Adrenocortical Carcinoma: A malignant neoplasm of the ADRENAL CORTEX. Adrenocortical carcinomas are unencapsulated anaplastic (ANAPLASIA) masses sometimes exceeding 20 cm or 200 g. They are more likely to be functional than nonfunctional, and produce ADRENAL CORTEX HORMONES that may result in hypercortisolism (CUSHING SYNDROME); HYPERALDOSTERONISM; and/or VIRILISM.Adrenal Cortex Neoplasms: Tumors or cancers of the ADRENAL CORTEX.Mitotane: A derivative of the insecticide DICHLORODIPHENYLDICHLOROETHANE that specifically inhibits cells of the adrenal cortex and their production of hormones. It is used to treat adrenocortical tumors and causes CNS damage, but no bone marrow depression.Adrenocortical Adenoma: A benign neoplasm of the ADRENAL CORTEX. It is characterized by a well-defined nodular lesion, usually less than 2.5 cm. Most adrenocortical adenomas are nonfunctional. The functional ones are yellow and contain LIPIDS. Depending on the cell type or cortical zone involved, they may produce ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and/or ANDROSTENEDIONE.Adrenal Cortex: The outer layer of the adrenal gland. It is derived from MESODERM and comprised of three zones (outer ZONA GLOMERULOSA, middle ZONA FASCICULATA, and inner ZONA RETICULARIS) with each producing various steroids preferentially, such as ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and ANDROSTENEDIONE. Adrenal cortex function is regulated by pituitary ADRENOCORTICOTROPIN.Carcinoma: A malignant neoplasm made up of epithelial cells tending to infiltrate the surrounding tissues and give rise to metastases. It is a histological type of neoplasm but is often wrongly used as a synonym for "cancer." (From Dorland, 27th ed)Cushing Syndrome: A condition caused by prolonged exposure to excess levels of cortisol (HYDROCORTISONE) or other GLUCOCORTICOIDS from endogenous or exogenous sources. It is characterized by upper body OBESITY; OSTEOPOROSIS; HYPERTENSION; DIABETES MELLITUS; HIRSUTISM; AMENORRHEA; and excess body fluid. Endogenous Cushing syndrome or spontaneous hypercortisolism is divided into two groups, those due to an excess of ADRENOCORTICOTROPIN and those that are ACTH-independent.Adrenal Gland Neoplasms: Tumors or cancer of the ADRENAL GLANDS.Adrenocorticotropic Hormone: An anterior pituitary hormone that stimulates the ADRENAL CORTEX and its production of CORTICOSTEROIDS. ACTH is a 39-amino acid polypeptide of which the N-terminal 24-amino acid segment is identical in all species and contains the adrenocorticotrophic activity. Upon further tissue-specific processing, ACTH can yield ALPHA-MSH and corticotrophin-like intermediate lobe peptide (CLIP).Hydrocortisone: The main glucocorticoid secreted by the ADRENAL CORTEX. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions.Myelolipoma: A rare benign tumor of the adrenal gland, several centimeters in diameter, composed in varying proportions of adipose tissue, lymphocytes, and primitive myeloid cells, probably a developmental abnormality. (Dorland, 27th ed)Adrenal Glands: A pair of glands located at the cranial pole of each of the two KIDNEYS. Each adrenal gland is composed of two distinct endocrine tissues with separate embryonic origins, the ADRENAL CORTEX producing STEROIDS and the ADRENAL MEDULLA producing NEUROTRANSMITTERS.Adrenal Rest Tumor: Neoplasm derived from displaced cells (rest cells) of the primordial ADRENAL GLANDS, generally in patients with CONGENITAL ADRENAL HYPERPLASIA. Adrenal rest tumors have been identified in TESTES; LIVER; and other tissues. They are dependent on ADRENOCORTICOTROPIN for growth and adrenal steroid secretion.Adrenalectomy: Excision of one or both adrenal glands. (From Dorland, 28th ed)Steroid 17-alpha-Hydroxylase: A microsomal cytochrome P450 enzyme that catalyzes the 17-alpha-hydroxylation of progesterone or pregnenolone and subsequent cleavage of the residual two carbons at C17 in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP17 gene, generates precursors for glucocorticoid, androgen, and estrogen synthesis. Defects in CYP17 gene cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL) and abnormal sexual differentiation.Carcinoma, Squamous Cell: A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)Adrenal Cortex Diseases: Pathological processes of the ADRENAL CORTEX.Carcinoma, Hepatocellular: A primary malignant neoplasm of epithelial liver cells. It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. The cells may be uniform or markedly pleomorphic, or form GIANT CELLS. Several classification schemes have been suggested.Adenoma: A benign epithelial tumor with a glandular organization.Feminization: Development of female secondary SEX CHARACTERISTICS in the MALE. It is due to the effects of estrogenic metabolites of precursors from endogenous or exogenous sources, such as ADRENAL GLANDS or therapeutic drugs.Adrenocortical Hyperfunction: Excess production of ADRENAL CORTEX HORMONES such as ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and/or ANDROSTENEDIONE. Hyperadrenal syndromes include CUSHING SYNDROME; HYPERALDOSTERONISM; and VIRILISM.17-Ketosteroids: Steroids that contain a ketone group at position 17.17-alpha-Hydroxyprogesterone: A metabolite of PROGESTERONE with a hydroxyl group at the 17-alpha position. It serves as an intermediate in the biosynthesis of HYDROCORTISONE and GONADAL STEROID HORMONES.Li-Fraumeni Syndrome: Rare autosomal dominant syndrome characterized by mesenchymal and epithelial neoplasms at multiple sites. MUTATION of the p53 tumor suppressor gene, a component of the DNA DAMAGE response pathway, apparently predisposes family members who inherit it to develop certain cancers. The spectrum of cancers in the syndrome was shown to include, in addition to BREAST CANCER and soft tissue sarcomas (SARCOMA); BRAIN TUMORS; OSTEOSARCOMA; LEUKEMIA; and ADRENOCORTICAL CARCINOMA.Endocrine Surgical Procedures: Surgery performed on any endocrine gland.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Aldosterone: A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.Steroidogenic Factor 1: A transcription factor and member of the nuclear receptor family NR5 that is expressed throughout the adrenal and reproductive axes during development. It plays an important role in sexual differentiation, formation of primary steroidogenic tissues, and their functions in post-natal and adult life. It regulates the expression of key steroidogenic enzymes.3-Hydroxysteroid Dehydrogenases: Catalyze the oxidation of 3-hydroxysteroids to 3-ketosteroids.Adrenal Cortex HormonesTumor Markers, Biological: Molecular products metabolized and secreted by neoplastic tissue and characterized biochemically in cells or body fluids. They are indicators of tumor stage and grade as well as useful for monitoring responses to treatment and predicting recurrence. Many chemical groups are represented including hormones, antigens, amino and nucleic acids, enzymes, polyamines, and specific cell membrane proteins and lipids.Aromatase: An enzyme that catalyzes the desaturation (aromatization) of the ring A of C19 androgens and converts them to C18 estrogens. In this process, the 19-methyl is removed. This enzyme is membrane-bound, located in the endoplasmic reticulum of estrogen-producing cells of ovaries, placenta, testes, adipose, and brain tissues. Aromatase is encoded by the CYP19 gene, and functions in complex with NADPH-FERRIHEMOPROTEIN REDUCTASE in the cytochrome P-450 system.Cell Line, Tumor: A cell line derived from cultured tumor cells.Carcinoma in Situ: A lesion with cytological characteristics associated with invasive carcinoma but the tumor cells are confined to the epithelium of origin, without invasion of the basement membrane.Dehydroepiandrosterone: A major C19 steroid produced by the ADRENAL CORTEX. It is also produced in small quantities in the TESTIS and the OVARY. Dehydroepiandrosterone (DHEA) can be converted to TESTOSTERONE; ANDROSTENEDIONE; ESTRADIOL; and ESTRONE. Most of DHEA is sulfated (DEHYDROEPIANDROSTERONE SULFATE) before secretion.Steroids: A group of polycyclic compounds closely related biochemically to TERPENES. They include cholesterol, numerous hormones, precursors of certain vitamins, bile acids, alcohols (STEROLS), and certain natural drugs and poisons. Steroids have a common nucleus, a fused, reduced 17-carbon atom ring system, cyclopentanoperhydrophenanthrene. Most steroids also have two methyl groups and an aliphatic side-chain attached to the nucleus. (From Hawley's Condensed Chemical Dictionary, 11th ed)Tomography, X-Ray Computed: Tomography using x-ray transmission and a computer algorithm to reconstruct the image.Prognosis: A prediction of the probable outcome of a disease based on a individual's condition and the usual course of the disease as seen in similar situations.Incidental Findings: Unanticipated information discovered in the course of testing or medical care. Used in discussions of information that may have social or psychological consequences, such as when it is learned that a child's biological father is someone other than the putative father, or that a person tested for one disease or disorder has, or is at risk for, something else.Carcinoma, Papillary: A malignant neoplasm characterized by the formation of numerous, irregular, finger-like projections of fibrous stroma that is covered with a surface layer of neoplastic epithelial cells. (Stedman, 25th ed)Tumor Cells, Cultured: Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.Antineoplastic Agents, Hormonal: Antineoplastic agents that are used to treat hormone-sensitive tumors. Hormone-sensitive tumors may be hormone-dependent, hormone-responsive, or both. A hormone-dependent tumor regresses on removal of the hormonal stimulus, by surgery or pharmacological block. Hormone-responsive tumors may regress when pharmacologic amounts of hormones are administered regardless of whether previous signs of hormone sensitivity were observed. The major hormone-responsive cancers include carcinomas of the breast, prostate, and endometrium; lymphomas; and certain leukemias. (From AMA Drug Evaluations Annual 1994, p2079)Neoplasm Staging: Methods which attempt to express in replicable terms the extent of the neoplasm in the patient.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Retroperitoneal NeoplasmsInhibins: Glycoproteins that inhibit pituitary FOLLICLE STIMULATING HORMONE secretion. Inhibins are secreted by the Sertoli cells of the testes, the granulosa cells of the ovarian follicles, the placenta, and other tissues. Inhibins and ACTIVINS are modulators of FOLLICLE STIMULATING HORMONE secretions; both groups belong to the TGF-beta superfamily, as the TRANSFORMING GROWTH FACTOR BETA. Inhibins consist of a disulfide-linked heterodimer with a unique alpha linked to either a beta A or a beta B subunit to form inhibin A or inhibin B, respectivelyGene Expression Regulation, Neoplastic: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.Fatal Outcome: Death resulting from the presence of a disease in an individual, as shown by a single case report or a limited number of patients. This should be differentiated from DEATH, the physiological cessation of life and from MORTALITY, an epidemiological or statistical concept.Blogging: Using an INTERNET based personal journal which may consist of reflections, comments, and often hyperlinks.National Cancer Institute (U.S.): Component of the NATIONAL INSTITUTES OF HEALTH. Through basic and clinical biomedical research and training, it conducts and supports research with the objective of cancer prevention, early stage identification and elimination. This Institute was established in 1937.

YM116, 2-(1H-imidazol-4-ylmethyl)-9H-carbazole, decreases adrenal androgen synthesis by inhibiting C17-20 lyase activity in NCI-H295 human adrenocortical carcinoma cells. (1/185)

The concentrations of androstenedione and dehydroepiandrosterone, products of C17-20 lyase, in the medium after a 6-hr incubation of NCI-H295 cells were decreased by YM116 (2-(1H-imidazol-4-ylmethyl)-9H-carbazole) (IC50: 3.6 and 2.1 nM) and ketoconazole (IC50: 54.9 and 54.2 nM). 17Alpha-hydroxyprogesterone, a product of 17alpha-hydroxylase, was increased by YM116 (1-30 nM) and by ketoconazole (10-300 nM) and then was decreased at higher concentrations of both agents (IC50: 180 nM for YM116, 906 nM for ketoconazole), indicating that YM116 and ketoconazole were 50- and 16.5-fold more specific inhibitors of C17-20 lyase, respectively, than 17alpha-hydroxylase. Compatible with these findings, progesterone, a substrate of 17alpha-hydroxylase, was increased by these agents. Cortisol production was inhibited by YM116 and ketoconazole (IC50: 50.4 and 80.9 nM, respectively). YM116 was a 14-fold more potent inhibitor of androstenedione production than cortisol production, whereas ketoconazole was a nonselective inhibitor of the production of both steroids. YM116 and ketoconazole inhibited the C17-20 lyase activity in human testicular microsomes (IC50: 4.2 and 17 nM, respectively). These results demonstrate that YM116 reduces the synthesis of adrenal androgens by preferentially inhibiting C17-20 lyase activity.  (+info)

Comparison of expression and regulation of the high-density lipoprotein receptor SR-BI and the low-density lipoprotein receptor in human adrenocortical carcinoma NCI-H295 cells. (2/185)

In rodents, cholesterol for adrenal steroidogenesis is derived mainly from high-density lipoproteins (HDL) via the HDL receptor, scavenger receptor-BI (SR-BI). In humans cholesterol for steroidogenesis is considered to be derived from the low-density lipoprotein (LDL) receptor pathway, and the contribution of SR-BI to that is unknown. In the present study SR-BI expression and regulation by steroidogenic stimuli was analysed in human adrenocortical cells and compared with LDL receptor expression. In addition, the functional contribution of both receptors for cholesteryl ester delivery to human adrenocortical cells was compared. Northern blot and reverse transcription-PCR amplification and sequence analysis demonstrated the presence of SR-BI mRNA in foetal and adult human adrenal cortex. Furthermore, SR-BI mRNA was expressed to similar levels in human primary adrenocortical and adrenocortical carcinoma NCI-H295 cells, indicating its presence in the steroid-producing cells. Treatment of NCI-H295 cells with 8Br-cAMP, a stimulator of glucocorticoid synthesis via the protein kinase A second messenger signal transduction pathway, resulted in an increase of both SR-BI and LDL receptor mRNA levels in a time- and dose-dependent manner. The induction of SR-BI and LDL receptor by cAMP was independent of ongoing protein synthesis and occurred at the transcriptional level. Ligand blot experiments indicated that a protein of similar size to SR-BI is the major HDL-binding protein in NCI-H295 cells. Western blot analysis demonstrated that cAMP treatment increased the levels of LDL receptor and, to a lesser extent, SR-BI protein in NCI-H295 cells. Binding and uptake of cholesterol was quantitatively smaller from HDL than from LDL, both in basal as well as in cAMP-stimulated cells. Scatchard analysis under basal conditions indicated that NCI-H295 cells express twice as many specific binding sites for LDL than for HDL. Dissociation constant values (Kd; in nm) were approximately five times higher for HDL than for LDL, indicating a lower affinity of HDL compared with LDL. The combined effects of these two parameters and the low cholesteryl ester content of HDL subfraction 3 (HDL3) contributes to a lower cholesteryl ester uptake from HDL than from LDL by the NCI-H295 cells. In conclusion, both the SR-BI and LDL receptor genes are expressed in the human adrenal cortex and coordinately regulated by activators of glucocorticoid synthesis. In contrast to rodents, in human adrenocortical cells the HDL pathway of cholesterol delivery appears to be of lesser importance than the LDL pathway. Nevertheless, the SR-BI pathway may become of major importance in conditions of functional defects in the LDL receptor pathway.  (+info)

The expression of inhibin/activin subunits in the human adrenal cortex and its tumours. (3/185)

Inhibins and activins are dimeric proteins of the transforming growth factor-beta superfamily which have been shown to be expressed in the adrenal cortex. Recent studies have suggested a role for these peptides in the pathogenesis and/or function of adrenal tumours. To investigate further their physiological and pathological roles, we have documented immunoreactivity for inhibin alpha, betaA and betaB subunits in normal adult and fetal human adrenals, in hyperplastic adrenals and in adrenal tumours. In the normal and hyperplastic adult gland, diffuse immunopositivity was demonstrated for beta subunits, suggesting that activins (beta beta dimers) can be expressed in all zones. Inhibin alpha was limited to the zona reticularis and the innermost zona fasciculata in the normal gland, extending centripetally into the zona fasciculata in hyperplasia, supporting a role for ACTH in the regulation of expression, and suggesting that expression of inhibins (alpha beta dimers) is restricted. Immunopositivity for all three subunits was seen in both fetal and definitive zones of the fetal cortex, indicating that both inhibins and activins could be expressed in both. Immunopositivity for all three subunits was seen in most adrenocortical tumours. Loss of immunopositivity for inhibin alpha in a subgroup of carcinomas might indicate a role in tumour progression. The greater intensity of staining for inhibin alpha in tumours associated with Cushing's syndrome again suggests a link with cortisol production.  (+info)

Autocrine role of IGF-II in proliferation of human adrenocortical carcinoma NCI H295R cell line. (4/185)

In adrenocortical tumors, the malignant phenotype is associated with rearrangements (paternal isodisomy) at the 11p15 locus and IGF-II gene overexpression, strongly suggesting that the IGF system is a major determinant of adrenocortical tumor progression. The aim of this study was to validate an in vitro model for investigating the involvement of the IGF system in adrenocortical tumorigenesis. We analyzed the production of IGF mRNA and proteins, IGF-binding proteins (IGFBPs) and IGF receptors by the NCI H295R cell line, which is derived from a human adult adrenocortical carcinoma. H295R cells were shown to proliferate for a long period (26 days) in the absence of serum or any added growth factor. Northern blot analyses showed high IGF-II mRNA contents in H295R cells. The cells secreted large amounts of IGF-II protein (14 ng/10(6) cells per 48 h) although no IGF-I protein was detected. Western ligand blot analyses of conditioned media detected the presence of large amounts of a 34 kDa protein, which was identified as IGFBP-2 by immunoblotting. The presence of high-affinity binding sites for IGF-I and IGF-II on H295R cells was shown by binding experiments using radiolabeled IGFs and confirmed by reverse transcription PCR analyses showing type 1 and type 2 IGF receptors. Proliferation of H295R cells was inhibited by anti-IGF-II antibody (45%) and by anti-type 1 IGF receptor antibody (53%) indicating that IGF-II is an autocrine growth factor for these cells and that its effects are, at least in part, mediated by the type 1 IGF receptor. These findings confirm the involvement of the IGF system in adrenocortical tumors and suggest that the H295R cell line is a suitable in vitro model for studying the molecular mechanisms of adrenocortical tumor proliferation.  (+info)

Lack of response to octreotide in Cushing's syndrome due to metastatic adrenocortical carcinoma. (5/185)

Functional metastatic adrenocortical carcinoma is an uncommon cause of Cushing's syndrome, which rarely responds to conventional treatment. A patient presenting with Cushing's syndrome secondary to adrenocortical carcinoma underwent surgical resection. Postoperatively, she developed metastatic disease resistant to conventional chemotherapy. Octreotide, a somatostatin analogue which is effective in the treatment of several types of neuroendocrine tumour, was tried to ameliorate her secretory symptoms, but without any therapeutic effect.  (+info)

Analysis of genomic alterations in sporadic adrenocortical lesions. Gain of chromosome 17 is an early event in adrenocortical tumorigenesis. (6/185)

Genetic changes underlying the tumorigenesis of sporadic adrenocortical tumors are poorly characterized. To search for characteristic genomic imbalances involved in adrenocortical tumors, we examined 41 adrenocortical lesions (12 carcinomas, 23 adenomas, and 6 hyperplasias) by comparative genomic hybridization. Our results show that genetic alterations are more frequent in malignant than in benign lesions and that they rarely occur in hyperplastic lesions. The most frequent DNA copy number changes in adrenocortical carcinomas included losses of 1p21-31, 2q, 3p, 3q, 6q, 9p, and 11q14-qter, as well as gains and amplifications of 5q12, 9q32-qter, 12q, and 20q. The genomic aberrations prevalently occurring in adrenocortical adenomas were gains of 17q, 17p, and 9q32-qter. Gains found in 2 of 6 adrenocortical hyperplastic lesions involved chromosome 17 or 17q only. These data indicate that oncogenes determining the early tumorigenesis of adrenocortical tumors may exist on chromosome 17 and that the number of genomic alterations is closely associated with tumor behavior in adrenocortical tumors.  (+info)

Changes in neoplastic cell features and sensitivity to mitotane during mitotane-induced remission in a patient with recurrent, metastatic adrenocortical carcinoma. (7/185)

A 58-year-old man had adrenocortical carcinoma in the right adrenal gland. The tumour secreted excessive cortisol and dehydroepiandrosterone-sulphate (DHEA-S), and had invaded the right hepatic lobe and vena cava. Eleven months after surgical tumour resection, the serum DHEA-S levels again increased. Local tumour recurrence and a metastasis was found in the lung. Eleven months after surgery chemotherapy with mitotane (o,p'-DDD) was initiated. Twelve weeks of mitotane reduced serum DHEA-S levels and caused these tumours to disappear. The patient was then treated with low-dose mitotane (1.5-2.0 g/day) for 2 years. Serum levels of mitotane remained at less than 10 microg/ml. Although such low serum levels of mitotane and delayed initiation of mitotane after surgery have been proposed to weaken the antineoplastic effect of mitotane, the patient had a remission for 2 years. However, there was then local re-recurrence with an increase in serum DHEA-S and death 4 months later. The histological features of neoplastic cells were quite different comparing tumour resected at surgery and tumour at autopsy. The latter had more frequent mitotic nuclei. This tumour was initially sensitive to mitotane, but later became insensitive.  (+info)

Expression of inhibin alpha in adrenocortical tumours reflects the hormonal status of the neoplasm. (8/185)

Inhibins are gonadal glycoprotein hormones whose main endocrine function is to inhibit pituitary FSH secretion. In addition to testes and ovaries, other steroid-producing organs are sites of inhibin alpha subunit expression. To study the role of inhibins in human adrenal gland, we screened a panel of 150 adrenals (10 normal adrenals, 25 adrenocortical hyperplasias, 65 adrenocortical adenomas, 30 adrenocortical carcinomas and 20 phaeochromocytomas) for inhibin alpha expression. mRNA levels of inhibin alpha subunit were studied in 57 samples and all tissues were stained immunohistochemically with an inhibin alpha subunit-specific antibody. Inhibin alpha mRNA was detected in all adrenocortical tissues. Virilizing adenomas possessed a 10-fold higher median inhibin alpha mRNA expression than did normal adrenals. Bilaterally and nodularly hyperplastic adrenals and other than virilizing adrenocortical tumours had their median inhibin alpha mRNA levels close to those of normal adrenals. Immunohistochemically, inhibin alpha subunit was detectable in all normal and hyperplastic adrenals, as well as in 73% of the adrenocortical tumours. However, the percentage of inhibin alpha-positive cells varied greatly in different tumour types. The median percentage of positive cells was 10 in non-functional and Conn's adenomas, 30 in Cushing's adenomas and 75 in virilizing adenomas. In malignant adrenocortical tumours the median percentage of inhibin alpha-immunopositive cells was 20 in non-functional carcinomas, 30 in Conn's carcinomas, 65 in Cushing's carcinomas and 75 in virilizing carcinomas. All phaeochromocytomas were negative for inhibin alpha subunit both at the mRNA level and immunohistochemically. Our data show that inhibin alpha subunit is highly expressed in both normal and neoplastic androgen-producing adrenocortical cells, with less expression in cortisol-producing and hardly any in aldosterone-producing cells. This suggests a specific role for inhibins in the regulation of adrenal androgen production. We did not find any significant difference in inhibin alpha expression between benign and malignant adrenocortical tumours. Thus inhibin alpha gene does not seem to have a tumour suppressor role in human adrenal cortex.  (+info)

Adrenocortical Carcinoma (Adrenal Cortex Cancer)-Pipeline Review, H1 2015. Summary. Global Markets Directs, Adrenocortical Carcinoma (Adrenal Cortex Cancer)-Pipeline Review, H1 2015, provides an overview of the Adrenocortical Carcinoma (Adrenal Cortex Cancer)s therapeutic pipeline.. This report provides comprehensive information on the therapeutic development for Adrenocortical Carcinoma (Adrenal Cortex Cancer), complete with comparative analysis at various stages, therapeutics assessment by drug target, mechanism of action (MoA), route of administration (RoA) and molecule type, along with latest updates, and featured news and press releases. It also reviews key players involved in the therapeutic development for Adrenocortical Carcinoma (Adrenal Cortex Cancer) and special features on late-stage and discontinued projects.. Global Markets Directs report features investigational drugs from across globe covering over 20 therapy areas and nearly 3,000 indications. The report is built using data ...
The Firm-ACT trial is the first ever conducted randomized controlled phase III trial in adrenocortical carcinoma (ACC), a rare malignancy with poor prognosis. It will provide results leading to the establishment of an urgently needed gold standard chemotherapy regimen for patients with locally advanced or metastatic ACC. To this end the trial compares the two most promising drug combinations investigated in phase II trials, considered by the International Consensus Conference on Adrenal Cancer (Ann Arbor/USA, 2003) as valuable first line treatments for advanced ACC. The first regimen consists of etoposide, doxorubicin, cisplatin plus mitotane (EDP-M), the second regiment employs streptozotocin plus mitotane (Sz-M). Over a period of five years this international trial will include 300 patients with advanced ACC from different European countries. Blood mitotane concentrations will be monitored, aiming at drug levels between 14 - 20 mg/L. Patients not responding to the first line treatment will ...
Rare Cancer News & Clinical Trials » Trial - Adrenocortical Carcinoma » Cabozantinib in Unresectable/Metastatic Adrenocortical ...
Adrenocortical carcinoma is a rare entity. However, it is the most common type of cancerous adrenal gland tumor with poor prognosis. Approximately 4 to 12 per 1 million people develop this type of tumor, which begins in the adrenal cortex. Adrenocortical carcinoma can occur at any age. Women tend to be diagnosed slightly more often than men. In most cases, the cause of cancerous adrenal gland tumor remains unknown. However, people with certain hereditary conditions have a higher risk. Adrenocortical carcinoma can be a functional or nonfunctional tumor. If the tumor is functional, it may produce hormones causing symptoms such as high blood pressure, low potassium level, heart palpitations, nervousness, feelings of anxiety or panic attacks, excessive perspiration, diabetes, Cushing syndrome, unexplained weight gain or weight loss, weakness, abdominal stretch marks, excessive hair growth, changes in genitalia, change in libido, etc. If the tumor is nonfunctional, symptoms occur because the tumor ...
... Summary Global Markets Directs latest Pharmaceutical and Healthcare disease pipeline guide Adrenocortical Carcinoma - Market research report and industry analysis - 10909461
Patients will be randomized 2:1 to receive either single agent OSI-906 (Arm A) or placebo (Arm B) and will be stratified according to prior systemic cytotoxic chemotherapy for ACC, and Eastern Cooperative Oncology Group (ECOG) performance status, and use of ,= 1 oral antihyperglycemic therapy at ...
Adrenocortical cancer (ACC) is a rare disease that is often difficult to diagnose, and therefore often presents at an advanced stage. Various cytotoxic treatments have been tried with little success. Evaluation of new diagnostic methods and improvement of medical therapies are therefore crucial.. The diagnostic potential of 11C-metomidate positron emission tomography (PET) was evaluated in eleven ACC patients. PET visualized all viable tumors with high tracer uptake, including two lesions that CT failed to detect. Necrotic or fibrotic tumors were PET negative. Medication with adrenal steroid inhibitors and chemotherapy may decrease the tracer uptake.. We performed a phase-II study with streptozocin and o,p-DDD (SO) combination therapy in 40 ACC patients. The SO therapy was found to have impact on the disease-free interval (P = 0.02) as well as on survival (P = 0.01) in patients who received adjuvant therapy after curative resection. Complete or partial response was obtained in 36.4% of patients ...
... , also called adrenal cortical carcinoma, is the formation of cancer in the outer layer (cortex) of an adrenal gland. This is the forum for discussing anything related to this health condition
TY - JOUR. T1 - Laparoscopic Versus Open Adrenalectomy for Adrenocortical Carcinoma. T2 - Surgical and Oncologic Outcome in 152 Patients: Editorial Comment. AU - Cadeddu, Jeffrey A. PY - 2011. Y1 - 2011. UR - http://www.scopus.com/inward/record.url?scp=84937218160&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=84937218160&partnerID=8YFLogxK. U2 - 10.1016/j.juro.2010.12.025. DO - 10.1016/j.juro.2010.12.025. M3 - Article. AN - SCOPUS:84937218160. VL - 185. SP - 1222. JO - Journal of Urology. JF - Journal of Urology. SN - 0022-5347. IS - 4. ER - ...
Aims: Structured multicentre efforts are needed if the prognosis of adrenocortical carcinoma (ACC) is to be improved. Data collection may be enhanced through standardised histopathological reporting using criteria such as the recently published Royal College of Pathologists (UK) minimum dataset (MDS). This study aimed to perform a clinicopathological review of the adult patients treated at the Royal Victoria Infirmary, Newcastle upon Tyne, in the 10 years preceding the MDS.. Methods: Case records were examined for all patients diagnosed with ACC between 1996 and 2006. Pathology was reviewed and compared with the Royal College of Pathologists MDS along with the original reports. A systematic evaluation of Ki-67 immunolabelling was also performed.. Results: Eleven patients with ACC were diagnosed and treated. Histopathological reporting according to the MDS identified more features of malignancy than in the original reports (8.5±1.2 versus 5.1±0.8, p,0.02). The median number of microscopic ...
Infinity also announced today that it is adding two additional cohorts to the combination expansion component of the study, one in mesothelioma and one in adrenocortical carcinoma (cancer of the adrenal gland). These two new cohorts are based in part ... ...
Würzburg, Josef-Schneider-Str. 2, 97080 Würzburg, Germany. Available online 3 June 2009. Adrenocortical carcinoma (ACC) is a rare and ...
Find research articles on adrenocortical carcinoma, which may include news stories, clinical trials, blog posts, and descriptions of active studies.
Learn more about Adrenocortical Carcinoma at Portsmouth Regional Hospital DefinitionCausesRisk FactorsSymptomsDiagnosisTreatmentPreventionrevision ...
Learn more about Adrenocortical Carcinoma at TriStar Southern Hills DefinitionCausesRisk FactorsSymptomsDiagnosisTreatmentPreventionrevision ...
Adrenocortical carcinoma is an unusual tumor that tends to be larger than 100 g at diagnosis. Malignant adrenocortical tumors of less than 50 g have been reported rarely. We studied a small adrenocortical carcinoma that weighed 40 g and metastasized 3 1/2 years following bilateral adrenalectomy. The malignancy of adrenocortical tumors is frequently difficult to determine. Two recent studies have proposed histologic criteria for determining the malignancy of adrenal cortical tumors. Since the tumor we studied was initially judged to be benign, we sought to determine whether an extensive evaluation of this tumor using these recent criteria could have identified the tumors potential for metastasizing ...
Adrenocortical cancer is an extremely rare tumor presenting with extensive locoregional spread at the time of diagnosis. Due to the diagnostic difficulties
Dr. Park conferred with experts in pathology. She communicated with oncologists at St. Judes Childrens Hospital in Tennessee, where the leading research on adrenocortical carcinoma is being performed by Dr. Rodriguez-Galindo and Dr. Rubiero. They shared their protocol for treating this rare disease with Dr. Park, and she changed Katies chemo regimen to follow the St. Judes teams protocol. Although the most current treatment was given, and the primary tumor was removed after 5 rounds of chemotherapy, the cancer recurred within a few months (in spite of follow-on drug therapy, as well). The thinking about adrenocortical carcinoma is that it is a slow-growing cancer; this was clearly not the case for Katie! Obviously, more needs to be known about pediatric cancer, which is the main reason why Katie wanted her Endowment to fund solid tumor research. Katies preference was that it fund adrenocortical carcinoma research, but since that is such a rare disease, her Endowment funds solid tumor ...
At the time of disease discovery there may be no symptoms (the tumor may be found incidentally on imaging). In other patients there may be symptoms of hormone excess or complaints referable to an abdominal mass. Hormone excess presents clinically as Cushings syndrome, virilization, feminization, or, less frequently, hypertension with hypokalemia. Hormone hypersecretion can be found in as many as 73%-79% of ACC patients, although not all patients have symptoms (2). In one study, amongst 45 ACC patients, routine biochemistry documented hormone excess in 33 (73%) with excess glucocorticoid and adrenal androgen in 12, isolated glucocorticoid in 11, isolated adrenal androgen in 7, and 17β-estradiol excess in combination with glucocorticoid and adrenal androgen excess in two and one, respectively. Steroid profiling revealed predominantly immature, early-stage steroid precursors, and their production most likely a consequence of altered expression of steroidogenic enzymes in variably undifferentiated ...
A 16-year-old girl with a masculinizing adrenal carcinoma treated surgically is presented. Following surgery a full clinical and steroid remission has been achieved, without any adjuvant chemotherapy. In the 7th year after the surgical treatment the patient became pregnant. Pregnancy and labour were uncomplicated. The patient continues in complete remission, and her son has been noted to have normal development at 21 mth of age.
The main limitation of studying this cancer type is the limited access to human samples, together with the lack of representative cell lines, and the absence of a reliable small animal model of disease. This has significantly challenged the study of this neoplasm for a long time. Additionally, it is difficult to successfully culture the ACC primary tumour cells for periods enough to carry out truly mechanistic studies in the lab. However, with new advances in tissue engineering techniques and biomaterials, we intend to reproduce an ACC tumour by culturing in 3D using collagen-I biomaterial and co-culturing with macrophages. Also, previous research within this field has informed us of several mutated genes such as Steroidogenic factor 1 or SF1. SF-1 is a nuclear receptor that belongs to the NR5A of orphan receptors which binds nuclear DNA. It is involved in adrenal and gonadal development, sexual determination, reproduction, and steroidogenesis. However, several other genes are mutated, and more ...
A new study showed staging system that incorporates the patients age better and predicts 5-year survival among patients with stages I/II ACC. Consideration should be given to include age in staging for ACC, because it may better inform providers about treatment and prognosis.[2] ...
Katies Comforters Guild is listed as one of the guilds that supports cancer research. The guilds connection to cancer research is 1) because Katie died of cancer, 2) our family and friends created the Katie Gerstenberger Endowment for Cancer Research in 2007 and 3) we began our work by sewing quilts for children in the cancer ward at Seattle Childrens Hospital - and weve now expanded to blanket the entire hospital. As you know, Katies endowment is for solid tumor research, to help find a cure for the kind of tumor she had (adrenocortical carcinoma). Since adrenocortical carcinoma is very rare, Katies endowment supports ALL solid tumor research with the income that is generated by the principal in the endowment. At last count, the principal was just over $100,000. ...
This page was last edited 16:23, 25 September 2017 by Mohammed Medhat. Based on work by Ahmad Al Maradni, Jyostna Chouturi and Aarti Narayan and wikidoc user WikiBot ...
This is an open-label Phase 1/2 study to assess the maximum tolerated dose of cintredekin besudotox (IL-13PE, hlLl3-PE38QQR) and the therapeutic respons
Diagnostic and prognostic value of nucleolar proteins in the regulation of tumor cells proliferation in patients with lung carcinoma and adrenocortical cancer
A rare disease in which cancer cells are found in the adrenal cortex. Cancer of the adrenal cortex is also called adrenocortical carcinoma. The inside layer of the adrenal gland is called the adrenal medulla. Cancer that starts in the adrenal medulla is called pheochromocytoma.
Health, ... Sol H. Weiss shareholder at law firm Anapol Schwartz Weiss Coha...Philadelphia (PRWEB) August 20 2008 -- a href http://www.anapolschw...Weiss is currently co-plaintiffs liaison counsel for more than 800 v...Active in the legal community Weiss is a member of the American Pen...,Anapol,,Schwartz,Attorney,Named,to,Executive,Committee,of,American,Association,for,Justice,medicine,medical news today,latest medical news,medical newsletters,current medical news,latest medicine news
The semi-automated fluorometric microculture cytotoxicity assay (FMCA), based on the measurement of fluorescence generated from cellular hydrolysis of fluorescein diacetate (FDA) by viable cells, was employed for cytotoxic drug sensitivity testing of tumor cells from patients with hematological or solid tumors. In total, 390 samples from 20 diagnoses were tested with up to 12 standard cytotoxic drugs. The technical success rate for different tumor types ranged from 67 to 95%. Fluorescence was linearly related to cell number but variably steep depending on tumor type. Samples from most solid tumors thus showed higher signal-to-noise ratios than hematological samples. A wide spectrum of in vitro drug activity was obtained, with acute leukemias and non-Hodgkins lymphomas being sensitive to almost all tested drugs, whereas renal and adrenocortical carcinomas were essentially totally resistant. Between these extremes were samples of breast and ovarian carcinomas and sarcomas. When in vitro response was
Background:. MicroRNA (miRNA)-503 is known to be down-regulated in several types of cancer, including oral, hepatocellular, gastric, and endometrial, suggesting that it plays a tumor-suppressor role in carcinogenesis. In contrast, other recent reports have demonstrated up-regulation of miR-503 in adrenocortical carcinoma, parathyroid carcinoma, and retinoblastoma, compared with adjacent normal tissues. Collectively, miR-503 shows tissue- or disease-specific expression patterns. However, to the best of our knowledge, miR-503 expression pattern, its clinical significance and molecular mechanism in colorectal cancer (CRC) have not been investigated.. Materials and Methods:. We analyzed miR-503 expression in a subset of 69 tissue samples from normal colonic mucosa (n = 20), adenoma (n = 29) and CRC (n = 20). Next, we further quantified miR-503 expression in a larger, independent cohort, which included CRC tissues from 181 patients, and investigated the clinical significance of miR-503 in CRC. In ...
Background:. MicroRNAs (miRNAs) are a class of small non-coding RNAs that inhibit gene expression by binding to 3` untranslated regions of mRNAs and inhibiting their translation. MiRNAs crucially affect cellular processes such as development, proliferation, differentiation and apoptosis, which are deregulated in cancer. MiR-503 is located at Xq26.3 and belongs to an extended miR-16 family of miRNAs. MiR-503 is down-regulated in several types of cancer, including oral, hepatocellular, gastric, and endometrial cancer, suggesting that it plays a tumour-suppressor role in carcinogenesis. In contrast, other recent reports have demonstrated up-regulation of miR-503 in adrenocortical carcinoma, parathyroid and retinoblastoma, compared with adjacent normal tissue. These results suggest that miR-503 shows tissue- or disease-specific expression patterns. However, miR-503 expression patterns in esophageal cancer (EC) and normal esophageal tissue have not been compared and the correlation of miR-503 ...
Clinical trial for Adrenocortical carcinoma , Cabazitaxel Activity in Patients With Advanced AdrenoCortical-Carcinoma Progressing After Previous Chemotherapy Lines
U.S. 1930 Census, Madison, Dane County, Wisconsin, population schedule, ED 13-31, sheets 10B-11A, house 181, family 274, family of J F Weiss [Joseph Weiss]; digital image, Ancestry.com (http://www.ancestry.com/search/db.aspx?dbid=6224&enc=1 : accessed 8 Aug 2012); citing NARA microfilm T626, roll 2566.. ...
Eric L. Weiss, MD is on CAP Network. CAP Network is a virtual workspace, to support collaboration among faculty, graduate students, postdocs and staff.
As with the DS1-MK3, the cooperation between Daniel Weiss and Softube has paid off, which is why the Compressor/Limiter with all its functions can also convince Weiss during testing. The result is an exceptionally clear and transparent sound that is simply fun to master. Advanced waveform metering, parameters such as attack, release, knee, ration, threshold, low pass and bandpass filters, a mid/side function and parallel compression are also included. In short, everything you need to get the most out of a signal.
Ronald Ehrenberg, industrial and labor relations; Anthony Ingraffea, civil and environmental engineering; and Paul Sherman, neurobiology and behavior, are the 2005 recipients of the Stephen H. Weiss Presidential Fellowships for effective, inspiring and distinguished teaching of undergraduate students. (November 09, 2005)
Visit Healthgrades for information on Dr. Barry Weiss, DDS Find Phone & Address information, medical practice history, affiliated hospitals and more.
Teklu, A. M., Tsegaye, E., Fekade, D., Hailemelak, A., Weiss, W. M., Hassen, E., Simmons, N., Zewdu, S., Berhan, Y., Getachew, A., Hagos, T., Alebachew, A., Damena, M., Sitotaw, Y., Assefa, Y., Medhin, G. & Ruff, A. J., Feb 1 2017, In : Ethiopian journal of health sciences. 27, p. 3-16 14 p.. Research output: Contribution to journal › Article ...
Alison Weiss, PhD is a member of the University of Cincinnati College of Medicine and Professor of Molecular Genetics, Biochemistry and Microbiology
Introductory Statistics 9th edition by Neil A. Weiss Test bank Questions Full Chapters are included Download Free Sample Do you need Solution manual for this
James M Weiss, M.D. specializes in Internal Medicine and Pulmonary and is located in Newport Beach, CA. Choose a doctor that chooses Hoag. Call (949) 566-8179
WEISS Steinpflegeprodukte is exhibiting the product Z.IMP at Stone tec 2015 in Nuremberg Germany. Search for further products and novelties.
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Fingerprint Fingerprint is based on mining the text of the persons scientific documents to create an index of weighted terms, which defines the key subjects of each individual researcher. ...
J:106993 Briancon N, Weiss MC, In vivo role of the HNF4alpha AF-1 activation domain revealed by exon swapping. EMBO J. 2006 Mar 22;25(6):1253-62 ...
Kiani S*, Chavez A*, Tuttle M, Hall RN, Chari R, Ter-Ovanesyan D, Qian J, Pruitt BW, Beal J, Vora S, Buchthal J, Kowal EJ, Ebrahimkhani MR, Collins JJ, Weiss R, Church G. Cas9 gRNA engineering for genome editing, activation and repression. Nat Methods. 2015 Sep 7. doi: 10.1038 (* co-first authors) ...
O. Francescangeli, V. Stanic, S. I. Torgova, A. Strigazzi, N. Scaramuzza, C. Ferrero, I. P. Dolbnya, T. M. Weiss, R. Berardi, L. Muccioli, S. Orlandi, and C. ...
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The structure was refined using the CNS program. The R value is 0.262 for 14484 reflections in the resolution range 15.0 to 1.8 Ångstroms with Fobs , 0.0 sigma(Fobs) and with I , 0.0 sigma(I) ...
Looking for online definition of adrenocortical carcinoma in the Medical Dictionary? adrenocortical carcinoma explanation free. What is adrenocortical carcinoma? Meaning of adrenocortical carcinoma medical term. What does adrenocortical carcinoma mean?
Mitotane (o,p′-DDD) is the standard treatment for advanced adrenocortical carcinoma (ACC). Monitoring of plasma mitotane levels is recommended to look for a therapeutic window between 14 and 20mg/L, but its positive predictive value requires optimization. We report the case of an ACC patient with a history of dyslipidemia treated with mitotane in whom several plasma mitotane levels ,30mg/L were found together with an excellent neurological tolerance. This observation led us to compare theoretical or measured o,p′-DDD and o,p′-DDE levels in a series of normolipidemic and dyslipidemic plasma samples to explore potential analytical issues responsible for an overestimation of plasma mitotane levels. We demonstrate an overestimation of mitotane measurements in dyslipidemic patients. Mitotane and o,p′-DDE measurements showed a mean 20% overestimation in hypercholesterolemic and hypertriglyceridemic plasma, compared with normolipidemic plasma. The internal standard p,p′-DDE measurements ...
TY - JOUR. T1 - Laparoscopic resection of adrenal cortical carcinoma. T2 - A cautionary note. AU - Gonzalez, Ricardo J.. AU - Shapiro, Suzanne. AU - Sarlis, Nicholas. AU - Vassilopoulou-Sellin, Rena. AU - Perrier, Nancy D.. AU - Evans, Douglas B.. AU - Lee, Jeffrey E.. AU - Inabnet, William B.. AU - Libutti, Steven K.. AU - Chen, Herbert. AU - Duh, Quan Yang. AU - Wilhelm, Scott. PY - 2005/12/1. Y1 - 2005/12/1. N2 - Background. While laparoscopic removal of small, benign, functioning adrenal tumors is accepted, laparoscopic resection of adrenal tumors that may be adrenal cortical carcinoma (ACC) remains controversial. Methods. The records of all patients with ACC evaluated at a single institution from 1991 through 2004 were reviewed retrospectively. Results. Among 170 patients with ACC, 153 patients underwent open anterior adrenalectomy, 6 underwent laparoscopic adrenalectomy, 1 was treated via an open flank approach, and 10 had no operation. At a median follow-up of 28 months, 115 (86%) of 133 ...
TY - JOUR. T1 - P-glycoprotein expression and multidrug resistance in adrenocortical carcinoma. AU - Flynn, Stuart D. AU - Murren, J. R.. AU - Kirby, W. M.. AU - Honig, J.. AU - Kan, L.. AU - Kinder, B. K.. PY - 1992. Y1 - 1992. N2 - Background. The response of adrenocortieal carcinoma (ACC) to adjuvant chemotherapy has been disappointing with no significant impact on survival. The normal adrenal cortex has very high levels of P-glycoprotein, an energy-dependent efflux pump of a variety of structurally unrelated chemotherapeutic agents. P-glycoprotein has been implicated as a cause of multidrug resistance in a variety of neoplasms. The purpose of this study was to evaluate P-glycoprotein expression in ACC. Methods. Eleven patients with ACC had paraffin-em bedded tumor evaluated for P-glycoprotein expression. These were analyzed by immunohistochemistry assay with a battery of four anti-P-glycoprotein antibodies (MRK-16, JSB-1, UIC-2, MDR). Results. All eleven cases showed intense, predominantly ...
Context: Adrenocortical cancer (ACC) is an aggressive tumor with a heterogeneous outcome. Prognostic stratification is difficult even based on tumor stage and Ki67. Recently integrated genomics studies have demonstrated that CpG islands hypermethylation is correlated with poor survival. Objective: The goal of this study was to confirm the prognostic value of CpG islands methylation on an independent cohort. Design: Methylation was measured by methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA). Setting: MS-MLPA was performed in a training cohort of 50 patients with ACC to identify the best set of probes correlating with disease-free survival (DFS) and overall survival (OS). These outcomes were validated in an independent cohort from 21 ENSAT centers. Patients: The validation cohort included 203 patients (64% women, median age 50 years, 80% localized tumors). Main Outcome Measures: DFS and OS. Results: In the training cohort, mean methylation of 4
The focus on the refinement, reduction and replacement of animal use in toxicity testing requires the development of cell-based systems that mimic the effects of xenobiotics in human tissues. The human adrenocortical carcinoma cell line, H295R, has been
The Official Patients Sourcebook on Adrenocortical Carcinoma: A Revised and Updated Directory for the Internet Age von Icon Health Publications und Buchbewertungen gibt es auf ReadRate.com. Bücher können hier direkt online erworben werden.
TY - JOUR. T1 - Mitotane enhances cytotoxicity of chemotherapy in cell lines expressing a multidrug resistance gene (mdr-1/P-glycoprotein) which is also expressed by adrenocortical carcinomas. AU - Bates, Susan E.. AU - Shieh, Ching Yi. AU - Mickley, Lyn A.. AU - Dichek, Helén L.. AU - Gazdar, Adi. AU - Loriaux, Donald (Lynn). AU - Fojo, Antonio Tito. PY - 1991/7. Y1 - 1991/7. N2 - P-Glycoprotein (Pgp), product of the mdr-1 gene, is a 130- to 180-kDa plasma membrane phosphoglycoprotein which mediates multidrug resistance in cell culture by increasing efflux of the natural product chemotherapeutic agents. High levels of expression of mdr-1/Pgp are found in both the normal adrenal and adrenocortical cancers. By RNA in situ hybridization the expression in adrenocortical cancer is shown to be widely distributed. The present study demonstrates that decreased drug accumulation mediated by mdr-1/Pgp can be overcome by clinically achieveable concentrations of mitotane (o,p′-DDD). The increase in drug ...
Abstract: Adrenocortical cancer (ACC) is a rare and aggressive endocrine tumor. The patient presented with a large retroperitoneum tumor and lung metastases. Removal of the adrenocortical tumor with part of the transverse colon and tail of the pancreas, spleen and kidney was successfully performed following chemotherapy. Levels of serum neuron-specific enolase (NSE) were found to be markedly high before surgery and may be clinically useful markers for monitoring tumor status during management. Immunohistochemical studies showed that the cancer cells were positive for NSE and overexpression of p53. We identified a novel germ line variant of the 177 mutant (Pro to Arg; P177R) of p53 by genomic sequencing. The genetic and biochemical data presented in this case confirm the importance of screening for p53 status in ACC with inherited cancer syndrome.. ...
Splenic arteriogastric fistula is a rare cause of upper gastrointestinal (GI) hemorrhage, only reported a handful of times in the literature. Herein, we present a case of a 49-year-old woman with metastatic adrenocortical carcincoma who developed a fistula between the splenic artery and gastric lumen as a result of local invasion of her primary tumor. This fistula led to several episodes of massive upper GI bleeding. Selective splenic artery embolization was successful in ceasing the GI bleed; however, the intervention was not timely enough for the patient to survive the hemorrhage. We outline several clinical and imaging findings to assist physicians with earlier detection of splenic arteriogastric fistulas, and advocate prophylactic selective splenic artery embolization when this rare but highly fatal entity is discovered.
Mitotane (o,p′-DDD) is the standard treatment for advanced adrenocortical carcinoma (ACC). Monitoring of plasma mitotane levels is recommended to look for a therapeutic window between 14 and 20mg/L, but its positive predictive value requires optimization. We report the case of an ACC patient with a history of dyslipidemia treated with mitotane in whom several plasma mitotane levels ,30mg/L were found together with an excellent neurological tolerance. This observation led us to compare theoretical or measured o,p′-DDD and o,p′-DDE levels in a series of normolipidemic and dyslipidemic plasma samples to explore potential analytical issues responsible for an overestimation of plasma mitotane levels. We demonstrate an overestimation of mitotane measurements in dyslipidemic patients. Mitotane and o,p′-DDE measurements showed a mean 20% overestimation in hypercholesterolemic and hypertriglyceridemic plasma, compared with normolipidemic plasma. The internal standard p,p′-DDE measurements ...
To date, renin-producing tumors are very rare, and most of them are of renal origin. Of these, the juxtaglomerular cell tumor was the most frequent. An extrarenal renin-producing tumor is extremely rare.6 Non-renal renin-producing tumors include carcinoma of the lung, pancreas, urinary bladder and ovary.7 To the best of our knowledge, there have been only two cases of renin-producing adrenal tumor reported before. Our case is the third such case reported but it is different to the case reported by Iimura et al. in the steroid synthetic pattern (tumor produced corticosteroids and sex steroids) and to the case of K. Yamanaka et al. in the characteristics of Cushings syndrome. Our case only exhibited hyperreninism, hyperaldosteronism and hypertension, but Cushings syndrome or steroid overproduction were not observed. Maybe the huge adrenal tumor could compress the renal artery, which might elevate the PRA. After immunohistochemical staining, the diagnosis of renin-producing adrenocortical ...
Purpose: To define a mitotane dose for pediatric patients with adrenocortical cancer (ACC) that maintains therapeutic plasma levels (TL) between 14 and 20 mu g/mL and to verify its antitumor efficacy in association with 8 cycles of cisplatin, etoposide, and doxorubicin (CED). Methods: Powdered mitotane was dissolved in a medium chain triglyceride oil and administered to 11 children with ACC (2.4 to 15.4 y of age); an initial low dose was increased to 4 g/m(2)/d. Ten of the 11 children had a germline TP53 R337H mutation. Mitotane plasma levels were determined using high-performance liquid chromatography. Results: The mitotane dose to maintain TL in 7 patients ranged from 1.0 to 5.3 g/m(2)/d. Six children reached mitotane levels of 10 mu g/mL in 3.6 months (1.5 to 5.0mo), whereas 5 children took 8 months (6.5 to 12.5 mo). Minor to partial tumor remission was found in 5 patients (, 1 y) and complete remission was found in 2 patients. Of the 3 patients who are alive at the time of report, 1 patient ...
This project is supported by the Canadian Institutes of Health Research (award #111062), Alberta Innovates - Health Solutions, and by The Metabolomics Innovation Centre (TMIC), a nationally-funded research and core facility that supports a wide range of cutting-edge metabolomic studies. TMIC is funded by Genome Alberta, Genome British Columbia, and Genome Canada, a not-for-profit organization that is leading Canadas national genomics strategy with funding from the federal government. Maintenance, support, and commercial licensing is provided by OMx Personal Health Analytics, Inc. Designed by Educe Design & Innovation Inc. ...
Purpose: Adrenocortical carcinoma (ACC) is a rare and aggressive cancer, and no current effective therapy is available for locally advanced and metastatic ACC. Drug repurposing is an emerging approach for identifying new indications for existing drugs, especially for rare cancers such as ACC. The objective of this study was to use quantitative high-throughput screening to identify agents with antineoplastic activity against ACC. Experimental Design: A screening of 4,292 compounds was performed on three ACC cell lines: BD140A, SW-13, and NCI-H295R. Results: Twenty-one active compounds were identified, with an efficacy of ,80% in all three cell lines. Of these, niclosamide showed higher efficacy and lower IC50 than established anti-ACC drugs. We then validated niclosamide-inhibited cellular proliferation in all three ACC cell lines. Next, we investigated the mechanism by which niclosamide inhibited ACC cell proliferation, and found that it induced caspase-dependent apoptosis and G1 cell cycle ...
... and its derivatives are active against the HIV virus 15 and the herpes simplex virus type 2. [35] [Lin TS, Schinazi. Selective inhibition of human immunodeficiency virus type 1replication by the (-) but not the (+) enantiomer of gossypol. Antimicrob Agents Chemother. 1989 Dec;33(12):2149-51]. A trial evaluated the therapeutic efficacy of gossypol for the treatment of metastatic carcinoma of the endometrium or ovary, and as an antiviral and interferon inducer in patients with AIDS [36] [Wu D. An overview of the clinical pharmacology and therapeutic potential of gossypol as a male contraceptive agent and in gynaecological disease. Drugs . 1989;38:333-341]. At low doses (30 mg/kg), the drug reduces 65% the tumor size and induces tumor mortality (8%) in nude-mice SW-13 adrenocortical carcinoma [24] [Wu, Y.W., Chik, C. L., Knazek, R. A., An in vitro and in vivo study of antitumor effects of gossypol on human SW-13 adrenocortical carcinoma, Cancer Res. 1989, 49, 3754 -3758.] . Furthermore, in ...
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Treatment:. The main method of adrenal tumor treatment is surgery.. At the first stage of tumor development, when the formation does not exceed 5 cm and there is no metastasis, laparoscopic removal is performed.. If the tumor has reached the second stage of development and has grown more than 5 cm, then the method of removal is determined by doctors based on MRI or CT.. At stage 3 of adrenal cancer, when the tumor affects the lymph nodes, a cavitary surgery is indicated. During removal, the surgeon examines nearby organs and tissues for the presence of metastases.. Adrenal cancer of the 4th stage is usually accompanied by metastatic sprouting in the tissue of the kidneys, liver, etc. Such tumors are not always operable. The possibility of prompt removal is determined by the doctor individually.. As additional treatment, other methods are used. Radiotherapy is actively used in pheochromocytomas.. A patient can get a radioactive isotope injection, which kills cancer cells, reducing the size of the ...
Note 2: Except for histologies that have strictly histology-based CS schemas (for example lymphoma), all cases with primary site adrenal gland (C74._) are coded with this schema. However, only adrenal cortical carcinomas will have AJCC stage derived (7th Edition only). Adrenal cortical carcinoma is identified as C74.0 (adrenal cortex) with histology 8010, 8140, or 8370 OR C74.9 (adrenal gland, NOS) with histology 8370 ...
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An interesting phenomenon consists of adrenal collision tumors. Thus a contiguous adrenal adenoma and metastasis results in the adenoma component displaying a signal loss on opposed-phase MR images and the metastatic component increasing in signal intensity. At times neither a biopsy nor a resected specimen allows adequate evaluation of an adrenocortical tumor if only histologic criteria are employed; immunohistologic staining is often helpful. Nevertheless, even then the true nature of a tumor may not be apparent. For example, CT and US discovered an incidental homogeneous adrenal tumor in a 43-year-old woman; endocrine tests revealed preclinical Cushings syndrome. An adrenalectomy was performed, and histology revealed an adrenocorticaltumor of undetermined nature, 4 months later the patient presented with a metastatic cortisol and androgen-producing adrenocortical carcinoma ...
Purpose: ,p,Adrenal incidentalomas must be differentiated from adrenocortical cancer (ACC). Currently, size, growth, and imaging characteristics determine the potential for malignancy but are imperfect. The aim was to evaluate whether urinary small molecules (,800 Da) are associated with ACC.,/p, ,p,Experimental Design:,/p, ,p,Preoperative fasting urine specimens from patients with ACC (n=19) and benign adrenal tumors (n=46) were analyzed by unbiased ultra performance liquid chromatography/mass spectrometry. Creatinine-normalized features were analyzed by Progenesis, SIMCA, and unpaired t-test adjusted by false discovery rate. Features with an AUC ,0.8 were identified through fragmentation patterns and database searches. All lead features were assessed in an independent set from patients with ACC (n=11) and benign adrenal tumors (n=46) and in a subset of tissue samples from patients with ACC (n=15) and benign adrenal tumors (n=15) in the training set.,/p, ,p,Results:,/p, ,p,Sixty-nine features ...
Yahashiri, A., Jorgenson, M. A. & Weiss, D. S. (2017). The SPOR Domain, a Widely Conserved Peptidoglycan Binding Domain That Targets Proteins to the Site of Cell Division. J Bacteriol, 199(14), e00118-17. PMID: 28396350.. Ransom, E. M., Weiss, D. S. & Ellermeier, C. D. (2016). Use of mCherryOpt Fluorescent Protein in Clostridium difficile. Methods Mol Biol, 1476, 53-67. PMID: 27507333.. Yahashiri, A., Jorgenson, M. A. & Weiss, D. S. (2015). Bacterial SPOR domains are recruited to septal peptidoglycan by binding to glycan strands that lack stem peptides. Proc Natl Acad Sci U S A, 112(36), 11347-52. PMID: 26305949.. Weiss, D. S. (2015). Last but not least: new insights into how FtsN triggers constriction during Escherichia coli cell division. (Vols. 95). (6), pp. 903-9. Mol Microbiol. PMID: 25571948.. Ransom, E. M., Ellermeier, C. D. & Weiss, D. S. (2015). Use of mCherry Red fluorescent protein for studies of protein localization and gene expression in Clostridium difficile. Appl Environ ...
Samuel Weiss is a neurobiologist. Weiss was an undergraduate at McGill University, where he received a B.Sc. in Biochemistry. He then went on to take his Ph.D. in Neurobiology at the University of Calgary. From 1983 to 1988 he held two postdoctoral fellowships funded by the AHFMR and the Medical Research Council of Canada (now the Canadian Institutes of Health Research), the first at the Centre de Pharmacologie-Endocologie, Montpellier, France, and the second at the University of Vermont College of Medicine. In 1985 Dr. Weiss and Fritz Sladeczek discovered the metabotropic glutamate receptor, currently an extremely important area of research for neurological disorders. Dr. Weiss was appointed Assistant Professor and MRC Scholar at The University of Calgary in 1988. In 1992, while working at the University of Calgary, Dr. Weiss and graduate student Brent Reynolds found cells in the brains of fetal and adult mice that divided to produce new cells. They claimed that they successfully isolated stem ...
Yin, A., Ettaieb, M. H. T., Swen, J. J., van Deun, L., Kerkhofs, T. M. A., van der Straaten, R. J. H. M., ... Moes, D. J. A. R. (2020). Population Pharmacokinetic and Pharmacogenetic Analysis of Mitotane in Patients with Adrenocortical Carcinoma: Towards Individualized Dosing. Clinical Pharmacokinetics. https://doi.org/10.1007/s40262-020-00913-y ...
Background: Adrenocortical carcinomas (ACCs) are among the most common childhood cancers occurring in infants affected with the Li-Fraumeni and Li- Fraumeni-like (LFS/LFL) syndromes, which are caused by dominant germline mutations in the TP53 gene. In Brazil, a particular mutation, occurring in the tetramerisation domain of the gene, p.R337H, is exceedingly common due to a founder effect and is strongly associated with ACC. In this report, we describe the phenotype and long-term clinical follow-up of a female child diagnosed with ACC and homozygous for the TP53 p.R337H founder mutation. Case presentation: At age 11 months, the patient was diagnosed with a virilising anaplastic adrenal cortical tumour, which was completely excised without disturbing the adrenal capsule. Family history was consistent with an LFL tumour pattern, and genotyping identified the TP53 p.R337H mutation in both alleles in genomic DNA from lymphocytes and fibroblasts. Haplotype analysis confirmed the occurrence of the ...
Prostaglandins can be synthesized in an adrenocortical carcinoma, and they can work in an autocrine or paracrine fashion. In rabbit chondrocyte and human squamous carcinoma cell lines, EGF induced the secretion of PGE2 via up-regulation of the activities of phospholipase A2 (PLA2) and COX-2 (Sato et al. 1997, Huh et al. 2003). This may suggest that PGE2 acts as a secondary factor to EGF in the up-regulation of aromatase expression. Therefore, we checked whether PGE2 was secreted from NCI-H295R cells in response to EGF. In this study, NCI-H295R cells secreted PGE2 in response to EGF (Fig. 13), and PGE2 increased aromatase activity to a greater extent than other prostaglandins (Fig. 6). The inhibition of EGF-induced aromatase expression with PGE2 receptor antagonists confirmed that PGE2 is the secondary factor of aromatase expression with EGF (Fig. 14). PGE1 also increased aromatase activity to a degree similar to that of PGE2, but EGF could not stimu- late NCI-H295R cells to secrete a sufficient ...
Adrenocortical carcinomas (ACC) are aggressive cancers originating in the cortex of the adrenal glands. Despite the overall poor prognosis, ACC outcome is heterogeneous. CTNNB1 and TP53 mutations are frequent in these tumors, but the complete spectrum of genetic changes remains undefined. Exome sequencing and SNP array analysis of 45 ACC revealed recurrent alterations in known drivers (CTNNB1, TP53, CDKN2A, RB1, MEN1) and genes not previously reported to be altered in ACC (ZNRF3, DAXX, TERT and MED12), which were validated in an independent cohort of 77 ACC. The cell-surface transmembrane E3 ubiquitin ligase ZNRF36 was the gene the most frequently altered (21%), and appears as a potential novel tumor suppressor gene related to the ß-catenin pathway.Our integrated genomic analyses led to the identification of two distinct molecular subgroups with opposite outcome. The C1A group of poor outcome ACC was characterized by numerous mutations and DNA methylation alterations, whereas the C1B group with ...
Adrenocortical tumors consist of benign adenomas and highly malignant carcinomas with a still incompletely understood pathogenesis. A total of 46 adrenocortical tumors (24 adenomas and 22 carcinomas) were investigated aiming to identify novel genes involved in adrenocortical tumorigenesis. High-resolution single nucleotide polymorphism arrays (Affymetrix) were used to detect copy number alterations (CNAs) and copy neutral losses of heterozygosity (cnLOH). Genomic clustering showed good separation between adenomas and carcinomas, with best partition including only chromosome 5, which was highly amplified in 17/22 malignant tumors. The malignant tumors had more relevant genomic aberrations than benign tumors, such as a higher median number of recurrent CNA (2631 vs 94), CNAs ,100 Kb (62.5 vs 7) and CN losses (72.5 vs 5.5), and a higher percentage of samples with cnLOH (91% vs 29%). Within the carcinoma cohort, a precise genetic pattern (i.e. large gains at chr 5, 7, 12, and 19, and losses at chr ...
... is an autosomal-dominant familial cancer syndrome that results in an increased lifelong risk of what are considered Li-Fraumeni syndrome spectrum tumors (e.g., soft tissue sarcoma, osteosarcoma, brain tumor, premenopausal breast cancer, adrenocortical carcinoma, leukemia, lung bronchoalveolar cancer), among others. About 3/4 of patients have a mutation in the gene encoding the p53 tumor suppressor protein (TP53). The cancers arent limited to those listed above, however, and patients can have a wide range of malignancies, including melanoma, germ-cell tumors, gastric carcinoma, Wilms tumor, lymphoma, and lung, laryngeal, prostate, and pancreatic cancers ...
The majority of LFS (about 70 percent) is caused by mutations in a gene on chromosome 17 known as p53. Mutations in p53 confer an increased risk for early onset breast cancer, childhood sarcoma, osteosarcoma, brain tumors, leukemia, and adrenocortical carcinoma.. People with a p53 mutation have a 50 percent chance of developing one of the associated cancers by age 40 and a 90 percent chance of developing cancer by age 60. Breast cancer appears to be the greatest risk for women, but less than 1 percent of all breast cancer is thought to be related to LFS. For those affected by LFS, breast cancers generally occur in premenopausal women.. The p53 gene is a tumor suppressor gene, which usually controls cell growth and cell death. Both copies of a tumor suppressor gene must be altered, or mutated, before a person will develop cancer. With LFS, the first mutation is inherited from either the mother or the father and is therefore present in all cells of the body. This is called a germline mutation. ...
The majority of LFS (about 70 percent) is caused by mutations in a gene on chromosome 17 known as p53. Mutations in p53 confer an increased risk for early onset breast cancer, childhood sarcoma, osteosarcoma, brain tumors, leukemia, and adrenocortical carcinoma.. People with a p53 mutation have a 50 percent chance of developing one of the associated cancers by age 40 and a 90 percent chance of developing cancer by age 60. Breast cancer appears to be the greatest risk for women, but less than 1 percent of all breast cancer is thought to be related to LFS. For those affected by LFS, breast cancers generally occur in premenopausal women.. The p53 gene is a tumor suppressor gene, which usually controls cell growth and cell death. Both copies of a tumor suppressor gene must be altered, or mutated, before a person will develop cancer. With LFS, the first mutation is inherited from either the mother or the father and is therefore present in all cells of the body. This is called a germline mutation. ...
FUNCTION: [Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene is one of several tumor-suppressing subtransferable fragments located in the imprinted gene domain of 11p15.5, an important tumor-suppressor gene region. Alterations in this region have been associated with the Beckwith-Wiedemann syndrome, Wilms tumor, rhabdomyosarcoma, adrenocortical carcinoma, and lung, ovarian, and breast cancer. This gene is imprinted, with preferential expression from the maternal allele. Mutations in this gene have been found in Wilms' tumor and lung cancer. This protein may act as a transporter of organic cations, and have a role in the transport of chloroquine and quinidine-related compounds in kidney. Several alternatively spliced transcript variants encoding different isoforms have been described. [provided by RefSeq, Oct 2015 ...
Another area of interest is the role of GATA factors in the regulation of steroidogenic cell differentiation. Our experimental system takes advantage of the observation that GATA-4 normally is expressed in gonadal but not adrenocortical steroidogenic cells of the adult mouse. Interestingly, certain inbred strains of mice develop sex steroid-producing adrenocortical neoplasms in response to prepubertal gonadectomy. This phenomenon is thought to reflect metaplasia of competent cells in the adrenal gland, which transform into gonadal-like stroma in response to changes in the hormonal milieu, and increased expression of GATA4 is a hallmark of this transformation. To examine the signaling pathways involved in this form of tissue-type switching, we have created new inbred and transgenic models of adrenocortical neoplasia .. ...
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Small, M; Lasser, weiss M.; and Daniel, V, "Release of immature cells from the thymus during solid tumor growth: identification by assay of tdt activity." (1979). Subject Strain Bibliography 1979. 4628 ...
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Adrenocortical Tumors: Improving the Practice of the Weiss System Through Virtual Microscopy: A National Program of the French Network INCa-COMETE. Tissier F, Aubert S, Leteurtre E, Al Ghuzlan A, Patey M, Decaussin M, Doucet L, Gobet F, Hoang C, Mazerolles C, Monges G, Renaudin K, Sturm N, Trouette H, Vacher-Lavenu MC, Viallon V, Baudin E, Bertagna X, Coste J, Libe R. Am J Surg Pathol. 2012 Aug;36(8):1194-1201. PMID: (...). ...
Genetic testing should be considered with adrenocortical carcinoma; carcinoid tumors; diffuse gastric cancer; fallopian tube/ ... leukaemia and adrenocortical carcinoma. Individuals with Li-Fraumeni syndrome often have multiple independent primary cancers. ... but also increases the risk of fallopian tube carcinoma and papillary serous carcinoma of the peritoneum. In men the risk of ... Nevoid basal cell carcinoma syndrome (NBCCS), also known as Gorlin syndrome, is an autosomal dominant cancer syndrome in which ...
80% of children with adrenocortical carcinoma and 2%-10% of childhood brain tumors have p53 mutations. ... a proband who is diagnosed with adrenocortical carcinoma or choroid plexus tumour, irrespective of family history ... lymphoma and adrenocortical carcinoma.. ~90% of females with LFS develop breast cancer by age 60 years; the majority of these ... adrenocortical carcinoma, leukemia or lung bronchoalveolar cancer - before age 46 years; ...
Allolio B, Fassnacht M (2006). "Adrenocortical Carcinoma: Clincal Update". J Clin Endocrinol Metab. 91 (6): 2027-2037. doi: ... excluding Cushing's Another cause for Cushing's syndrome is adrenocortical carcinoma (ACC). This is a rare form of cancer with ...
MBZ significantly inhibited cancer cell growth, migration, and metastatic formation of adrenocortical carcinoma, both in vitro ... Martarelli D, Pompei P, Baldi C, Mazzoni G (April 2008). "Mebendazole inhibits growth of human adrenocortical carcinoma cell ...
... was introduced in 1960 for the treatment of adrenocortical carcinoma. Mitotane is the INN, USAN, BAN, and JAN of ... 1888-. ISBN 1-4557-1126-8. Hahner S, Fassnacht M (April 2005). "Mitotane for adrenocortical carcinoma treatment". Current ... Mitotane has been produced by Bristol Myers Squibb SpA but it is marketed as an orphan drug for adrenocortical carcinoma due to ... "Adjuvant mitotane treatment for adrenocortical carcinoma". N Engl J Med. 356 (23): 2372-2380. doi:10.1056/NEJMoa063360. PMID ...
It was initially isolated in 1980 from a 48-year-old female patient diagnosed with adrenocortical carcinoma. The initial ... Wang T, Rainey WE (2012). "Human Adrenocortical Carcinoma Cell Lines". Mol. Cell. Endocrinol. 351 (1): 58-65. doi:10.1016/j.mce ... "Establishment and characterization of a human adrenocortical carcinoma cell line that expresses multiple pathways of steroid ... Rainey WE, Saner K, Schimmer BP (2004). "Adrenocortical cell lines". Mol. Cell. Endocrinol. 228 (1-2): 23-38. doi:10.1016/j.mce ...
Chen, David Y. T.; Sosa, RE; Scherr, DS (2004). "Treatment of adrenocortical carcinoma: Contemporary outcomes". Current Urology ... Barocas, DA; Mathew, S; Delpizzo, JJ; Vaughan Ed, ED; Sosa, RE; Fine, RG; Akhtar, M; Scherr, DS (2007). "Renal cell carcinoma ... Barocas, DA; Rabbani, F; Scherr, DS; Vaughan Ed, ED (2006). "A population-based study of renal cell carcinoma and prostate ... Raman, JD; Scherr, DS (2007). "Management of patients with upper urinary tract transitional cell carcinoma". Nature Clinical ...
Mir-210 has been suggested as a useful biomarker to distinguish adrenocortical carcinoma from adrenocortical adenoma. in ... It was found that miR-181a and miR-181c are overexpressed in Papillary Thyroid Carcinoma tumors, sufficiently to successfully ... It has been shown that conserved miR-181 family were upregulated in EpCAM+ AFP+ Hepatocellular carcinoma (HCC) cells and EpCAM+ ... "The role of microRNA genes in papillary thyroid carcinoma". Proceedings of the National Academy of Sciences of the United ...
More recently JAG1 expression has been found to be altered in breast cancer and adrenocortical carcinoma patients. Mouse models ... Simon DP, Giordano TJ, Hammer GD (2012). "Upregulated JAG1 enhances cell proliferation in adrenocortical carcinoma". Clin. ... with both poor overall breast cancer survival rates and an enhancement of tumor proliferation in adrenocortical carcinoma ... "Gene alterations identified by expression profiling in tumor-associated endothelial cells from invasive ovarian carcinoma". ...
Mebendazole inhibits growth of human adrenocortical carcinoma cell lines implanted in nude mice. Cancer Chemotherapy and ...
"The role of microRNA deregulation in the pathogenesis of adrenocortical carcinoma". Endocrine Related Cancer. 18 (6): 643-655. ... "Alteration of microRNA profiles in squamous cell carcinoma of the head and neck cell lines by human papillomavirus". Head & ... "Potentially important microRNA cluster on chromosome 17p13.1 in primary peritoneal carcinoma". Modern Pathology. 22 (2): 197- ...
"The role of microRNA deregulation in the pathogenesis of adrenocortical carcinoma". Endocrine Related Cancer. 18 (6): 643-655. ... "Effect of YB-1 on the regulation of micro RNA expression in drug-sensitive and drug-resistant gastric carcinoma cells". ... "Differential expression of microRNAs in human parathyroid carcinomas compared with normal parathyroid tissue". Endocrine ... "Integrative molecular bioinformatics study of human adrenocortical tumors: MicroRNA, tissue-specific target prediction, and ...
A phase III clinical trial found that linsitinib did not increase survival in patients with adrenocortical carcinoma. As of ... Linsitinib was granted orphan drug designation for adrenocortical carcinoma in March 2012. Phase II clinical trials were ... versus placebo for patients with locally advanced or metastatic adrenocortical carcinoma: a double-blind, randomised, phase 3 ... initiated for multiple myeloma, ovarian cancer, hepatocellular carcinoma, and NSCLC, but subsatisfactory results caused ...
2010) The role of microRNA deregulation in the pathogenesis of adrenocortical carcinoma. Endocr Relat Cancer. (2011) Primary ... 2004) Expression Profiling of Adrenocortical Tumors Suggests a Molecular Signature of Malignancy. (2005) Differential RNA ... 2008) Transcriptional profiling enables molecular classification of adrenocortical tumours. European Journal of Endocrinology ... Accuracy of centinel node in papillary thyroid carcinoma (2001) Quality of life in bariatric surgery (2002) Utilidad de la ...
80% of children with adrenocortical carcinoma and 2%-10% of childhood brain tumors have p53 mutations. 2%-3% of osteosarcomas, ... lymphoma and adrenocortical carcinoma. ~90% of females with LFS develop breast cancer by age 60 years; the majority of these ... adrenocortical carcinoma, leukemia or lung bronchoalveolar cancer - before age 46 years; and at least one of the following: at ... tumour spectrum and the first of which occurred before age 46 years a proband who is diagnosed with adrenocortical carcinoma or ...
MBZ significantly inhibited cancer cell growth, migration, and metastatic formation of adrenocortical carcinoma, both in vitro ... "Mebendazole inhibits growth of human adrenocortical carcinoma cell lines implanted in nude mice". Cancer Chemother. Pharmacol. ...
"Regression of hypertrophic osteopathy in a cat after surgical excision of an adrenocortical carcinoma". J Am Anim Hosp Assoc. ...
"Effect of oestrogen or cyproterone acetate treatment on adrenocortical function in prostate carcinoma patients". Acta ... van Wayjen RG, van den Ende A (1981). "Effect of cyproterone acetate on pituitary-adrenocortical function in man". Acta ... Torri V, Floriani I (2005). "Cyproterone acetate in the therapy of prostate carcinoma". Arch Ital Urol Androl. 77 (3): 157-63. ... Stivel MS, Kauli R, Kaufman H, Laron Z (1982). "Adrenocortical function in children with precocious sexual development during ...
Mir-210 has been suggested as a useful biomarker to distinguish adrenocortical carcinoma from adrenocortical adenoma. mir-210 ... "Analysis of circulating microRNAs in adrenocortical tumors". Laboratory Investigation; A Journal of Technical Methods and ...
... adrenocortical carcinoma and some adrenal pheochromocytomas. Most adrenal pheochromocytomas and all adrenocortical adenomas are ... Adrenocortical carcinoma (ACC) is a rare, highly aggressive cancer of adrenal cortical cells, which may occur in children or ... Due to their location deep in the retroperitoneum, most adrenocortical carcinomas are not diagnosed until they have grown quite ... Functional adrenocortical adenomas are surgically curable. Most of the adrenocortical adenomas are less than 2 cm in greatest ...
... esophageal carcinoma, ovarian serous cystadenocarcinoma, lung squamous cell carcinoma, adrenocortical carcinoma, Diffuse Large ... kidney papillary carcinoma, clear cell kidney carcinoma, breast ductal carcinoma, renal cell carcinoma, cervical cancer ( ... hepatocellular carcinoma, Head and neck (oral) squamous cell carcinoma, thyroid carcinoma, bladder urothelial carcinoma - ... squamous cell carcinoma of the head and neck, colon cancer, rectal cancer, bladder cancer, kidney clear cell carcinoma, ovarian ...
... for example adrenocortical carcinoma and non-small cell lung cancer (NSCLC). This drug was being developed by Pfizer, but they ... and pharmacokinetics of the anti-IGF-1R monoclonal antibody figitumumab in patients with refractory adrenocortical carcinoma". ...
Adrenocortical carcinoma. *Islet cell carcinoma (endocrine pancreas). *Multiple endocrine neoplasia syndrome. *Parathyroid ... spindle cell carcinoma, and small-cell carcinoma.[citation needed] ... Cancers are usually named using -carcinoma, -sarcoma or -blastoma as a suffix, with the Latin or Greek word for the organ or ... For example, the most common type of breast cancer is called ductal carcinoma of the breast. Here, the adjective ductal refers ...
... is expressed in adrenocortical neoplasms but not in renal cell and hepatocellular carcinomas". Appl. Immunohistochem. Mol. ...
... such as Cushing's syndrome and hyperaldosteronism in adrenocortical carcinoma. Analogs of gonadotropin-releasing hormone (GnRH ... including renal cell carcinoma and melanoma. List of hormonal alkylating antineoplastic agents DeVita, Vincent T.; Hellman, ...
Small cell carcinoma, a common cause of ACTH secreted ectopically. *Congenital adrenal hyperplasia, diseases in the production ... ACTH acts by binding to cell surface ACTH receptors, which are located primarily on adrenocortical cells of the adrenal cortex ... These actions are probably necessary to supply the enhanced energy needs of adrenocortical cells stimulated by ACTH.[9] ... "Mitochondrial-genome-encoded RNAs: differential regulation by corticotropin in bovine adrenocortical cells". Proceedings of ...
Carcinoma. Adrenocortical Carcinoma. Neoplasms, Glandular and Epithelial. Neoplasms by Histologic Type. Neoplasms. ... Trial in Locally Advanced and Metastatic Adrenocortical Carcinoma Treatment (FIRM-ACT). This study has been completed. ... The Firm-ACT trial is the first ever conducted randomized controlled phase III trial in adrenocortical carcinoma (ACC), a rare ... Further study details as provided by Martin Fassnacht, Collaborative Group for Adrenocortical Carcinoma Treatment:. Primary ...
Mitotane (o,p′-DDD) is the standard treatment for advanced adrenocortical carcinoma (ACC). Monitoring of plasma mitotane levels ...
Adrenocortical Carcinoma. Carcinoma. Neoplasms, Glandular and Epithelial. Neoplasms by Histologic Type. Neoplasms. ... Study Rationale Adrenocortical carcinoma (ACC) is a very rare disease with a high risk of relapse after radical surgery. The ... Efficacy of Adjuvant Mitotane Treatment in Prolonging Recurrence-free Survival in Patients With Adrenocortical Carcinoma at Low ... Adjuvant mitotane treatment for adrenocortical carcinoma. N Engl J Med. 2007 Jun 7;356(23):2372-80. ...
Mitotane associated with cisplatin, etoposide, and doxorubicin in advanced childhood adrenocortical carcinoma - Mitotane ... Purpose: To define a mitotane dose for pediatric patients with adrenocortical cancer (ACC) that maintains therapeutic plasma ...
Adrenocortical hyperfunction has occurred in association with carcinomas not originating in the adrenal glands. These cancers ... Three patients have been studied: (1) a 23-year-old female with a small-cell carcinoma of the thyroid with extensive metastases ... Adrenocortical Hyperfunction in Cancer. B. J. Kennedy, M.D., F.A.C.P. ... Adrenocortical Hyperfunction in Cancer.. Ann Intern Med. 1961;54:1045. doi: 10.7326/0003-4819-54-5-1045_2 ...
... adrenocortical and thyroid follicular carcinoma, and ovarian cysts). These associations constitute a distinct clinical syndrome ... Primary pigmented nodular adrenocortical disease (PPNAD) is a pituitary-independent, primary adrenal form of hypercortisolism ... Primary pigmented nodular adrenocortical disease (PPNAD) is a pituitary-independent, primary adrenal form of hypercortisolism ... Adrenocortical Hyperfunction. Adrenal Gland Diseases. Endocrine System Diseases. Melanosis. Hyperpigmentation. Pigmentation ...
Bevacizumab plus capecitabine as a salvage therapy in advanced adrenocortical carcinoma. Eur J Endocrinol; 2010 Feb;162(2):349- ... Shin YM: Hepatic adrenal rest tumor mimicking hepatocellular carcinoma. Korean J Hepatol; 2010 Sep;16(3):338-41. [Fulltext ... Title] Hepatic adrenal rest tumor mimicking hepatocellular carcinoma.. *[MeSH-major] Adrenal Rest Tumor / radiography. Liver ... the mass expressed the adrenal 4-binding protein and several enzymes involved in the synthesis of adrenocortical steroids. ...
The prevalence of adenomas and carcinomas in dogs with functioning adrenocortical tumors is approximately equal, and the right ... Bilateral adrenocortical tumors resulting in hyperadrenocorticism are exceedingly rare in dogs. In a retrospective study ... The following is a case report of a dog that was diagnosed with hyperadrenocorticism due to bilateral adrenocortical tumors and ... Primary adrenocortical neoplasia has been diagnosed in 10 to 20% of dogs with hyperadrenocorticism. ...
Adrenocortical Carcinoma Medicine & Life Sciences * Peritoneal Neoplasms Medicine & Life Sciences * Adrenalectomy Medicine & ... Laparoscopic resection of adrenal cortical carcinoma : A cautionary note. In: Surgery. 2005 ; Vol. 138, No. 6. pp. 1078-1086. ... Laparoscopic resection of adrenal cortical carcinoma: A cautionary note. Ricardo J. Gonzalez, Suzanne Shapiro, Nicholas Sarlis ... Fingerprint Dive into the research topics of Laparoscopic resection of adrenal cortical carcinoma: A cautionary note. ...
Adrenocortical carcinoma (ACC) is a cancer of the adrenal glands. The adrenal glands are two triangle-shaped glands. One gland ... Adrenocortical carcinoma treatment (Adult) (PDQ) - health professional version. www.cancer.gov/types/adrenocortical/hp/ ... Adrenocortical carcinoma (ACC) is a cancer of the adrenal glands. The adrenal glands are two triangle-shaped glands. One gland ... Allolio B, Fassnacht M. Adrenocortical carcinoma. In: Jameson JL, De Groot LJ, de Kretser DM, et al, eds. Endocrinology: Adult ...
Find research articles on adrenocortical carcinoma, which may include news stories, clinical trials, blog posts, and ... A molecular characterization of adrenocortical carcinoma, a rare cancer of the adrenal cortex, analyzed 91 cases for ...
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Resection of adrenocortical carcinoma is less complete and local recurrence occurs sooner and more often after laparoscopic ... For decades, little progress was made in improving outcomes for patients with adrenocortical carcinoma (ACC). During the past ... Evaluation, staging, and surgical management for adrenocortical carcinoma: an update from the SSO Endocrine and Head and Neck ... Linsitinib (OSI-906) versus placebo for patients with locally advanced or metastatic adrenocortical carcinoma: a double-blind, ...
Natural History and Tissue Acquisition Study of Adrenocortical Carcinoma. *Adrenocortical Carcinoma. Observational. *National ... 65 Studies found for: Adrenocortical carcinoma. Also searched for Adrenocortical cancer and Adrenal carcinoma. See Search ... Single Agent Pembrolizumab in Subjects With Advanced Adrenocortical Carcinoma. *Adrenocortical Carcinoma. *Drug: Pembrolizumab ... A Study of OSI-906 in Patients With Locally Advanced or Metastatic Adrenocortical Carcinoma. *Adrenocortical Carcinoma ...
... were adrenocortical carcinoma and 34.7% were metastasis [7, 8]. Patients with adrenocortical carcinoma are usually 40-50 years ... A Rare Adrenal Incidentaloma That Mimics Adrenocortical Carcinoma. Kedar Lavingia, Ramyar Torabi, Samuel W. Kim, Marybeth S. ... The suspicion for adrenocortical carcinoma usually prompts adrenalectomy.. 1. Introduction. Adrenal hemangiomas are rare benign ... Due to the difficulty in distinguishing the lesion from an adrenocortical carcinoma on imaging and due to the small risk of ...
Most adrenocortical tumors are functioning. Find evidence-based information on adrenocortical carcinoma including treatment and ... Adrenocortical carcinoma is also called cancer of the adrenal cortex. A tumor of the adrenal cortex may be functioning or ... Adrenocortical Carcinoma Treatment. More information. * Unusual Cancers of Childhood Treatment (PDQ®)-Health Professional ... NCI does not have PDQ evidence-based information about prevention of adrenocortical carcinoma.. More information. * Cancer ...
ACC is capable of secreting excess adrenocortical hormones, which can compound morbidity and compromise clinical outcomes. ... Adrenocortical carcinoma (ACC) is a rare malignancy with a poor prognosis. ... Treatment of Adrenocortical Carcinoma. November 3, 2019 Adrenocortical carcinoma (ACC) is a rare malignancy with a poor ... ACC is capable of secreting excess adrenocortical hormones, which can compound morbidity and compromise clinical outcomes. By ...
Adrenocortical carcinoma is a rare tumor, with incidence of 1-2 per million population annually. Adrenocortical carcinoma has a ... Oncocytic adrenal cortical carcinoma Myxoid adrenal cortical carcinoma Carcinosarcoma Adenosquamous adrenocortical carcinoma ... Adrenocortical carcinoma (ACC, adrenal cortical carcinoma, adrenal cortical cancer, adrenal cortex cancer, etc.) is an ... Adrenocortical adenoma Renal cell carcinoma Adrenal medullary tumors Hepatocellular carcinoma The only curative treatment is ...
Adrenocortical carcinoma. Definition. Adrenocortical carcinoma (ACC) is a cancer of the adrenal glands. The adrenal glands are ... PDQ: adrenocortical carcinoma treatment - health professional version. Updated June 02, 2015. Cancer.gov. www.cancer.gov/types/ ... Allolio B, Fassnacht M. Adrenocortical carcinoma. In: Jameson JL, De Groot LJ, de Kretser DM, et al, eds. Endocrinology: Adult ...
... adrenocortical carcinoma) from the Cleveland Clinic, including symptoms, treatment options & more. ... Adrenocortical carcinoma may be cured if treated at an early stage.. Stages of Adrenocortical Carcinoma. *After adrenocortical ... Stage I Adrenocortical Carcinoma. Treatment of stage I adrenocortical carcinoma may include the following:. *Surgery ( ... Stage II Adrenocortical Carcinoma. Treatment of stage II adrenocortical carcinoma may include the following:. *Surgery ( ...
Carcinoma. Adrenocortical Carcinoma. Neoplasms, Glandular and Epithelial. Neoplasms by Histologic Type. Neoplasms. ... Surgery and Heated Chemotherapy for Adrenocortical Carcinoma. The safety and scientific validity of this study is the ... Adrenocortical carcinoma (ACC) is a rare tumor of the adrenal gland. Few people who develop this disease live more than 5 years ... Adrenocortical Carcinoma Peritoneal Carcinomatosis Drug: Cisplatin Procedure: Cytoreductive surgery Drug: sodium thiosulfate ...
Learn more about Adrenocortical Carcinoma at Portsmouth Regional Hospital DefinitionCausesRisk ... Adrenocortical carcinoma is cancer of the adrenal cortex. The adrenal glands are 2 glands located above each kidney. The glands ... Approximately 40% of people with adrenocortical carcinoma do not secrete any hormone. These people do not have any specific ... Adrenocortical carcinoma is discovered as part of a physical examination for abdominal pain. ...
Adrenocortical carcinoma is cancer of the adrenal cortex. The adrenal glands are two glands located above each kidney. The ... The cause of adrenocortical carcinoma is unknown.. Risk Factors. A genetic defect may cause adrenocortical cancer in some ... Adrenocortical carcinoma is cancer of the adrenal cortex. The adrenal glands are two glands located above each kidney. The ... Approximately 40 percent of people with adrenocortical carcinoma do not secrete any hormone. These people do not have any ...
Adrenocortical carcinoma is a rare disease in which malignant (cancer) cells form in the outer layer of the adrenal gland. ... Stage IV Adrenocortical Carcinoma. Treatment of stage IV adrenocortical carcinoma may include the following as palliative ... Stages of Adrenocortical Carcinoma. After adrenocortical carcinoma has been diagnosed, tests are done to find out if cancer ... Recurrent Adrenocortical Carcinoma. Recurrent adrenocortical carcinoma is cancer that has recurred (come back) after it has ...
Adrenocortical Carcinoma. (Cancer of the Adrenal Cortex; Adrenal Cortical Carcinoma; Adrenal Cancer). by Amanda Barrett, MA ... Adrenocortical carcinoma is cancer of the adrenal cortex. The adrenal glands are 2 glands located above each kidney. The glands ... General information about adrenocortical carcinoma. National Cancer Institute website. Available at: ...(Click grey area to ... Approximately 40% of people with adrenocortical carcinoma do not secrete any hormone. These people do not have any specific ...
  • The Firm-ACT trial is the first ever conducted randomized controlled phase III trial in adrenocortical carcinoma (ACC), a rare malignancy with poor prognosis. (clinicaltrials.gov)
  • Study Rationale Adrenocortical carcinoma (ACC) is a very rare disease with a high risk of relapse after radical surgery. (clinicaltrials.gov)
  • Primary pigmented nodular adrenocortical disease (PPNAD) is a pituitary-independent, primary adrenal form of hypercortisolism characterized by (a) resistance to suppression by dexamethasone and abolition of the normal diurnal rhythm of cortisol secretion, and (b) distinctive, bilateral, histopathologic changes of the adrenal glands, such as the formation of variably sized, pigmented nodular adenomas, loss of normal zonation and atrophy of the extranodular cortex. (clinicaltrials.gov)
  • We describe the landscape of somatic genomic alterations of 66 chromophobe renal cell carcinomas (ChRCCs), based on multidimensional and comprehensive characterization, including mitochondrial DNA (mtDNA) and whole genome sequencing. (nih.gov)
  • The purpose of this report is to relate a patient with morbid obesity that underwent bariatric surgery and after that developed the Cushing's syndrome caused by an adrenocortical carcinoma. (scielo.br)
  • these often appear normal in Cushing's In the alcoholic patient with pseudo-Cushing's, admission to hospital (and avoidance of alcohol) will result in normal midnight cortisol levels within five days, excluding Cushing's Another cause for Cushing's syndrome is adrenocortical carcinoma (ACC). (wikipedia.org)
  • Mitotane, sold under the brand name Lysodren, is a steroidogenesis inhibitor and cytostatic antineoplastic medication which is used in the treatment of adrenocortical carcinoma and Cushing's syndrome. (wikipedia.org)
  • Second, a minority (about 15%) of adrenocortical adenomas are "functional", meaning that they produce glucocorticoids, mineralcorticoids, and/or sex steroids, resulting in endocrine disorders such as Cushing's syndrome, Conn's syndrome (hyperaldosteronism), virilization of females, or feminization of males. (wikipedia.org)
  • It can also be used for the treatment of hyperadrenocortical syndromes, such as Cushing's syndrome and hyperaldosteronism in adrenocortical carcinoma. (wikipedia.org)
  • Amphenone B was tested in humans in the mid-1950s as a potential treatment for cortisol-dependent conditions such as Cushing's syndrome and adrenocortical carcinoma. (wikipedia.org)
  • They have been used to inhibit corticosteroid synthesis in the treatment of Cushing's syndrome and adrenocortical carcinoma, and ketoconazole has also been used to inhibit androgen production in the treatment of prostate cancer. (wikipedia.org)
  • Squamous cell carcinoma related oncogene regulates angiogenesis through vascular endothelial growth factor-A". Annals of Surgical Oncology. (wikipedia.org)
  • Global Markets Direct's latest Pharmaceutical and Healthcare disease pipeline guide Adrenocortical Carcinoma - Pipeline Review, H1 2017, provides an overview of the Adrenocortical Carcinoma (Oncology) pipeline landscape. (marketresearch.com)
  • Moreover, according to the study by Medscape, 2017, adrenocortical carcinoma accounted for 0.02-0.2% of all cancer-related deaths, globally. (coherentmarketinsights.com)
  • They should not be confused with adrenocortical "nodules", which are not true neoplasms. (wikipedia.org)
  • Their research and discovery in the abstract of Li and Dr. Fraumeni's paper described their method and results as, "A search of the Cancer Family Registry of the National Cancer Institute revealed 24 kindreds with the syndrome of sarcoma, breast carcinoma, and other neoplasms in young patients. (wikipedia.org)
  • Symptoms of adrenocortical carcinoma include pain in the abdomen. (clevelandclinic.org)
  • The symptoms of adrenocortical carcinoma may present differently in adults and children. (ning.com)
  • 1. Current coexisting malignancy other than basal cell carcinoma. (knowcancer.com)
  • History of prior malignancy, except for cured non-melanoma skin cancer, cured in situ cervical carcinoma, or other treated malignancies with no evidence of disease for at least three years. (centerwatch.com)
  • Adrenocortical carcinoma (ACC) is a rare malignancy, the prognosis of which is mainly dependent on stage at diagnosis. (ovid.com)
  • Adrenocortical carcinoma (ACC) is a rare and heterogeneous malignancy, and most of the diagnostic and therapeutic strategies are not fully established according to criteria of evidence-based medicine. (medicdebate.org)
  • Caze C, Pucheux J, Orain I, Angoulvanti D (2014) Massive Pulmonary Embolism Revealing a Giant Adrenocortical Carcinoma. (omicsonline.org)
  • Global Markets Direct's Pharmaceutical and Healthcare latest pipeline guide Adrenocortical Carcinoma (Adrenal Cortex Cancer) - Pipeline Review, H2 2018, provides comprehensive information on the therapeutics under development for Adrenocortical Carcinoma (Adrenal Cortex Cancer) (Oncology), complete with analysis by stage of development, drug target, mechanism of action (MoA), route of administration (RoA) and molecule type. (reportsnreports.com)
  • Also, in March 2018, the University of Colorado Anschutz Medical Campus presented new models to identify genetic targets and test promising treatments in adrenocortical carcinoma at the ENDO Conference, thus exploring new therapeutic options for the patients. (coherentmarketinsights.com)
  • Adrenocortical Carcinoma, Hereditary, also known as adrenocortical carcinoma, pediatric , is related to li-fraumeni syndrome 2 and adenoid cystic carcinoma , and has symptoms including fever and flank pain . (malacards.org)
  • Using in situ hybridization with SF-1 cRNA specific probe detected gene transcripts in adrenocortical cells, Leydig cells, and ovarian theca and granulosa cells. (wikipedia.org)
  • Figitumumab (previously CP-751871) is a monoclonal antibody targeting the insulin-like growth factor-1 receptor that was investigated for the treatment of various types of cancer, for example adrenocortical carcinoma and non-small cell lung cancer (NSCLC). (wikipedia.org)