the selective cholesterol uptake in these cells.

Adrenal Cortex↗
PubMed1996

Adrenal Medullary Nodules in Beckwith-Wiedemann Syndrome Resemble Extra-Adrenal Paraganglia.

Clues to mechanisms regulating development and tumorigenesis may be provided by studies of unusual diseases. Beckwit-Wiedemann syndrome (BWS) is a rare congenital disorder apparently related to abnormal regulation of insulin-like growth factor-2 (IGF-2) production. IGF2 mRNA has been previously localized to the chief cells of extra-adrenal paraganglia and to adult, but not fetal, adrenal medulla. Expression of IGF-2 by neuroblastomas has been hypothesized to reflect extra-adrenal paraganglionic differentiation. In the adrenals of a fetus with 8W5, we have observed both increased numbers of chromaffin cells and organoid nodules resembling extra-adrenal paraganglia. Immunoreactive IGF-2 was observed in both cell types, but was also observed in chromaffin cells in the normal fetal adrenal. The findings suggest autocrine or paracrine influences of IGF-2 in regulating the number and phenotype of cells derived from sympathoadrenal precursors in the developing adrenal medulla as well as in extra-adrenal paraganglia. These results have implications for the interpretation of data from neuroblastoma studies.

Journal Article↗
PubMed1984

The computed tomography-guided adrenal biopsy. An alternative to surgery in adrenal mass diagnosis.

A series of 16 patients with adrenal masses were biopsied percutaneously under computed tomography (CT) guidance with 18- to 22-gauge modified Chiba needles. Adrenal adenomas, cysts, metastases, melanoma, and adrenal hemorrhage were identified. Of nine oncologic patients, four had adrenal metastases, while five had other nonmalignant adrenal masses. Thus, an adrenal mass in an oncologic patient is not always metastases. No complications occurred. The diagnostic evaluation of an adrenal mass in selected cases should include CT-guided percutaneous aspiration as a safe and reliable alternative to open surgical biopsy. CT-guided biopsy can be performed as an outpatient procedure, avoiding the cost of hospitalization and the morbidity of surgery.

Adenoma↗
PubMed2003

Immunohistochemical study of heat shock proteins 27, 60 and 70 in the normal human adrenal and in adrenal tumors with suppressed ACTH production.

Heat shock proteins (HSPs) are known to protect cells against various aggressions and to assist in the correct folding of nascent proteins as well as in the recovery of denatured ones. HSP70 increases its levels in the cell in response to any stress and is induced by ACTH in the adrenal gland. HSP60 is located in the mitochondria and assists in the folding of mitochondrial peptides. HSP27 is the only small HSP that is stress-induced. HSP27 and HSP70 are known to protect cells against apoptosis while, on the contrary, HSP60 is proapoptotic, increasing caspases maturation. We studied the expression of these HSPs in human adrenal tissue both in the normal glands (12 cases) and in tumoral tissue from cortisol producing adrenal adenomas (6 cases). Besides being neoplastic, these cells live in a particular ambience of lack of ACTH due to the suppression of the hypothalamic-pituitary ACTH secretion induced by the elevated levels of cortisol. HSP27 is highly expressed in the normal adrenal and shows a marked reduction of expression in Cushing's adrenal tissue. Although with overall lower levels of expression in the normal adrenal, HSP70 exhibited a similar pattern of reduction in tumoral tissue. HSP60, on the other hand, increased significantly and consistently in adrenal Cushing tumors. Besides the possible consequences of incorrect folding of nascent peptides, the alterations observed in tumoral tissue seem to act in an apoptotic direction. The only factor that we observed that could be contributing to these changes was the lack of plasma ACTH.

Adrenal Gland Neoplasms↗
PubMed1988

Age-related changes in adrenal size during the first year of life in normal newborns, infants and patients with congenital adrenal hyperplasia due to 21-hydroxylase deficiency: comparison of ultrasound and hormonal parameters.

An adrenal size index (ASI) was specifically designed to improve ultrasound evaluation of adrenal size in the 1st year of life. In 84 newborns and infants, ASI and plasma dehydroepiandrosterone sulphate (DHEA-S) concentrations were determined to study in vivo changes in adrenal size and cortical zonal composition. ASI was higher (P less than 0.0001) in the first 2 postnatal weeks (median 60.5 mm2) than in the rest of the first year (median 39.6 mm2) and showed a negative correlation with chronological age (r = -0.41). A positive correlation existed between DHEA-S concentrations and ASI (r = 0.29) as well as ASI relative to body weight (r = 0.57). These data and changes in gland echogenicity are consistent with histopathological observations that the early decrease in adrenal size is due to involution of the fetal zone. In four patients with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase (21-OHase) deficiency, ASI and plasma concentrations of pre-defect steroid were determined. Two patients with severe salt loss had markedly elevated ASI, which returned to normal during treatment. Two patients without severe salt loss had pretreatment ASI in the upper normal range, which decreased with treatment. Our findings indicate that ASI is useful in assessing physiological changes in adrenal size and, in conjunction with DHEA-S determinations, in adrenal cortex composition. ASI may aid in the early diagnosis of the salt-losing variety of 21-OHase deficiency. ASI is an instantaneously available tool which, in addition to biochemical and clinical data, can be used to monitor treatment of 21-OHase deficiency.

Adrenal Glands↗
PubMed1983

Suppression and stimulation of mineralocorticoid hormones (MCH) in the simple virilizing form of congenital adrenal hyperplasia (CAH) evaluated by the quantitation in adrenal venous blood.

Four untreated female patients with the nonsalt-losing form of congenital virilizing adrenal hyperplasia (21-hydroxylase deficiency) (21-OHD) maintained on a daily sodium intake of 120 m-equiv were studied by bilateral adrenal vein catheterization. Simultaneous right and left adrenal and peripheral blood samples were collected for determination of cortisol (F), progesterone (P), 17-hydroxyprogesterone (17-OHP), aldosterone (Aldo), and deoxycorticosterone (DOC). All patients were studied during sequential ACTH suppression (30 min after intravenous administration of 4 mg of dexamethasone) and stimulation (5 min after intravenous administration of 250 micrograms beta-ACTH [cosyntropin]). Basal peripheral concentrations of Aldo, DOC, P and 17-OHP were increased, whereas F concentrations were in the lower limit of the normal range. Dexamethasone suppressed adrenal secretion in all subjects. Subsequent adrenal stimulation by ACTH increased P, 17-OHP and DOC, whereas F returned to only control levels. DOC responses to ACTH in the adrenal vein effluents correlated significantly with Aldo responses but not with the 17-OHP increments, suggesting that the adrenal responses of Aldo and DOC to ACTH are events that probably occur in the same zone.

17-alpha-Hydroxyprogesterone↗
PubMed1994

Ovarian suppression with triptorelin and adrenal stimulation with adrenocorticotropin in functional hyperadrogenism: role of adrenal and ovarian cytochrome P450c17 alpha.

OBJECTIVES: To validate combined ovarian suppression with triptorelin and adrenal stimulation with ACTH in the diagnosis of female hyperandrogenism and to provide new insights into the adrenal-ovarian relationship present in this disorder. DESIGN: Comparison of sexual steroids and basal and ACTH-stimulated steroid levels before and after ovarian suppression induced by triptorelin. SETTING: Department of Endocrinology, Hospital Ramón y Cajal, Madrid, Spain. PARTICIPANTS: Thirty-nine nonselected women with hyperandrogenism. MAIN OUTCOME MEASURES: Serum levels of T, 17-hydroxyprogesterone (17-OHP), 17-hydroxy-pregnenolone, DHEA and DHEAS, androstenedione (delta 4-A), 11-deoxycortisol, and cortisol. RESULTS: Elevated T independent of ovarian suppression pointed to an adrenal disorder in six patients (one with an androgen-producing adenoma, two with late-onset 21-hydroxylase deficiency, three with functional adrenal hyperandrogenism). Nineteen patients had functional ovarian hyperandrogenism as elevated T normalized after ovarian suppression and were subdivided into ovDHEAS+ (n = 7) and ovDHEAS = (n = 12) subgroups depending on the presence of DHEAS hypersecretion. Finally, 14 patients had idiopathic hirsutism according to normal T before and after ovarian suppression. Comparisons of initial hormonal values between groups and with reference values obtained from normal women (n = 11) disclosed in functional adrenal hyperandrogenism an elevation of T and basal and stimulated DHEAS, delta 4-A, and 17-OHP with respect to normal women. These abnormalities were also present in ovDHEAS+ except for basal delta 4-A, which was normal, whereas only T and stimulated 17-OHP were elevated in ovDHEAS =. In the idiopathic group all steroids were normal with the exception of a mild elevation in stimulated DHEAS. CONCLUSIONS: These results show a continuum of abnormalities in hyperandrogenic women, suggesting an enhanced cytochrome P450c17 alpha activity in the adrenal and the ovary as the shared mechanism between functional adrenal hyperandrogenism and functional ovarian hyperandrogenism.

Adenoma↗
PubMed1990

Adrenal insufficiency from bilateral adrenal hemorrhage.

Bilateral adrenal hemorrhage is a rare cause of adrenal insufficiency in adults. Because of the nonspecific manifestations of adrenal insufficiency, antemortem diagnosis is difficult. Serial computed tomographic scans of the abdomen are a valuable adjunct in confirming the diagnosis of bilateral adrenal hemorrhage, which manifests as round or oval adrenal masses of high density that subsequently decrease in both size and density. The diagnosis should be suspected in any complex highly stressful illness, in the postoperative period, or in the presence of a coagulopathy in conjunction with hypotension, fever, or electrolyte disturbances. Herein we describe five patients in whom the computed tomographic scans suggested or confirmed the presence of bilateral adrenal hemorrhage. In three of the five patients, the presence of a circulating lupus anticoagulant was demonstrated. Once the diagnosis of adrenal hemorrhage is suspected, steroid replacement therapy should be initiated promptly.

Adrenal Gland Diseases↗
PubMed1997

Adrenal incidentalomas. Diagnostic workup of the incidentally discovered adrenal mass.

The incidentally discovered adrenal mass is a diagnostic dilemma veterinarians are likely to face with increasing frequency in the coming years. Dogs and cats may be more prone to functional adrenal lesions than are humans. Most adrenal tumors are benign, but a significant number of adrenocortical carcinomas (approximately 12%) and metastatic lesions within the adrenal glands (3% to 34%) do occur. Evaluation for hypertension, hypokalemia, and loss of hypothalamic-pituitary-adrenal responsiveness to a low dose of dexamethasone is appropriate for all patients with adrenal incidentalomas. The value of clinical and historical signs of hormonal overexpression should not be underestimated. More invasive or expensive diagnostic testing should be predicted on suspicions raised by the history and clinical signs. New diagnostic clinicopathologic tests, including plasma CgA and serum DHEAS, should be investigated in veterinary patients. Advanced diagnostic imaging using nuclear scintigraphy and chemical-shift MRI may offer veterinarians sensitive and specific noninvasive tools to consider for the evaluation of these patients. Patients with large masses, tumors with signs of malignancy, or productive adrenal tumors (plus or minus cortisol-producing tumors in which chemical ablation with mitotane can be attempted) should be considered candidates for exploratory surgery.

Adrenal Gland Neoplasms↗
PubMed2002

Adrenal growth is controlled by expression of specific pro-opiomelanocortin serine protease in the outer adrenal cortex.

As previous work had shown that extreme N-terminal fragments of the ACTH precursor pro-opiomelanocortin (POMC) not containing gamma-melanotropin (gamma-MSH) were active adrenal mitogens but an antiserum raised against gamma-MSH paradoxically also inhibited adrenal growth we proposed that the adrenal mitogen is processed from pro-gamma-MSH by a neurally controlled protease at the growing adrenal. To this end we have characterised a novel serine protease (named adrenal secretory protease (AsP) as Psort predicted a leader motif) which is expressed at the glomerulosa/fasciculata boundary where mitosis takes place. The expression of AsP was also found to be essential for mitosis of the adrenal cortical tumor Y1 cell-line in POMC containing media and 3D homology modeling revealed the presence of a catalytic pocket flanked by the classical His/Asp/Ser motifs. An usual feature of the model was a cluster of arginine residues on the underside of the protease suggesting that this basically charged face would tend to retain it on the cell surface on secretion-immunocytochemistry using an antiserum raised against a synthetic peptide spanning residues 1-25 of AsP showed that this was the case for Y1 cells. Specificity of AsP (affinity purified from Y1 media) was demonstrated by its inability to cleave model substrates for either trypsin or pro-hormone converting enzymes but was able to cleave an internally quenched POMC (44-55) model peptide. Interestingly mass spectral analysis of products of the latter predicts that the protease cleaves between the bond between Val52 and Met53 suggesting the natural adrenal mitogen is POMC (1-52).

Adrenal Cortex↗
PubMed1994

Early adrenal hypofunction in patients with organ-specific autoantibodies and no clinical adrenal insufficiency.

Idiopathic Addison's disease occurs frequently in association with other organ-specific autoimmune diseases, and autoantibodies to adrenal cortex are markers of this condition. A variable asymptomatic period with subtle adrenal dysfunction may precede the onset of clinical manifestations. We studied the pituitary-adrenal axis by measuring plasma ACTH, cortisol, and 17 alpha-hydroxyprogesterone after ovine CRH (100 micrograms as an iv bolus) stimulation in 19 patients with organ-specific autoimmune disease and adrenal autoantibodies, in whom adrenal steroids were normal under baseline conditions and normally responsive to a standard ACTH stimulation test (250 micrograms). In all subjects, oCRH produced a normal increase in plasma ACTH. Plasma cortisol, which was normoresponsive in 11 subjects, showed little or no increase in 8 subjects. Two of these patients developed overt adrenal failure after 1 yr. The 17 alpha-hydroxyprogesterone response to oCRH, tested in 10 of 19 patients, paralleled that of plasma cortisol, excluding a steroidogenic block at the 21-hydroxylase site. Our data demonstrate the existence of a very early phase of Addison's disease in which adrenal function shows an impaired response to ovine CRH-stimulated ACTH.

17-alpha-Hydroxyprogesterone↗
PubMed1997

Ribonucleic acid expression of the clustered imprinted genes, p57KIP2, insulin-like growth factor II, and H19, in adrenal tumors and cultured adrenal cells.

The recently cloned cyclin-dependent kinase inhibitor gene p57KIP2 is genomically imprinted and located on human chromosome 11p15.5. This region contains two other imprinted genes, insulin-like growth factor II (IGF-II) and H19, both of which seem to be implicated in adrenal neoplasms. We analyzed the expression of the putative tumor suppressor p57KIP2 gene by Northern blotting in normal and hyperplastic adrenals, adrenocortical tumors, and pheochromocytomas. The expression of p57KIP2 messenger ribonucleic acid (mRNA) correlated positively with H19 and negatively with IGF-II RNA in adrenocortical tissues. p57KIP2 mRNA (and H19 RNA) was abundantly expressed in normal human adrenals, adrenocortical adenomas from patients with Cushing's or Conn's syndrome or without clinical evidence of hormone overproduction, hyperplastic adrenals, and tumor-adjacent adrenal tissues, in which IGF-II mRNA expression was low. In most adrenocortical carcinomas and virilizing adrenal adenomas, very low levels of both p57KIP2 and H19 RNAs were observed, whereas IGF-II was highly expressed. In pheochromocytomas, p57KIP2 and H19 RNA expression was highly variable, but on the average it was about 45% and 27%, respectively, of that in normal and tumor-adjacent adrenals. In cultured adrenocortical cells, ACTH and dibutyryl cAMP treatment slightly reduced the predominant 1.7-kilobase (kb) transcript of p57KIP2 gene, but induced a 2.5-kb transcript with a simultaneous increase in H19 RNA expression. The stimulatory effect of ACTH on the 2.5-kb p57KIP2 and H19 transcript accumulation was enhanced by exogenous IGF-II and IGF-I. Our data show that p57KIP2 and H19 RNAs are expressed usually in parallel in normal and pathological adrenocortical tissues. The decreased expression of both p57KIP2 and H19 RNAs in conjunction with elevated IGF-II mRNA expression in hormonally active adrenocortical carcinomas suggests that the loss of expression of the putative tumor suppressor genes p57KIP2 and H19 may be involved in the pathogenesis of these neoplasms.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Effects of long-term phenobarbital treatment on the thyroid and adrenal axis and adrenal function tests in dogs.

Phenobarbital can interfere with the thyroid axis in human beings and rats by accelerating hepatic thyroxine metabolism because of enzyme induction. In human beings, it also can interfere with the low-dose dexamethasone suppression test (LDDST) used to assess adrenal function by accelerating dexamethasone metabolism. This effect can cause a lack of suppression of pituitary ACTH and subsequent adrenal cortisol release after dexamethasone administration. The effects of phenobarbital on the thyroid axis, the adrenal axis, and adrenal function tests were prospectively investigated in 12 normal, adult dogs. Phenobarbital was administered at 5 mg per kilogram of body weight (range, 4.8-6.6 mg/kg) PO q12h for 29 weeks, resulting in therapeutic serum concentrations (20-40 microg/mL). Serum total thyroxine (TT4), free thyroxine (FT4) by equilibrium dialysis, total triiodothyronine (TT3), thyrotropin (TSH), and cholesterol were determined before and during phenobarbital treatment. LDDST, ACTH stimulation tests, and ultrasonographic evaluation of the adrenal glands were performed before and during treatment. TT4 and FT4 decreased significantly (P < or = .05), TT3 had minimal fluctuation, TSH had only a delayed compensatory increase, and cholesterol increased during phenobarbital treatment. The delayed increase in TSH, despite persistent hypothyroxinemia, suggests that accelerated hepatic thyroxine elimination may not be the only effect of phenobarbital on the thyroid axis. There was no significant effect of phenobarbital on either of the adrenal function tests. With the methods employed, we did not find any effects of the drug on the hormonal equilibrium of the adrenal axis.

Adrenal Gland Diseases↗
PubMed1999

Testicular adrenal rest tissue in congenital adrenal hyperplasia: comparison of MR imaging and sonographic findings.

OBJECTIVE: The purpose of our study was to describe the MR features of testicular adrenal rest tissue in patients with congenital adrenal hyperplasia and to compare the usefulness of MR imaging with that of sonography for the detection of testicular adrenal rest tissue. SUBJECTS AND METHODS: Nineteen patients with congenital adrenal hyperplasia underwent MR imaging and gray-scale and color Doppler sonography of the testicles during the same visit to our institution. Findings were compared. RESULTS: MR features of testicular adrenal rest tissue included the following: isointensity (71% of the masses) and slight hyperintensity (29% of the masses) relative to normal testicular tissue on T1-weighted images; hypointensity relative to normal testicular tissue on T2-weighted images (100% of the masses); and diffuse enhancement on contrast-enhanced T1-weighted images (85% of the masses). MR imaging and sonography revealed the testicular lesions equally well. Eleven (58%) of 19 patients had normal findings on MR imaging and sonography. Eight (42%) of 19 patients had 14 intratesticular masses detected by both imaging techniques. CONCLUSION: MR imaging and sonography are equally useful in the detection of testicular adrenal rest tissue. Because sonography is more accessible to most institutions and is less expensive, it is the imaging technique of choice for the detection of testicular adrenal rest tissue.

Adolescent↗
PubMed2004

[Mantle cell lymphoma markedly infiltrated into adrenal glands with adrenal insufficiency].

A 66-year-old male was admitted to our hospital complaining of bilateral hypochondrial pain, back pain and loss of weight in May, 2002. Superficial lymph nodes were not palpable on admission. The leukocyte count was 3430/microl, hemoglobin concentration, 13.0g/dl, and platelet count, 174000/microl. LDH, soluble IL-2 receptor, ACTH and cortisol values were out of the normal range (LDH 1368IU/l, sIL-2R 2630U/ml, ACTH 132pg/ml, cortisol 7.4microg/dl). Abdominal CT scan showed bilateral adrenal masses, and abnormal uptake of Ga-scintigraphy was seen correspondent with the bilateral adrenal masses. The histological diagnosis of bilateral adrenal masses cannot be performed because of the bleeding tendency, but atypical cells were observed in the patient's bone marrow aspirate. Surface marker analysis of atypical cells showed CD5+, cyclin D1+, CD19+, CD20+ and HLA-DR+. From these results we diagnosed this case as a mantle cell lymphoma (stage IV B) markedly infiltrated into the adrenal glands with adrenal insufficiency. The bilateral adrenal masses dramatically reduced in size after CHOP chemotherapy with hydrocortisone supplementation. We report on the present case and summarize the reports of adrenal grand-infiltrating lymphomas.

Adrenal Gland Neoplasms↗
PubMed2001

[Transposition of pedicled adrenal gland for the treatment of adrenal medullary hyperplasia].

OBJECTIVE: To investigate the operative modes for adrenal medullary hyperplasia. METHODS: 8 cases of adrenal medullary hyperplasia were treated with transposition of pedicled adrenal gland. The inferior and the medial blood vessel of adrenal gland were ligated. The superior blood vessel of adrenal gland was formed a 5.0- 6.0 cm pedicle and dragged to the subcutaneous of dorsum. RESULT: After follow-up for an average of 2 years, only 1 of the 8 patients did not recover as a result of psychosis and others had no symptoms but normal endocrine results. CONCLUSION: Transposition of the pedicled adrenal gland is a simple and satisfied way to treat patients with adrenal medullary hyperplasia.

Adrenal Glands↗
PubMed1990

Immunopathology of adrenal and renal cortical tumors. Coordinated change in antigen expression is associated with neoplastic conversion in the adrenal cortex.

A series of adrenal cortical adenomas (ACA) and carcinomas (ACC), as well as normal adrenal cortex have been studied by a panel of 11 antibodies to characterize antigenic changes that may distinguish these morphologically similar entities. Normal adrenal cortex and ACA express low-molecular weight cytokeratin intermediate filaments. However, none of the six primary or seven metastatic ACCs were found to express detectable levels of cytokeratins. In contrast, vimentin was seen in all ACCs studied and was heterogeneously expressed by ACAs. However, its expression was usually confined to stromal elements of the normal adrenal cortex. We conclude that adrenal cortical cells undergo characteristic changes in intermediate filament expression during the process of neoplastic conversion and malignant transformation. Undetectable expression of cytokeratins and strong expression of vimentin is associated with malignant adrenal cortical lesions. In addition, we examined the antigenic phenotype of a series of primary renal cell carcinomas (RCC). Renal cell carcinomas express cytokeratins, while ACCs do not. The majority of primary RCCs express Lewis blood group isoantigens (most commonly Lewis X), while ACAs and ACCs do not. The panel of antibodies described here may help to distinguish morphologically similar lesions of like histogenesis (ACAs vs. ACCs) and lesions of different histogenesis (adrenal vs. renal) on the basis of their composite antigenic phenotypes.

Adenoma↗
PubMed1988

Apparent stronger expression in the human adrenal cortex than in the human adrenal medulla of Mr 170,000-180,000 P-glycoprotein.

A monoclonal antibody (MAb), MRK 16, specific to Adriamycin-resistant human myelogenous leukemia cell line K562, was used to examine whether the antigen molecules (P-glycoprotein) recognized by the MAb are present in the adrenals. The materials examined included 61 human adrenals and several cell lines. Immunohistochemical analysis revealed that almost all of the human adrenal specimens (59 out of 61) were stained positively with MAb MRK 16 and that the antigen was strongly expressed even in cases where anticancer agents had not been given. Immunoprecipitation showed that the Mr 170,000-180,000 glycoprotein was present in all of the adult adrenals but not in fetal and neonatal adrenals. Furthermore, fluorescence image analysis revealed that the P-glycoprotein was more strongly expressed in the cortex than in the medulla, showing a tendency to occur in cell clusters in the latter area. The cell lines derived from animal adrenals (SW-13, Y-1, and PC-12) showed no positive staining with MAb MRK 16. It is suggested that this glycoprotein may be related to maturation of the adrenal, in which it possibly plays a physiological role.

ATP Binding Cassette Transporter, Subfamily B, Mem↗