Dermatitis, Exfoliative: The widespread involvement of the skin by a scaly, erythematous dermatitis occurring either as a secondary or reactive process to an underlying cutaneous disorder (e.g., atopic dermatitis, psoriasis, etc.), or as a primary or idiopathic disease. It is often associated with the loss of hair and nails, hyperkeratosis of the palms and soles, and pruritus. (From Dorland, 27th ed)Erythema Multiforme: A skin and mucous membrane disease characterized by an eruption of macules, papules, nodules, vesicles, and/or bullae with characteristic "bull's-eye" lesions usually occurring on the dorsal aspect of the hands and forearms.Dermatitis Herpetiformis: Rare, chronic, papulo-vesicular disease characterized by an intensely pruritic eruption consisting of various combinations of symmetrical, erythematous, papular, vesicular, or bullous lesions. The disease is strongly associated with the presence of HLA-B8 and HLA-DR3 antigens. A variety of different autoantibodies has been detected in small numbers in patients with dermatitis herpetiformis.Adrenal Insufficiency: Conditions in which the production of adrenal CORTICOSTEROIDS falls below the requirement of the body. Adrenal insufficiency can be caused by defects in the ADRENAL GLANDS, the PITUITARY GLAND, or the HYPOTHALAMUS.Dermatitis, Seborrheic: A chronic inflammatory disease of the skin with unknown etiology. It is characterized by moderate ERYTHEMA, dry, moist, or greasy (SEBACEOUS GLAND) scaling and yellow crusted patches on various areas, especially the scalp, that exfoliate as dandruff. Seborrheic dermatitis is common in children and adolescents with HIV INFECTIONS.Stevens-Johnson Syndrome: Rare cutaneous eruption characterized by extensive KERATINOCYTE apoptosis resulting in skin detachment with mucosal involvement. It is often provoked by the use of drugs (e.g., antibiotics and anticonvulsants) or associated with PNEUMONIA, MYCOPLASMA. It is considered a continuum of Toxic Epidermal Necrolysis.Addison Disease: An adrenal disease characterized by the progressive destruction of the ADRENAL CORTEX, resulting in insufficient production of ALDOSTERONE and HYDROCORTISONE. Clinical symptoms include ANOREXIA; NAUSEA; WEIGHT LOSS; MUSCLE WEAKNESS; and HYPERPIGMENTATION of the SKIN due to increase in circulating levels of ACTH precursor hormone which stimulates MELANOCYTES.Giant Cell Arteritis: A systemic autoimmune disorder that typically affects medium and large ARTERIES, usually leading to occlusive granulomatous vasculitis with transmural infiltrate containing multinucleated GIANT CELLS. The TEMPORAL ARTERY is commonly involved. This disorder appears primarily in people over the age of 50. Symptoms include FEVER; FATIGUE; HEADACHE; visual impairment; pain in the jaw and tongue; and aggravation of pain by cold temperatures. (From Adams et al., Principles of Neurology, 6th ed)Purpura, Thrombocytopenic, Idiopathic: Thrombocytopenia occurring in the absence of toxic exposure or a disease associated with decreased platelets. It is mediated by immune mechanisms, in most cases IMMUNOGLOBULIN G autoantibodies which attach to platelets and subsequently undergo destruction by macrophages. The disease is seen in acute (affecting children) and chronic (adult) forms.Adrenal Hyperplasia, Congenital: A group of inherited disorders of the ADRENAL GLANDS, caused by enzyme defects in the synthesis of cortisol (HYDROCORTISONE) and/or ALDOSTERONE leading to accumulation of precursors for ANDROGENS. Depending on the hormone imbalance, congenital adrenal hyperplasia can be classified as salt-wasting, hypertensive, virilizing, or feminizing. Defects in STEROID 21-HYDROXYLASE; STEROID 11-BETA-HYDROXYLASE; STEROID 17-ALPHA-HYDROXYLASE; 3-beta-hydroxysteroid dehydrogenase (3-HYDROXYSTEROID DEHYDROGENASES); TESTOSTERONE 5-ALPHA-REDUCTASE; or steroidogenic acute regulatory protein; among others, underlie these disorders.Immune Reconstitution Inflammatory Syndrome: Exuberant inflammatory response towards previously undiagnosed or incubating opportunistic pathogens. It is frequently seen in AIDS patients following HAART.Infertility, Male: The inability of the male to effect FERTILIZATION of an OVUM after a specified period of unprotected intercourse. Male sterility is permanent infertility.Infertility, Female: Diminished or absent ability of a female to achieve conception.Infertility: Inability to reproduce after a specified period of unprotected intercourse. Reproductive sterility is permanent infertility.Syndrome: A characteristic symptom complex.Spermatozoa: Mature male germ cells derived from SPERMATIDS. As spermatids move toward the lumen of the SEMINIFEROUS TUBULES, they undergo extensive structural changes including the loss of cytoplasm, condensation of CHROMATIN into the SPERM HEAD, formation of the ACROSOME cap, the SPERM MIDPIECE and the SPERM TAIL that provides motility.Sperm Motility: Movement characteristics of SPERMATOZOA in a fresh specimen. It is measured as the percentage of sperms that are moving, and as the percentage of sperms with productive flagellar motion such as rapid, linear, and forward progression.Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains SPERMATOZOA and their nutrient plasma.Sperm Count: A count of SPERM in the ejaculum, expressed as number per milliliter.Semen Analysis: The quality of SEMEN, an indicator of male fertility, can be determined by semen volume, pH, sperm concentration (SPERM COUNT), total sperm number, sperm viability, sperm vigor (SPERM MOTILITY), normal sperm morphology, ACROSOME integrity, and the concentration of WHITE BLOOD CELLS.Cyclotrons: Devices for accelerating charged particles in a spiral path by a constant-frequency alternating electric field. This electric field is synchronized with the movement of the particles in a constant magnetic field.Doxycycline: A synthetic tetracycline derivative with similar antimicrobial activity.Fourier Analysis: Analysis based on the mathematical function first formulated by Jean-Baptiste-Joseph Fourier in 1807. The function, known as the Fourier transform, describes the sinusoidal pattern of any fluctuating pattern in the physical world in terms of its amplitude and its phase. It has broad applications in biomedicine, e.g., analysis of the x-ray crystallography data pivotal in identifying the double helical nature of DNA and in analysis of other molecules, including viruses, and the modified back-projection algorithm universally used in computerized tomography imaging, etc. (From Segen, The Dictionary of Modern Medicine, 1992)Mass Spectrometry: An analytical method used in determining the identity of a chemical based on its mass using mass analyzers/mass spectrometers.Lipids: A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)Spectrometry, Mass, Electrospray Ionization: A mass spectrometry technique used for analysis of nonvolatile compounds such as proteins and macromolecules. The technique involves preparing electrically charged droplets from analyte molecules dissolved in solvent. The electrically charged droplets enter a vacuum chamber where the solvent is evaporated. Evaporation of solvent reduces the droplet size, thereby increasing the coulombic repulsion within the droplet. As the charged droplets get smaller, the excess charge within them causes them to disintegrate and release analyte molecules. The volatilized analyte molecules are then analyzed by mass spectrometry.Lipid Metabolism: Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.Chromatography, High Pressure Liquid: Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.Cell Aging: The decrease in the cell's ability to proliferate with the passing of time. Each cell is programmed for a certain number of cell divisions and at the end of that time proliferation halts. The cell enters a quiescent state after which it experiences CELL DEATH via the process of APOPTOSIS.Glycerophospholipids: Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine.Lymphangioma: A benign tumor resulting from a congenital malformation of the lymphatic system. Lymphangioendothelioma is a type of lymphangioma in which endothelial cells are the dominant component.Lymphangioma, Cystic: A cystic growth originating from lymphatic tissue. It is usually found in the neck, axilla, or groin.ThymineDatura: A plant genus of the family SOLANACEAE. Members contain TROPANES. The common name of trumpet flower is also sometimes used for GELSEMIUM.ValeratesPeriodicals as Topic: A publication issued at stated, more or less regular, intervals.Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.Carbolines: A group of pyrido-indole compounds. Included are any points of fusion of pyridine with the five-membered ring of indole and any derivatives of these compounds. These are similar to CARBAZOLES which are benzo-indoles.Editorial Policies: The guidelines and policy statements set forth by the editor(s) or editorial board of a publication.Authorship: The profession of writing. Also the identity of the writer as the creator of a literary production.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)Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals.Veterinary Drugs: Drugs used by veterinarians in the treatment of animal diseases. The veterinarian's pharmacological armamentarium is the counterpart of drugs treating human diseases, with dosage and administration adjusted to the size, weight, disease, and idiosyncrasies of the species. In the United States most drugs are subject to federal regulations with special reference to the safety of drugs and residues in edible animal products.Education, Veterinary: Use for general articles concerning veterinary medical education.Surgery, Veterinary: A board-certified specialty of VETERINARY MEDICINE, requiring at least four years of special education, training, and practice of veterinary surgery after graduation from veterinary school. In the written, oral, and practical examinations candidates may choose either large or small animal surgery. (From AVMA Directory, 43d ed, p278)Schools, Veterinary: Educational institutions for individuals specializing in the field of veterinary medicine.Pathology, Veterinary: The field of veterinary medicine concerned with the causes of and changes produced in the body by disease.Veterinarians: Individuals with a degree in veterinary medicine that provides them with training and qualifications to treat diseases and injuries of animals.Legislation, Veterinary: Laws and regulations, pertaining to the field of veterinary medicine, proposed for enactment or enacted by a legislative body.Chickenpox Vaccine: A live, attenuated varicella virus vaccine used for immunization against chickenpox. It is recommended for children between the ages of 12 months and 13 years.Hirschsprung Disease: Congenital MEGACOLON resulting from the absence of ganglion cells (aganglionosis) in a distal segment of the LARGE INTESTINE. The aganglionic segment is permanently contracted thus causing dilatation proximal to it. In most cases, the aganglionic segment is within the RECTUM and SIGMOID COLON.Urogenital Abnormalities: Congenital structural abnormalities of the UROGENITAL SYSTEM in either the male or the female.Ependymoma: Glioma derived from EPENDYMOGLIAL CELLS that tend to present as malignant intracranial tumors in children and as benign intraspinal neoplasms in adults. It may arise from any level of the ventricular system or central canal of the spinal cord. Intracranial ependymomas most frequently originate in the FOURTH VENTRICLE and histologically are densely cellular tumors which may contain ependymal tubules and perivascular pseudorosettes. Spinal ependymomas are usually benign papillary or myxopapillary tumors. (From DeVita et al., Principles and Practice of Oncology, 5th ed, p2018; Escourolle et al., Manual of Basic Neuropathology, 2nd ed, pp28-9)Search Engine: Software used to locate data or information stored in machine-readable form locally or at a distance such as an INTERNET site.Anal Canal: The terminal segment of the LARGE INTESTINE, beginning from the ampulla of the RECTUM and ending at the anus.Sacrum: Five fused VERTEBRAE forming a triangle-shaped structure at the back of the PELVIS. It articulates superiorly with the LUMBAR VERTEBRAE, inferiorly with the COCCYX, and anteriorly with the ILIUM of the PELVIS. The sacrum strengthens and stabilizes the PELVIS.Teratoma: A true neoplasm composed of a number of different types of tissue, none of which is native to the area in which it occurs. It is composed of tissues that are derived from three germinal layers, the endoderm, mesoderm, and ectoderm. They are classified histologically as mature (benign) or immature (malignant). (From DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1642)Nasolacrimal Duct: A tubular duct that conveys TEARS from the LACRIMAL GLAND to the nose.Lacrimal Duct Obstruction: Interference with the secretion of tears by the lacrimal glands. Obstruction of the LACRIMAL SAC or NASOLACRIMAL DUCT causing acute or chronic inflammation of the lacrimal sac (DACRYOCYSTITIS). It is caused also in infants by failure of the nasolacrimal duct to open into the inferior meatus and occurs about the third week of life. In adults occlusion may occur spontaneously or after injury or nasal disease. (Newell, Ophthalmology: Principles and Concepts, 7th ed, p250)Thanatophoric Dysplasia: A severe form of neonatal dwarfism with very short limbs. All cases have died at birth or later in the neonatal period.Pituitary Adenylate Cyclase-Activating Polypeptide: A multi-function neuropeptide that acts throughout the body by elevating intracellular cyclic AMP level via its interaction with PACAP RECEPTORS. Although first isolated from hypothalamic extracts and named for its action on the pituitary, it is widely distributed in the central and peripheral nervous systems. PACAP is important in the control of endocrine and homeostatic processes, such as secretion of pituitary and gut hormones and food intake.Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide: A family of G-protein-coupled receptors that share significant homology with GLUCAGON RECEPTORS. They bind PITUITARY ADENYLATE CYCLASE ACTIVATING POLYPEPTIDE with high affinity and trigger intracellular changes that influence the behavior of CELLS.Vasoactive Intestinal Peptide: A highly basic, 28 amino acid neuropeptide released from intestinal mucosa. It has a wide range of biological actions affecting the cardiovascular, gastrointestinal, and respiratory systems and is neuroprotective. It binds special receptors (RECEPTORS, VASOACTIVE INTESTINAL PEPTIDE).Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type IReceptors, Vasoactive Intestinal Peptide: Cell surface proteins that bind VASOACTIVE INTESTINAL PEPTIDE; (VIP); with high affinity and trigger intracellular changes which influence the behavior of cells.Receptors, Pituitary Hormone: Cell surface proteins that bind pituitary hormones with high affinity and trigger intracellular changes influencing the behavior of cells. Since many pituitary hormones are also released by neurons as neurotransmitters, these receptors are also found in the nervous system.Neuropeptides: Peptides released by NEURONS as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells.Receptors, Vasoactive Intestinal Peptide, Type II: A pituitary adenylate cyclase-activating peptide receptor subtype found in LYMPHOCYTES. It binds both PACAP and VASOACTIVE INTESTINAL PEPTIDE and regulates immune responses.Receptors, Vasoactive Intestinal Polypeptide, Type I: A pituitary adenylate cyclase-activating polypeptide receptor subtype that binds both PACAP and VASOACTIVE INTESTINAL PEPTIDE. It is found predominately in the BRAIN.Pituitary Gland: A small, unpaired gland situated in the SELLA TURCICA. It is connected to the HYPOTHALAMUS by a short stalk which is called the INFUNDIBULUM.

Medroxyprogesterone acetate inhibits interleukin 6 secretion from KPL-4 human breast cancer cells both in vitro and in vivo: a possible mechanism of the anticachectic effect. (1/2596)

Interleukin 6 (IL-6) is a multifunctional cytokine. Recent reports suggest that circulating IL-6 secreted from tumour cells plays an important role in cancer-induced cachexia. Medroxyprogesterone acetate (MPA) has been used as an endocrine therapeutic agent for patients with breast cancer. It has been suggested that MPA decreases serum IL-6 levels and preserves the bodyweight of patients with advanced breast cancer. However, the mechanisms of action responsible for the anticachectic effect of MPA have not been elucidated. Therefore, the effects of MPA on IL-6 secretion were studied both in vitro and in vivo using a human breast cancer cell line, KPL-4, which secretes IL-6 into medium and induces cachexia when injected into female nude mice. MPA (10-1000 nM) dose-dependently decreased basal IL-6 secretion into medium, and also suppressed tumour necrosis factor (TNF-alpha)-induced IL-6 secretion. Both basal and TNF-alpha-induced IL-6 mRNA levels were dose-dependently lowered by MPA. Moreover, intramuscular injections of MPA (100 mg kg(-1) twice a week) into nude mice bearing KPL-4 transplanted tumours significantly decreased serum IL-6 levels without affecting tumour growth and preserved the bodyweight of recipient mice. These findings suggest that suppression of IL-6 secretion from tumour cells, at least in part, causes the anticachectic effect of MPA.  (+info)

The somatostatin analog octreotide inhibits growth of interleukin-6 (IL-6)-dependent and IL-6-independent human multiple myeloma cell lines. (2/2596)

Somatostatin and its analogs can inhibit growth in several cell types, in part by interfering with insulin-like growth factor-I (IGF-I) signaling. Our previous studies point to the importance of paracrine and autocrine IGF-I in the support of growth and survival of human multiple myeloma (MM) cell lines. In this report, we have investigated the potential role of a somatostatin analog, octreotide, in regulating growth and/or survival in MM. The results show that all MM cell lines express functional somatostatin receptors (sst). The MM cell lines express the subtypes sst2, sst3, and predominantly sst5 as determined by reverse-transcriptase polymerase chain reaction and fluorescence-activated cell sorter analysis. Octreotide inhibited the growth of both the interleukin-6 (IL-6)-dependent and the IL-6-independent MM cell lines. The effect is mainly cytostatic, resulting in 25% to 45% growth inhibition, and in three of eight of the MM cell lines a weak induction of apoptosis was recorded. Our results also show that octreotide may act as an inducer of apoptosis in primary B-B4(+) plasma cells isolated from bone marrow of MM patients. In conclusion, the results show a novel pathway for growth inhibition of MM cells: the activation of somatostatin receptor signaling.  (+info)

Increased activator protein-1 DNA binding and c-Jun NH2-terminal kinase activity in human breast tumors with acquired tamoxifen resistance. (3/2596)

Human breast tumors that are initially responsive to tamoxifen (TAM) eventually relapse during treatment. Estrogen receptor (ER) expression and function are often preserved in these tumors, and clinical evidence suggests that this relapse may be related to TAM's known agonistic properties. ER can interact with the activator protein-1 (AP-1) transcription factor complex through protein-protein interactions that are independent of ER DNA binding and, in certain ER-positive cells, this may allow TAM to exert an agonist response on AP-1-regulated genes. We, therefore, assessed both AP-1 DNA binding and the known AP-1 activating enzyme, c-Jun NH2-terminal kinase (JNK), in a panel of 30 ER-positive primary human breast tumors with acquired TAM resistance, as compared to a matched panel of 27 untreated control ER-positive breast tumors and a separate control set of 14 primary tumors, which included 7 ER-positive tumors that were growth-arrested by 3 months of preoperative TAM. AP-1 DNA binding activity was measured from cryopreserved tumor extracts using a labeled oligonucleotide probe containing a consensus AP-1 response element by electrophoretic mobility shift assay. JNK was first extracted from the tumor lysates by incubation over a Sepharose-bound c-Jun(1-89) fusion protein, and its activity was then measured by chemiluminescent Western blot by detection of the phosphorylated product using a phospho-Jun(Ser-63)-specific primary antibody. The set of control ER-positive breast tumors growth arrested by TAM showed no significant difference from untreated control tumors in their AP-1 DNA binding and JNK activities. In contrast, there was a significant (P < 0.001) increase in mean AP-1 DNA binding activity for the panel of ER-positive TAM-resistant (TAM-R) tumors as compared to its matched control panel of untreated tumors. Mean JNK activity in the TAM-R tumors was also significantly higher than that found in the untreated tumors (P = 0.038). Overall, there was no significant correlation between JNK activity and AP-1 DNA binding; however, regression analysis showed that, for any given level of JNK activity, the TAM-R tumors possessed a 3.5-fold increase in AP-1 DNA binding activity as compared to the untreated tumors. These findings indicate that, when compared to untreated ER-positive primary breast tumors, TAM-R tumors demonstrate significantly increased levels of AP-1 DNA binding and JNK activity, consistent with experimental models suggesting that TAM-stimulated ER-positive tumor growth may be mediated by enhanced AP-1 transcriptional activity. These observations support the need for further evaluation of these markers in breast tumors as predictors of TAM resistance.  (+info)

In vivo localization of [(111)In]-DTPA-D-Phe1-octreotide to human ovarian tumor xenografts induced to express the somatostatin receptor subtype 2 using an adenoviral vector. (4/2596)

Adenoviral vectors, encoding genes for cell surface antigens or receptors, have been used to induce their high level expression on tumor cells in vitro and in vivo. These induced antigens and receptors can then be targeted with radiolabeled antibodies or peptides for potential radiotherapeutic applications. The purpose of this study was to determine a dosing schema of an adenoviral vector encoding the human somatostatin receptor subtype 2 (AdCMVhSSTr2) for achieving the highest tumor localization of [(111)In]-DTPA-D-Phe1-octreotide, which binds to this receptor, in a human ovarian cancer model as a prelude to future therapy studies. AdCMVhSSTr2 was produced and used to induce hSSTr2 on A427 human nonsmall cell lung cancer cells and on SKOV3.ipl human ovarian cancer cells in vitro, as demonstrated by competitive binding assays using [125I]-Tyr1-somatostatin and [(111)In]-DTPA-D-Phe1-octreotide. Mice bearing i.p. SKOV3.ip1 tumors administered 1 x 10(9) plaque-forming units of AdCMVhSSTr2 i.p. 5 days after tumor cell inoculation, followed by an i.p. injection of [(111)In]-DTPA-D-Phe1-octreotide 2 days later, showed a range of 15.3-60.4% median injected dose/gram (ID/g) in tumor at 4 h after injection compared with 3.5% ID/g when [125I]-Tyr1-somatostatin was administered and 0.3% ID/g when the negative control peptide [125I]-mIP-bombesin was administered. Mice administered a control adenoviral vector encoding the gastrin-releasing peptide receptor did not have tumor localization of [(111)In]-DTPA-D-Phe1-octreotide (<1.6% ID/g), demonstrating specificity of [(111)In]-DTPA-D-Phe1-octreotide for the AdCMVhSSTr2 induced tumor cells. In another set of experiments, the tumor localization of [(111)In]-DTPA-D-Phe1-octreotide was not different 1, 2, or 4 days after AdCMVhSSTr2 injection (31.8, 37.7, and 40.7% ID/g, respectively; P = 0.88), indicating that multiple injections of radiolabeled peptide can be administered with equivalent uptake over a 4-day period. [(111)In]-DTPA-D-Phe1-octreotide tumor localization in animals administered AdCMVhSSTr2 on consecutive days or 2 days apart was 22.4% ID/g and 53.2% ID/g, respectively (P = 0.009) when [(111)In]-DTPA-D-Phe1-octreotide was given 1 day after the second AdCMVhSSTr2 injection. There was no difference in [(111)In]-DTPA-D-Phe1-octreotide localization after a single AdCMVhSSTr2 injection (40.7% ID/g) or two injections of AdCMVhSSTr2 given 1 (45.9% ID/g) or 2 (53.2% ID/g) days apart, where [(111)In]-DTPA-D-Phe1-octreotide was given in each case 4 days after the first AdCMVhSSTr2 injection (P = 0.65). Therefore, two AdCMVhSSTr2 injections did not increase [(111)In]-DTPA-D-Phe1-octreotide tumor localization compared with one injection, which eliminates concerns about an immune response to a second dose of AdCMVhSSTr2. This will be the basis for a therapeutic protocol with multiple administrations of an octreotide analogue labeled with a therapeutic radioisotope.  (+info)

The aromatase inactivator 4-hydroxyandrostenedione (4-OH-A) inhibits tamoxifen metabolism by rat hepatic cytochrome P-450 3A: potential for drug-drug interaction of tamoxifen and 4-OH-A in combined anti-breast cancer therapy. (5/2596)

Tamoxifen (tam), an anti-breast cancer agent, is metabolized into tam-N-oxide by the hepatic flavin-containing monooxygenase and into N-desmethyl- and 4-hydroxy-tam by cytochrome P-450s (CYPs). Additionally, tam is metabolically activated by hepatic CYP3A, forming a reactive intermediate that binds covalently to proteins. Tam and 4-hydroxyandrostenedione (4-OH-A) are currently used to treat breast cancer, and it has been contemplated that 4-OH-A be given concurrently with tam to contravene potential tumor resistance to tam. Because alterations in tam metabolism may influence its therapeutic efficacy, the effect of 4-OH-A on tam metabolism was examined. Incubation of tam with liver microsomes from phenobarbital-treated rats, in the presence of 4-OH-A (10-100 microM), resulted in marked inhibition of tam-N-demethylation and tam covalent binding and in decreased tam-N-oxide accumulation; however, there was no inhibition of the formation of 4-hydroxy-tam and of 3,4-dihydroxytamoxifen. These findings indicate that 4-OH-A inhibits CYP3A, but not P-450(s) that catalyze tam 4-hydroxylation. The diminished tam-N-oxide accumulation could be due to decreased N-oxide formation and/or due to increased N-oxide reduction. Incubation of tam-N-oxide with liver microsomes containing heat-inactivated flavin-containing monooxygenase demonstrated that 4-OH-A increases the accumulation of tam, possibly by diminishing its P-450-mediated metabolism. Kinetic studies indicate that 4-OH-A is a competitive inhibitor of CYP3A, but not a time-dependent inactivator. Consequently, the concurrent treatment of tam and 4-OH-A may result in increased tam half-life and thus could potentiate the therapeutic efficacy of tam and diminish the potential side effects of tam by inhibiting its covalent binding to proteins and possibly to DNA.  (+info)

Lack of evidence from HPLC 32P-post-labelling for tamoxifen-DNA adducts in the human endometrium. (6/2596)

Tamoxifen is associated with an increased incidence of endometrial cancer in women. It is also a potent carcinogen in rat liver and forms covalent DNA adducts in this tissue. A previous study exploring DNA adducts in human endometria, utilizing thin layer chromatography 32P-postlabelling, found no evidence for adducts in tamoxifen-treated women [Carmichael,P.L., Ugwumadu,A.H.N., Neven,P., Hewer,A.J., Poon,G.K. and Phillips,D.H. (1996) Cancer Res., 56, 1475-1479]. However, subsequent work utilizing HPLC 32P-post-labelling [Hemminki,K., Ranjaniemi,H., Lindahl,B. and Moberger,B. (1996) Cancer Res., 56, 4374-4377] suggested that very low levels could be detected. We have sought to investigate this question further by reproducing the HPLC methodology at two centres, and analysing endometrial DNA from 20 patients treated with 20 mg/day tamoxifen for between 22 and 65 months. Liver DNA isolated from tamoxifen-treated rats was used as a positive control. We found no convincing evidence for tamoxifen-derived DNA adducts in human endometrium. HPLC elution profiles of post-labelled DNA from tamoxifen-treated women were indistinguishable from those obtained with DNA from 14 untreated women and from six women taking toremifene, an analogue of tamoxifen.  (+info)

Kleine-Levin and Munchausen syndromes in a patient with recurrent acromegaly. (7/2596)

Hypothalamic disease often affects the patients' personality and this also applies to pituitary tumors with suprasellar extension. We report on a patient with a 12-year history of recurrent acromegaly, treated with three transphenoidal operations, single field radiation therapy and bromocriptine/octreotide administration. During the course of follow-up she presented with self-inflicted anemia and Kleine-Levin syndrome (hypersomnia, hyperphagia and hypersexuality). Furthermore, she developed post-radiation necrosis within the right temporal lobe. Whether her neurological and personality disorders result - at least partially - from the acromegaly or the temporal lobe necrosis remains unclear.  (+info)

Expression of prostate-specific antigen (PSA) correlates with poor response to tamoxifen therapy in recurrent breast cancer. (8/2596)

Prostate-specific antigen (PSA) is a serine protease which may play a role in a variety of cancer types, including breast cancer. In the present study, we evaluated whether the level of PSA in breast tumour cytosol could be associated with prognosis in primary breast cancer, or with response to tamoxifen therapy in recurrent disease. PSA levels were determined by enzyme-linked immunosorbent assay (ELISA) in breast tumour cytosols, and were correlated with prognosis in 1516 patients with primary breast cancer and with response to first-line tamoxifen therapy in 434 patients with recurrent disease. Relating the levels of PSA with classical prognostic factors, low levels were more often found in larger tumours, tumours of older and post-menopausal patients, and in steroid hormone receptor-negative tumours. There was no significant association between the levels of PSA with grade of differentiation or the number of involved lymph nodes. In patients with primary breast cancer, PSA was not significantly related to the rate of relapse, and a positive association of PSA with an improved survival could be attributed to its relationship to age. In patients with recurrent breast cancer, a high level of PSA was significantly related to a poor response to tamoxifen therapy, and a short progression-free and overall survival after start of treatment for recurrent disease. In Cox multivariate analyses for response to therapy and for (progression-free) survival, corrected for age/menopausal status, disease-free interval, site of relapse and steroid hormone receptor status, PSA was an independent variable of poor prognosis. It is concluded that the level of PSA in cytosols of primary breast tumours might be a marker to select breast cancer patients who may benefit from systemic tamoxifen therapy.  (+info)

*List of hormonal alkylating antineoplastic agents

This is a list of dual hormonal and alkylating antineoplastic agents. Estramustine phosphate (Emcyt, Estracyt; Leo 299, NSC- ...

*Prednisone

Antineoplastic Agents, Hormonal (2009). Retrieved 9-11-2010 RIEMER, AD (April 1958). "Application of the newer corticosteroids ...

*Alkylating antineoplastic agent

List of hormonal alkylating antineoplastic agents "Alkylating Agents". US National Library of Medicine. Retrieved 2 August 2014 ... An alkylating antineoplastic agent is an alkylating agent used in cancer treatment that attaches an alkyl group (CnH2n+1) to ... The platinum agents are also sometimes described as nonclassical. Alkylating antineoplastic agents have limitations. Their ... University of Nebraska page on alkylating agent drugs Alkylating antineoplastic agents at the US National Library of Medicine ...

*Hormonal therapy (oncology)

List of hormonal alkylating antineoplastic agents DeVita, Vincent T.; Hellman, Samuel; Rosenberg, Steven A., eds. (2005). ... Selective estrogen receptor modulators (SERMs) are an important class of hormonal therapy agents which act as antagonists of ... although another class of hormonal agents, aromatase inhibitors, now have an expanding role in that disease. One effective ... Hormonal therapy in oncology is hormone therapy for cancer and is one of the major modalities of medical oncology ( ...

*Cytestrol acetate

List of hormonal alkylating antineoplastic agents Oborotov, A. V.; Smirnova, Z. S.; Osetrova, I. P.; Polozkova, A. P.; ... Cytestrol acetate is a steroidal antiestrogen and an alkylating antineoplastic agent (i.e., chemotherapeutic) which was ...

*Alestramustine

List of hormonal alkylating antineoplastic agents List of estrogen esters NCI Thesaurus. "Alestramustine". Retrieved 24 June ... G. W. A. Milne (1 July 2000). Ashgate Handbook of Antineoplastic Agents. Wiley. p. 5. ISBN 978-0-566-08382-2. KD Tripathi (30 ... is a nitrogen mustard alkylating antineoplastic drug that was never marketed. It is the L-alanine ester of estramustine, which ...

*Estromustine

List of hormonal alkylating antineoplastic agents List of estrogen esters Bruce A. Chabner; Dan L. Longo (7 December 2011). ... is a major active metabolite of the cystotatic estrogen and nitrogen mustard alkylating antineoplastic agent estramustine ...

*ICI-85966

List of hormonal alkylating antineoplastic agents List of estrogen esters J. Elks (14 November 2014). The Dictionary of Drugs: ... nonsteroidal estrogen and alkylating antineoplastic agent of the stilbestrol group and a cytostatic nitrogen mustard ester of ...

*Estramustine

List of hormonal alkylating antineoplastic agents List of estrogen esters J. Elks (14 November 2014). The Dictionary of Drugs: ... Estramustine (INN, USAN, BAN) is a synthetic, steroidal estrogen and alkylating antineoplastic agent which was never marketed. ...

*Estradiol mustard

List of hormonal alkylating antineoplastic agents List of estrogen esters J. Elks (14 November 2014). The Dictionary of Drugs: ... steroidal estrogen and alkylating antineoplastic agent and a chlorphenacyl nitrogen mustard-coupled estrogen ester that was ... 898-. ISBN 978-1-4757-2085-3. Asai M, Takeuchi H, Okada H (1978). "In vivo interaction between steroidal alkylating agents and ... V. H. T. James; J. R. Pasqualini (22 October 2013). Hormonal Steroids: Proceedings of the Sixth International Congress on ...

*Prednimustine

List of hormonal alkylating antineoplastic agents List of corticosteroid esters J. Elks (14 November 2014). The Dictionary of ... 868-. ISBN 978-3-88763-075-1. I.K. Morton; Judith M. Hall (6 December 2012). Concise Dictionary of Pharmacological Agents: ...

*Sturamustine

List of hormonal alkylating antineoplastic agents List of androgen esters J. Elks (14 November 2014). The Dictionary of Drugs: ... that was developed as an alkylating antineoplastic agent (i.e., a chemotherapy drug) for the treatment of hormone-dependent ...

*Atrimustine

List of hormonal alkylating antineoplastic agents List of estrogen esters J. Elks (14 November 2014). The Dictionary of Drugs: ... Ohsawa N, Yamazaki Z, Wagatsuma T, Isurugi K (1984). "[Bestrabacil: a possible target-oriented anticancer agent]". Gan to ... is a nitrogen mustard alkylating antineoplastic drug that was under development in Japan by Kureha Chemicals (now Kureha ...

*Phenestrol

List of hormonal alkylating antineoplastic agents List of estrogen esters J. Elks (14 November 2014). The Dictionary of Drugs: ... nonsteroidal estrogen and alkylating antineoplastic agent (i.e., chemotherapy drug) and a chlorphenacyl nitrogen mustard ester ... Lagova ND, Sof'ina ZP, Shkodinskaia EN, Kurdiumova KN, Valueva IM (1988). "[The antineoplastic activity of testiphenon]". Vopr ...

*Cortifen

List of hormonal alkylating antineoplastic agents List of corticosteroid esters Lagova ND, Kiselev VI, Kurdiumova KN, Sof'ina ... is a synthetic glucocorticoid corticosteroid and cytostatic alkylating antineoplastic agent which was developed in Russia for ... V.; Khalanskii, A. S.; Gershtein, E. S.; Gerasimova, G. K. (1999). "Dependence of antitumor effect of hormonal cytostatic ...

*Testifenon

List of hormonal alkylating antineoplastic agents List of androgen esters Lagova ND, Sof'ina ZP, Shkodinskaia EN, Kurdiumova KN ... and an alkylating antineoplastic agent (i.e., chemotherapeutic) that was never marketed. It is an androgen ester - specifically ... Valueva IM (1988). "[The antineoplastic activity of testiphenon]". Vopr Onkol (in Russian). 34 (11): 1363-8. PMID 3201773. ...

*N-Desmethylenzalutamide

... an NSAA which is used as a hormonal antineoplastic agent in the treatment of metastatic prostate cancer. It has similar ...

*LS-1727

... that was developed as an alkylating antineoplastic agent but was never marketed. List of hormonal alkylating antineoplastic ... nitrosocarbamates as potential anticancer agents". J. Med. Chem. 43 (8): 1484-8. doi:10.1021/jm990417j. PMID 10780904. J. Elks ... agents List of androgen esters § Nandrolone esters Reynolds RC, Tiwari A, Harwell JE, Gordon DG, Garrett BD, Gilbert KS, Schmid ...

*Estramustine phosphate

... is a dual alkylating antineoplastic agent (i.e., a chemotherapy drug) of the nitrogen mustard type and hormonal antineoplastic ... agent of the estrogen type that is used in the treatment of prostate cancer. Estramustine phosphate is indicated, in the United ...

*ORM-15341

... an NSAA which is under development as a hormonal antineoplastic agent for the treatment of metastatic prostate cancer. ... Both agents show much higher affinity and more potent inhibition of the AR relative to the other NSAAs enzalutamide and ...

*9α-Bromo-11-ketoprogesterone

Alan C. Sartorelli; David G. Johns (27 November 2013). Antineoplastic and Immunosuppressive Agents. Springer Science & Business ... 185-. ISBN 978-3-642-65806-8. GOLDENBERG IS, HAYES MA (1959). "Hormonal therapy of metastatic female breast carcinoma. I. 9 ... Tyler, Edward T. (1959). "FERTILITY PROMOTING AND INHIBITING EFFECTS OF NEW STEROID HORMONAL SUBSTANCES". Journal of the ...

*Cancer

Chemotherapy is the treatment of cancer with one or more cytotoxic anti-neoplastic drugs (chemotherapeutic agents) as part of a ... The primary ones include surgery, chemotherapy, radiation therapy, hormonal therapy, targeted therapy and palliative care. ... Hormones are important agents in sex-related cancers, such as cancer of the breast, endometrium, prostate, ovary and testis and ... Traditional chemotherapeutic agents act by killing cells that divide rapidly, a critical property of most cancer cells. ...

*Megestrol acetate

MGA is used mainly as an appetite stimulant in a variety of conditions and as an antineoplastic agent in the treatment of ... MGA has also been used as a hormonal contraceptive in combination with an estrogen at relatively low doses. In addition to its ... Kenneth A. Foon (1998). Biological and Hormonal Therapies of Cancer. Springer. p. 73. ISBN 978-0-7923-9997-1. Retrieved 2 June ... Ian Morton; Ian K. M. Morton; Judith M. Hall (1999). Concise Dictionary of Pharmacological Agents: Properties and Synonyms. ...

*Estrogen ester

... as well as the nitrogen mustard alkylating antineoplastic agent estramustine phosphate. Estrogen esters also occur naturally in ... Estrogen esters are used in hormone therapy and as hormonal contraceptives, among other indications. The first estrogen ester ...

*Management of prostate cancer

... as well as the combined estrogenic and nitrogen mustard alkylating antineoplastic agent estramustine phosphate. Newer estrogens ... Hormonal therapy can decrease levels of DHT by interrupting this pathway at any point. There are several forms of hormonal ... However, hormonal therapy rarely cures prostate cancer because cancers that initially respond to hormonal therapy typically ... Hormonal therapy is, therefore, usually used when cancer has spread from the prostate. It may also be given to certain men ...

*Chemotherapy

... possible roles for hormonal and non-hormonal attenuating agents". Human Reproduction Update. 20 (5): 759-774. doi:10.1093/ ... Antineoplastic Agents in Encyclopedia of Molecular Pharmacology, 2nd Edition, Volume 1. Eds. Offermanns S and Rosenthal W. ... The increased use of antineoplastic agents in veterinary oncology also puts these workers at risk for exposure to these drugs. ... Healthcare workers exposed to antineoplastic agents take precautions to keep their exposure to a minimum. There is a limitation ...
In a meta-analysis reported in JAMA Oncology, Spring et al found that neoadjuvant endocrine therapy was associated with outcomes similar to those with chemotherapy in women with estrogen receptor-positive breast cancer.. Similar Outcomes. The analysis included 3,490 patients from 20 randomized trials of neoadjuvant therapy containing ≥ 1 endocrine therapy arm. Compared with combination chemotherapy, endocrine therapy alone was associated with a similar clinical response rate (odds ratio [OR] = 1.08, P = .85), radiologic response rate (OR = 1.38, P = .12), and breast-conserving surgery rate (OR = 0.65, P = .07), with endocrine therapy alone being associated with reduced toxicity. Compared with tamoxifen, aromatase inhibitor use was associated with a better clinical response rate (OR = 1.69, P , .001), radiologic response rate (OR = 1.49, P , .001), and breast-conserving surgery rate (OR = 1.62, P , .001). Compared with endocrine therapy alone, dual combination therapy with growth factor pathway ...
ER-positive breast cancer is commonly treated with adjuvant endocrine therapies. Adjuvant endocrine treatment has been shown to increase overall survival and in light of recent studies is likely to be recommended for even longer duration in the adjuvant setting (40, 41). However, many patients do not benefit from these therapies and predictors for response or resistance to endocrine treatment are urgently needed. In this study, we report a meta-analysis of two genome-wide studies and two validation datasets for identifying genetic variants associated with breast cancer-related mortality specifically after adjuvant endocrine treatment. In a meta-analysis involving individuals treated with adjuvant endocrine therapy, we identified SNP rs8113308 specifically and significantly predicting outcome after endocrine treatment. We were further able to show that among patients with ER-positive tumors, there is a significant interaction between the rs8113308 and endocrine treatment, indicating a predictive, ...
Researchers examine the effect of different adjuvant endocrine therapies on disease recurrence in premenopausal women with ER+ breast cancer.
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Learn about the veterinary topic of Hormonal Agents. Find specific details on this topic and related topics from the Merck Vet Manual.
Prosigna is indicated for use in postmenopausal women with hormone receptor-positive, node-negative (Stage I or II) or node-positive (Stage II or IIIA) early-stage breast cancer to be treated with adjuvant endocrine therapy.. ...
Prosigna is indicated for use in postmenopausal women with hormone receptor-positive, node-negative (Stage I or II) or node-positive (Stage II or IIIA) early-stage breast cancer to be treated with adjuvant endocrine therapy.. ...
In this investigation, we delineate a pathway involving the MutL complex, along with ATM, CHK2, and CDK4/6 that is required for ER+HER2− tumors to respond to endocrine therapy (Fig. 6G). When components of this pathway are poorly expressed or lost through mutation, feedback control on CDK4/6 is defective. This allows the cell cycle to proceed despite DNA mismatches, thereby promoting the growth of high mutation load ER+ breast cancers that are intrinsically resistant to endocrine treatment, but still sensitive to CDK4/6i.. The sequential triple biopsy design of the NeoPalAna trial was executed to determine the effects of CDK4/6i on ER+ HER2− tumors where intrinsic endocrine therapy resistance had been demonstrated. Consistent with our model, CDK4/6i was uniformly effective in suppressing residual proliferation in MutL−ER+ breast cancers, with almost undetectable Ki67 levels after approximately 2 weeks of palbociclib exposure. In contrast, the degree to which each mutant MutL allele or ...
DI-fusion, le Dépôt institutionnel numérique de lULB, est loutil de référencementde la production scientifique de lULB.Linterface de recherche DI-fusion permet de consulter les publications des chercheurs de lULB et les thèses qui y ont été défendues.
Clinical equipoise exists around the optimal time to start adjuvant endocrine therapy in patients who will receive post-operative radiotherapy for breast cancer. Patients receive either concurrent or sequential endocrine and radiation therapy, where concurrent therapy consists of endocrine therapy started before, with or during radiotherapy, while sequential treatment is defined as endocrine therapy starting after the completion of radiotherapy. A recent survey of Canadian oncologists showed that the main reason for prescribing sequential endocrine therapy was a concern that concurrent endocrine therapy and radiotherapy would worsen the toxicity of endocrine treatment. This is despite the absence of any clinical trial evidence to support this. Indeed, a recent systematic review by our group was unable to confirm or refute whether increased toxicities, related to the timing of endocrine therapy and radiotherapy actually exist in clinical practice. The investigators are therefore proposing a ...
BACKGROUND: As trials of 5 years of tamoxifen in early breast cancer mature, the relevance of hormone receptor measurements (and other patient characteristics) to long-term outcome can be assessed increasingly reliably. We report updated meta-analyses of the trials of 5 years of adjuvant tamoxifen. METHODS: We undertook a collaborative meta-analysis of individual patient data from 20 trials (n=21,457) in early breast cancer of about 5 years of tamoxifen versus no adjuvant tamoxifen, with about 80% compliance. Recurrence and death rate ratios (RRs) were from log-rank analyses by allocated treatment. FINDINGS: In oestrogen receptor (ER)-positive disease (n=10,645), allocation to about 5 years of tamoxifen substantially reduced recurrence rates throughout the first 10 years (RR 0.53 [SE 0.03] during years 0-4 and RR 0.68 [0.06] during years 5-9 [both 2p|0.00001]; but RR 0.97 [0.10] during years 10-14, suggesting no further gain or loss after year 10). Even in marginally ER-positive disease (10-19 fmol/mg
Although mechanisms of acquired resistance to endocrine therapy have been identified in estrogen receptor-positive (ER+) breast cancer, the causes of intrinsic resistance, present at the time of diagnosis, are less well understood. Haricharan and colleagues linked loss of the MutL mismatch repair (MMR) complex to intrinsic resistance to endocrine therapy. MMR has two damage-sensing complexes: MutS and MutL. In patients with ER+ breast cancer, endocrine therapy resistance was associated with dysregulation of MutL but not MutS. In ER+ breast cancer cell lines, silencing of MutL complex genes promoted resistance to endocrine therapy (including estrogen deprivation, a surrogate for aromatase inhibitor exposure, fulvestrant, and tamoxifen) by preventing CHK2-mediated inhibition of CDK4/6, resulting in deregulated CDK4/6 activity that drove endocrine therapy resistance. Further, mutations that dysregulated MutL promoted resistance to endocrine therapy in patient-derived xenograft models. Response to ...
The majority of breast cancer patients discontinues todays standard adjuvant treatment (endocrine therapy) due to side effects and reduced quality of life. Thereby, most side effects are unspecific, suggesting a role of psychological factors as patients´ expectations (nocebo effects). Moreover, patients are not informed sufficiently about their treatment.. Using a longitudinal design, the nature and onset of adverse side effects and their association to treatment related expectations are investigated. Postoperative patients with hormone receptor-positive breast cancer are assessed before the start of adjuvant treatment. All patients receive standardized, additional information about endocrine therapy. Expectations about side effects, knowledge and satisfaction with the enhanced information are assessed before and after informing patients. Side effects, quality of life and adherence are measured three months, two and five years after start of medication intake.. It will be analyzed if patients ...
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BACKGROUND:The cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitor palbociclib, in combination with fulvestrant therapy, prolongs progression-free survival among patients with hormone-receptor-positive, human epidermal growth factor receptor 2 (HER2)-negative advanced breast cancer. We report the results of a prespecified analysis of overall survival. METHODS:We randomly assigned patients with hormone-receptor-positive, HER2-negative advanced breast cancer who had progression or relapse during previous endocrine therapy to receive palbociclib plus fulvestrant or placebo plus fulvestrant. We analyzed overall survival; the effect of palbociclib according to the prespecified stratification factors of presence or absence of sensitivity to endocrine therapy, presence or absence of visceral metastatic disease, and menopausal status; the efficacy of subsequent therapies after disease progression; and safety. RESULTS:Among 521 patients who underwent randomization, the median overall survival was 34.9 ...
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(Medical Xpress)-A University of Cincinnati (UC) cancer biology team reports breakthrough findings about specific cellular mechanisms that may help overcome endocrine (hormone) therapy-resistance in patients with estrogen-positive ...
Conclusion The benefit of Pin HER2+ early BC is maintained, with the greatest benefit continuing to be observed in the node positive population. With longer follow-up, the benefit of P no longer appears to depend on HR status. Continued follow up of patients is very important to determine possible benefit for OS. A calendar-driven third interim OS analysis is planned in 2.5 years, and the event-driven final OS analysis is planned when 640 deaths have occurred.. Addition of S-1 to Post-operative Endocrine Therapy Improves Outcomes for Patients with Hormone Receptor-positive, HER2-negative Breast Cancer:. ABSTRACT Publication Number: GS1-09 Addition of S-1 to endocrine therapy in the post-operative adjuvant treatment of hormone receptor-positive and human epidermal growth factor receptor 2-negative primary breast cancer: A multicenter, open-label, phase 3 randomized trial(POTENT trial). Masakazu Toi, Shigeru Imoto, Takanori Ishida, Yoshinori Ito, et al.. ...
In this issue of Clinical Cancer Research, Fox and colleagues report a prospective tamoxifen dose-escalation study in patients with low endoxifen concentrations during treatment (1). Tamoxifen is highly effective for preventing recurrence of hormone receptor (HR+) breast cancer; however, approximately 15% of patients will recur within 5 years despite adjuvant treatment (2). Tamoxifen is believed to be a prodrug with part of the antiestrogen activity attributed to endoxifen, which is produced primarily via CYP2D6-catalyzed metabolism. There is substantial variability in endoxifen concentration in patients on tamoxifen treatment, and there is some evidence that patients with low endoxifen concentrations during tamoxifen treatment are at increased risk of cancer recurrence (3, 4). On the basis of this putative association between endoxifen concentration and tamoxifen treatment efficacy, several studies have prospectively dose-escalated patients who have low-activity CYP2D6 genotype and predicted, ...
ESMO is a Swiss-registered not-for-profit organisation. All funding for this site is provided directly by ESMO or via grants from the sponsors and supporters.. Via L. Taddei 4, 6962 Viganello - Lugano - CH © Copyright 2017 European Society for Medical Oncology All rights reserved worldwide.. ...
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I am so glad I found this blog! Ive been on tamoxifen for 14 months. They really should have a warning label that says will alter your life on the bottle!!!! I had stage 1b BC ER/PR positive at age 38, did not reach my lymph nodes, thank god, no chemo or radiation. I quickly became depressed after I started taking the tamoxifen, I thought I was going through depression due to all the fear & scare I had gone through. Plus my reconstruction had been very painful & couldnt find any answers as to why it was so painful, so I was depressed. My period was normal until I took the tamoxifen, it changed to every 5 to 6 weeks instead of 4 & was very light. Over time it went back to my regular flow & time. I decided to start a period tracker app on my phone, thought it would be a good idea. About 6 months after taking tamoxifen I noticed that my mood was like a light switch & the depression was so bad, plus cramps body aches,loss of sex drive, fog you name it. The brain fog is the worst for me I cant ...
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Neoadjuvant endocrine therapy in the management of breast cancer is woefully underutilized by U.S. clinicians, according to advocates of this approach who made their case at the 2016 Miami Breast Canc.... ...
Steroid hormones mediate critical lineage-specific developmental and physiologic responses. They function by binding their cognate receptors, which are transcription factors that drive specific gene expression programs. The requirement of most prostate cancers for androgen and most breast cancers for estrogen has led to the development of endocrine therapies that block the action of these hormones in these tumors. While initial endocrine interventions are successful, resistance to therapy often arises. We will review how steroid receptor-dependent genomic signaling is affected by genetic alterations in endocrine therapy resistance. The detailed understanding of these interactions will not only provide improved treatment options to overcome resistance, but, in the future, will also be the basis for implementing precision cancer medicine approaches.. ...
This is a two stage study, with an initial dose escalation phase I study and subsequent double blind randomised phase II controlled trial. Eligible patients are post-menopausal women with metastatic ER+ breast cancer not suitable for surgical resection. Patients should be suitable for endocrine treatment, but have received no more than 3 previous lines of endocrine treatment and up to 1 line of chemotherapy for metastatic disease. They will also have had progressive disease during treatment with an aromatase inhibitor. Following the dose-escalation in stage 1, patients will be randomised to receive fulvestrant plus either placebo or 480mg (or maximum tolerated dose) of AZD5363 oral capsules or tablets taken once daily. Patients will receive fulvestrant in combination with either placebo or AZD5363 until disease progression. Patients may continue to receive fulvestrant and AZD5363/placebo treatment even after the last trial visit. ...
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Evidence-based recommendations on hormonal therapies (anastrozole/exemestane/letrozole) as extra treatment for early oestrogen-receptor-positive breast cancer
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Breast cancers with high-level estrogen sensitivity had a significantly greater risk of late recurrence, possibly indicating a need for more than 5 years of adjuvant hormonal therapy, British investig
Here is some moderately good news for women with breast cancer: taking Tamoxifen for 10 years rather than the prescribed five reduces the risk of cancer recurrence and, ultimately, death from the disease.
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Before you begin using a medication, be sure to inform your doctor of any medical conditions or allergies you may have, any medications you are taking, whether you are pregnant or breast-feeding, and any other significant facts about your health. These factors may affect how you should use this medication.. Blood clots: Tamoxifen may increase the chance of developing blood clots in the lungs or legs. This chance may be further increased if tamoxifen is given with other forms of chemotherapy. If you have a history of blood clots, discuss with your doctor how this medication may affect your medical condition, how your medical condition may affect the dosing and effectiveness of this medication, and whether any special monitoring is needed.. A blood clot in the blood vessels of the brain can prevent blood from reaching parts of the brain, causing a stroke. If you experience signs of a stroke such as confusion, difficulty speaking, loss of coordination, sudden headache or vision changes, contact ...
Do not become pregnant while taking this medicine or for 2 months after stopping this medicine. Stop taking this medicine if you get pregnant or think you are pregnant and contact your doctor. This medicine may harm your unborn baby. Women who can possibly become pregnant should use birth control methods that do not use hormones during tamoxifen treatment and for 2 months after therapy has stopped. Talk with your health care provider for birth control advice ...
Description and results of LEA, clinical trial comparing bevacizumab + endocrine therapy versus endocrine therapy in advanced breast cancer (metastatic)
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Hormonal therapy is a treatment that corrects hormone levels by adjusting them up or down. Hormones are part of your endocrine system and act as chemical messengers in your body to control different bodily functions. For example, insulin is a hormone that helps regulate your metabolism and how your body uses food for energy.
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TY - JOUR. T1 - Adjuvant endocrine therapy in postmenopausal breast cancer. AU - Ingle, James N.. PY - 2003/1/1. Y1 - 2003/1/1. N2 - Adjuvant endocrine therapy with tamoxifen has a clearly established benefit in postmenopausal women with resected early breast cancer that expresses the estrogen receptor and/or progesterone receptor. Whereas there is a vast and long experience with tamoxifen, the major focus of clinical trials over the past 6 years has involved the study of the third-generation aromatase inhibitors. Recently published data from the Arimidex, Tamoxifen, Alone or in Combination (ATAC) trial, which involved only postmenopausal women and is the largest adjuvant trial ever conducted, has demonstrated superior efficacy for anastrozole over tamoxifen alone or in combination with anastrozole. These data have engendered a great deal of discussion as to whether they provide a sufficient basis for changing the standard of practice in terms of choice of agent. Currently, a case can be made ...
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A significant amount of data has accumulated suggesting an important role for translational dysregulation in many cancer lineages, including breast cancer. It remained unclear, however, which of these alterations are the most significant determinants of cancer progression and poor patient outcomes. We sought to determine the association of translational regulators with clinical-pathologic factors and survival outcomes in hormone receptor-positive breast cancer. We found that high eEF2, S6, pS6 S240/244, p4E-BP1 T70, and low pdcd4 were significantly associated with node positivity. High p4E-BP1 T36/47, p4E-BP1 S65, p4E-BP1 T70 as well as total 4E-BP1 were associated with worse RFS. High p4E-BP1 T70 and pS6 S235/236, and low pdcd4, were associated with worse OS. In the multivariable analysis, in addition to positive nodes, high p4E-BP1 S65 remained a significant predictor of lower RFS. High pS6 S235/236, eEF2K and low pdcd4 were associated with lower OS. These results confirm that translational ...
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Adjuvant endocrine therapy has made a significant impact in improving overall survival for women with hormone receptor (HR)-positive breast cancer. The anti-estrogen tamoxifen is the most widely used therapy, although in postmenopausal women, aromatase inhibitors (AIs) have further improved outcomes either as an alternative to tamoxifen for 5 years, or given in sequential fashion following initial tamoxifen therapy. However, late recurrence remains perhaps the biggest risk in HR-positive breast cancer, with more than half all recurrences occurring beyond 5 years since primary diagnosis. As such, the current debate is whether extended AI or prolonged tamoxifen therapy should be given, and if so, to whom. We review some of the recent studies that have addressed this question and demonstrated further reduction in risk of recurrence, and discuss the clinical issues that face women and their health care providers in determining who should use which drug, and for how long.. ...
We present a single-cell application to determine PIK3CA mutations in CTCs, which uncovered the degree of intra-patient heterogeneity in patients with metastatic hormone receptor-positive breast cancer (HR+ MBC) and high CTC count (>10 CTCs/7.5mL). Using CellSearch and DEPArray we isolated circulating tumor cells (CTCs) and white blood cells (WBCs) from peripheral blood and sequenced PIK3CA exons 9 and 20 by targeted amplicon sequencing. Comparative analysis between the primary tumor (PT, n=27 patients), circulating cell-free DNA (cfDNA, n=31 patients), single (n=146 CTCs) and pools (n=70 CTC suspensions, ranging 5-120 cells/suspension) of CTCs from 26 patients and metastases/DTCs (n=11 patients) was performed. Mutations were frequent in PT (15/27 (55.5%)) and showed slight and substantial agreement with cfDNA (n=21; kappa=0.14) and CTCs (n=22; kappa=0.6733), respectively. A wild-type genotype in WBCs indicates a high specificity. Inter-compartmental concordance was observed in 13/18 (72.2%) ...
The estrogen receptor (ER) drives the growth of most luminal breast cancers and is the primary target of endocrine therapy. Although ER blockade with drugs such as tamoxifen is very effective, a major clinical limitation is the development of endocrine resistance especially in the setting of metastatic disease. Preclinical and clinical observations suggest that even following the development of endocrine resistance, ER signaling continues to exert a pivotal role in tumor progression in the majority of cases. Through the analysis of the ER cistrome in tamoxifen-resistant breast cancer cells, we have uncovered a role for an RUNX2-ER complex that stimulates the transcription of a set of genes, including most notably the stem cell factor SOX9, that promote proliferation and a metastatic phenotype. We show that up-regulation of SOX9 is sufficient to cause relative endocrine resistance. The gain of SOX9 as an ER-regulated gene associated with tamoxifen resistance was validated in a unique set of ...
Tamoxifen remains a widely used hormone therapy for pre and postmenopausal women with hormone receptor positive breast cancer in both adjuvant and metastatic disease settings. Resistance to this well tolerated and cost-effective drug limits its use. Only an improved understanding of the mechanisms of tamoxifen resistance will provide the basis for overcoming this phenomenon. Expression profiles from tamoxifen-resistant and sensitive MCF7 derived breast cancer cell lines were prepared, using Affymetrix HG_U133A cDNA microarrays. The data generated was analysed to identify novel pathways and genes associated with tamoxifen resistance or sensitivity. Selected genes, whose expression correlates with response to tamoxifen, were validated using RT-PCR in cell lines and following this, in situ hybridisation and immunohistochemistry on cell lines. Functional analyses of these genes were carried out: genes that were down-regulated in tamoxifen resistant MCF7 cells (HRASLS3, CTSD, CAXII) were selectively ...
OBJECTIVES. Primary. To determine the change from baseline to post-treatment Ki67 values in ER-positive, HER2-negative ILC tissue derived from postmenopausal women awaiting definitive surgery or further neoadjuvant treatment who are randomized to 21-24 days of neoadjuvant endocrine treatments with fulvestrant (two 250 mg IM injections given on day 1), anastrozole (1mg given orally daily), or tamoxifen (20mg given orally daily).. Secondary. - To evaluate ER protein expression in ILC tissues at baseline and following neoadjuvant endocrine therapy.. - To evaluate PR protein expression in ILC tissues at baseline and following neo-adjuvant endocrine therapy.. - To evaluate ER-related and ILC-specific candidate gene mRNA expression in ILC tissues at baseline and following neoadjuvant endocrine therapy in an effort to identify biomarkers of endocrine response and putative drivers of endocrine resistance in ILC.. - To evaluate associations between changes in Ki67 in ILC tissues following neoadjuvant ...
Background We designed the randomized phase III LEA study of first-line bevacizumab in combination with endocrine therapy, to address the hypothesis that anti-VEGF treatment can prevent resistance to endocrine therapy in patients (pts) with advanced breast cancer sensitive to such treatment.. Methods A multicentre, binational, randomised, open label, phase III study investigated the addition of Bevacizumab (B) 15mg/kg every 3 weeks to an endocrine therapy (ET) with letrozole or fulvestrant (250mg/4 weeks) as first-line therapy in metastatic breast cancer. Postmenopausal pts with HER2-negative and hormone-receptor-positive breast cancer were eligible. The primary objective was to compare progression-free survival (PFS) in the treatment arms. Secondary objectives were overall survival, time to treatment failure, overall response rate, response duration, clinical benefit rate and safety. The recruitment was completed in September 2011. Efficacy analysis will be triggered after 270 events.. Results ...
Modeling suggests that among patients who are wild type for CYP2D6, 5-year disease-free survival outcomes are similar to or perhaps even superior with tamoxifen than with aromatase inhibitors. Endocrine therapy tailored to CYP2D6 genotype could be considered for women who are newly diagnosed with br …
After surgery, women diagnosed with breast cancer face the risk of the breast cancer coming back (recurrence). Recurrence can happen at any time. But the risk of recurrence is highest during the first 3 years after treatment. To lower the risk of recurrence in postmenopausal women diagnosed with hormone-receptor-positive early breast cancer, hormonal therapy usually is prescribed for 5 years after the initial treatment. Treatment that comes after surgery or another initial treatment is called adjuvant therapy.. For years, tamoxifen was the hormonal therapy of choice for women diagnosed with hormone-receptor-positive early breast cancer. But in 2005, large clinical studies showed that aromatase inhibitors worked better than tamoxifen to reduce the risk of the cancer coming back in postmenopausal women diagnosed with hormone-receptor-positive breast cancer. So aromatase inhibitors - Arimidex (chemical name: anastrozole), Aromasin (chemical name: exemestane), and Femara (chemical name: letrozole) - ...
Our study shows a higher proliferative state, as determined by MIB-1 index, of benign endometrial epithelium in postmenopausal tamoxifen users when compared with untreated women. However, this was not reflected by the histomorphology of the epithelium or by mitotic figures in standard haematoxylin and eosin staining. On the contrary, the epithelium in tamoxifen users remained thin whereas the stroma became cell rich. However, the MIB-1 index in the stroma was also very low. The increased MIB-1 index in the endometrial epithelium might be indicative of an increased proliferative inclination in this subgroup of postmenopausal tamoxifen users. The fact that the control groups (II and IV) comprise endometrial tissue from women without breast cancer could be a source of bias, because breast and endometrial cancer share several risk factors. Another potential source of bias is the fact that there were more symptomatic patients in the tamoxifen users with benign endometrium (group I) than in non-users ...
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While overall there was no significant difference in the response rates observed after two by two grouping, a trend did favour oophorectomy (or ovarian ablation) with respect to treatment activity. In fact, the best response rate was observed in patients allocated to this treatment (46.6% OR -95% CL: 21.2-72.9) while the lowest rate was observed in patients treated with oophorectomy plus tamoxifen (11.1% OR: CL: -3.4-25.6). Response to goserelin and goserelin plus tamoxifen was 27.2% (+/- 18.6) and 45% (+/- 21.8), respectively. Logistical regression analysis suggested that there might be a different interaction between tamoxifen and goserelin or oophorectomy (ovarian irradiation), respectively. Nevertheless, patient survivals were comparable, irrespective of allocated treatment. This indicates that two by two grouping has some value with respect to treatment efficacy and shows that oophorectomy (or ovarian irradiation) and goserelin have comparable efficacies. Tamoxifen did not improve the ...
Associations between high levels of ERβ2 protein (immunoscore) or mRNA (qRTPCR) and improved outcome have been seen, but only the qRTPCR results are significant in the clinically relevant ERα + cohort. It is therefore important to establish the relationship between mRNA and protein levels in clinical samples. Notably, most previous RTPCR-based analyses have failed to take into account the possible translational control when assigning biological or clinical relevance to ERβ isoform expression.. When assessing the relationship between immunostaining and qRTPCR for paired samples from each case, no correlation was seen between levels of protein and mRNA for ERβ2 [Pearson (%+) -0.12 P = 0.24; and Spearman (Allred) -0.08 P = 0.40]. This is in contrast to ERα in the same cohort [Pearson (%+) 0.30 P = 0.003; Spearman (Allred) 0.50 P = 1.0 × 10-6], but a similar lack of correlation was seen previously for ERβ1 [9]. Due to tissue heterogeneity, any mRNA analysis of tissue homogenates without ...
Ending up being an anabolic task item, booster boosts testosterone hormonal agents quantity which to rises muscle mass cells leads subsequently. Additionally, testogen results gathered in the direction of this hormonal agents somatic advantages would certainly be the rise in skeletal dimension, bone growth and also density. That is muscle mass enhancement covered in a tablet computer for any person muscular tissue mass structure high strength and also fan enlightened gamers readily available. Oddly sufficient, as basic metabolic process is boosted by testosterone, these booster items might perhaps be the feasible methods to repair the body fat problems. The Diary of Clinical Endocrinology uploaded an analysis mentioning the outcomes of regional fat dimension and also supplements on whole body and also entry. Based upon clinical truths, raised levels of this hormonal agent subsequently lead to a significant basic minimized quantity of neighborhood well as full excess fat in subjects affected ...
My ob/gyn told me that only a percentage of women stop getting periods altogether while on tamoxifen (I forget what the percentage was; Ill have to get back to you on that). Many (if not most) women still get periods, either regularly or sporadically. Im a few days late as well, Jill, but KNOW Im not pregnant Can tamoxifen stop your period if youre 41? hi there, im 35 and had primary breast cancer two years ago. chemo cause my periods to stop for a bit but they then came back about a year after chemo finished. Ive been on tamoxifen for over 18 months and have been getting regular periods but much, much lighter than before. As Im also BRCA1 my.. Int J Gynecol Bribe. May;19(4) doi: /IGC.0bea47cbe. Mill of tamoxifen on the endometrium and the united cycle of premenopausal receptor cancer patients. Buijs C(1), Willemse PH, de Vries EG, Ten Hoor KA, Boezen HM, Hollema H, Mourits MJ. Bishop information: (1)Department of. In ma, tamoxifen stop menstruation I suffer some terrible harsh tamoxifen ...
Our thyroid is actually a really important glandular in our body. It lies somewhere during our frontal back. It is actually only a little glandular however very seriously requires bunches of attention. It is actually the glandular that generates thyroxin, which is a quite crucial bodily hormone for our body. Without it, our body units are going to not work effectively. The hormonal agents are accountable for the rate of metabolism of the body system that is actually why the thyroid needs to be regularly operating well.. There are pair of primary ailments that could be associated with the thyroid glandular. One is hyperthyroidism which is actually the condition when the glandular is actually creating excessive of the hormonal agents. When the glandular is certainly not creating the proper quantity of thyroxin, an additional is the hypothyroidism which happens. Only a little bit of variation can really impact a whole lot into our body. That appertains caring for it is actually extremely ...
Makes what if I can take fresenius nolvadex breast cancer cell lines o 20 mg para. Kessar side effects al 20 preis dcis tamoxifen after bilateral mastectomy.Tamoxifen 20mg Hexal:. Die Liste ist aufsteigend nach Preis sortiert und entspricht den unverbindlichen Preisempfehlungen des. Tamoxifen Al 20. Tabletten.Tamoxifen Al 20 Tabletten 30 St von Aliud Pharma Gmbh bei Petersberg-Apotheke Schrift: A-, A , A+. E-Mail-Adresse. Passwort. Samstag, 16. April 2016. Preis 14,36.Aldactacine rezeptfrei kaufen, hohe qualität und schnelle lieferung. Den besten preis auf Aldactacine und rabatte. Apotheke Deutschland für sie.. . coupons how long does it take to feel the effects of lexapro does metformin hcl 500 mg tablet help you with pcos feldene 20 mg. tamoxifen while on cycle. al.Erfolgreiche Teilnahme am Rolf-Joseph-Preis 2015 Erfolgreiche Teilnahme am Rolf-Joseph-Preis 2015. Die Untertertia C hat mit verschiedenen Beiträgen an dem.Tamoxifen AL 20 Zur Anwendung bei Erwachsenen Wirkstoff: Tamoxifen 20 mg ...
If you seek medical attention for any reason, be sure to tell your doctor that you take tamoxifen or have taken tamoxifen.. For women: Tamoxifen may make you more fertile. It is best to use some type of birth control while you are taking it. However, do not use oral contraceptives ("the Pill") since they may change the effects of tamoxifen. Tell your doctor right away if you think you have become pregnant while taking this medicine.. ...
Tamoxifen decreases breast cancer recurrence, mortality, and breast cancer risk in high-risk women. Despite these proven benefits, tamoxifen use is often limited due to side effects. We identified pre
Blood samples will be collected before and during hormone therapy in all patients treated with aromatase inhibitors. In case of tamoxifen therapy, blood samples will only be collected during tamoxifen therapy. Patients will have the ability to collect their fecal samples and fill in the questionnaire up to 2 days before or during regular hospital visits. It will take 5 minutes to fill in the questionnaire. All other procedures can take place during regular hospital visits. Taken all together, only the additional blood collection introduces a minimal burden to the patients ...
Taking tamoxifen for 10 years rather than 5 years reduces the likelihood of recurrence and mortality from breast cancer, according to a study.
Р Р Р done on two patients by Golchet et al. Ann Ophthalmol 25170-172 20 Johnson SM (1998) Neurotrophic corneal defects after diode laser cycloablation. 100, Taking (1996) 72. Injection test solution (a) and reference solution (a).
Tamoxifen blocks the actions of estrogen, a female hormone. Certain types of breast cancer require estrogen to grow. Tamoxifen is used to treat some types of breast cancer in men and women. Tamoxifen is also used to lower a womans chance of developing breast cancer if she has a high risk (such as a family history of...
All women on tamoxifen receive the standard dose of 20mg QD, irrespective of the use of potential CYP2D6 inhibitors, and are not tested for CYP2D6 polym
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Wish I could help you but I am first getting into vitamins. Just added e and calcium with mag. to my multi. Debby suzanne new wrote: , , I am using GENISOY protein powder. So far I have just tried the , chocolate (very tasty). Using soy is new to me so now I am trying to , experiment with tofu. Any suggestions will be appreciated. I am going to , everything in my power to stay healthy! , Your friend Suzanne , , , Lillian wrote: , , , , Sizanne, do you make your own soy shakes? your friend, lillian , , , , , , ----- Original Message ----- , , From: suzanne new ,[email protected], , , To: ,[email protected], , , Sent: Tuesday, July 06, 1999 2:11 PM , , Subject: Re: [MOL] Tamoxifen , , , , , Hi deb: I started on Tamoxifen about 3 months ago. Like you I had a , , lot , , , of thinking to do before I decided to take it. I got most of my , , , information over the form and as you know this drug is not without , , risk! , , , So far so good. The worst side effects I have experienced so far ar ...
Peptides are very important compounds that are frequently synthesized in all living organisms, and also offer mostly to control physical processes. Peptide hormonal agents as well as neuropeptides manage several procedures in the human body. Peptides are involved in the procedure of regrowth and development of cells, correct functioning of the immune system, body metabolic… Read More ». ...
Goetz MP, Knox SK, Suman VJ, Rae JM, Safgren SL, Ames MM, Visscher DW, Reynolds C, Couch FJ, Lingle WL, Weinshilboum RM, Fritcher EG, Nibbe AM, Desta Z, Nguyen A, Flockhart DA, Perez EA, Ingle JN: The impact of cytochrome P450 2D6 metabolism in women receiving adjuvant tamoxifen. Breast Cancer Res Treat. 2007 Jan;101(1):113-21. Epub 2006 Nov 18. [PubMed:17115111 ...
Dear all, My 9 years old son has been taking Tamoxifen for 2 months now. He is taken care of by a wonderful team in Hadassah Hospital, Jerusalem.The drug consi…
Dear all, My 9 years old son has been taking Tamoxifen for 2 months now. He is taken care of by a wonderful team in Hadassah Hospital, Jerusalem.The drug consi…
In this study no increase in the incidence of stroke was observed with 10 years of tamoxifen therapy, though endometrial cancer risk was higher in this arm. Endometrial cancer is often detected early, when it can often be treated successfully. The researchers estimate that for every endometrial cancer death that occurs as a side effect of long-term tamoxifen, there would be 30 deaths from breast cancer prevented ...
Bosom cancer is one of the main sources of death for ladies. This is the reason it is critical that each lady ought to think about this and figure out how to evaluate themselves in the event that they have added to the condition or are inclined to creating it. It is likewise vital that they comprehend that bosom malignancy is preventable and in addition treatable if the illness has been gotten on amid its initial stages. Knowing how to self-look at such is urgent for any lady. On the off chance that they have been esteemed by their specialist as having the condition or have a high risk in creating it, they will undoubtedly be approached to purchase tamoxifen citrate for either counteractive action or treatment. On the off chance that you purchase tamoxifen citrate, you are better guaranteed in getting over the ailment when contrasted with not doing anything by any means.. The best strategy is dependably counteractive action. On the off chance that you are viewed as high hazard, then it is ...
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FiSL-aiKcenС ССвСРРРС1cl irecuРРР1Р. Occurring exclusively in patients with renal tamoxifen mellГ©khatГЎsa, the first case series was published in 2000 115. B. Tamoxifen mellГ©khatГЎsa the rigid transform this is not the case, but a solution is nevertheless possible.
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Research presented at the American Academy of Dermatologys summer meeting showcases how hormonal therapy can be used to treat acne in women older than 20.
It should be observed that ASTRO has managed to come up with a list entirely made up of things NOT to do. Even the Ten Commandments had only 70% "shall-nots." I was particularly impressed by Wise Choice #1, which implies that women age 50 and above do not warrant treatment currently considered standard. We previously dealt with the possibly overstated encouragement for treatment with hormonal therapy alone vs. radiation therapy and hormonal therapy.full in women over 70 wondering if that was being overly discriminatory!!!. Perhaps there will later "Wise Choices" about what we should be doing, but in the meantime it might be worth evaluating these five items. Why were there five rather than four, six, or ten? It is because five is a sacred number in Freemasonry, or that there are five elements in Feng Shui? Is it a reference to the pentagram? Or, more ominously, is it a sign of a fifth column working within our profession, especially considering that the announcement was made only shortly before ...
BACKGROUND Tamoxifen is frequently used for the treatment of hormone receptor positive breast cancer (BC). Mainly CYP2D6 is responsible for the transformation to therapeutically active metabolites, but CYP2C19, CYP2C9 and CYP2B6 also are involved. We investigated the impact of polymorphisms within the genes encoding these CYP enzymes on the relapse-free time (RFT) in patients with BC. METHODS Ninety-nine patients with hormone receptor positive BC, who had undergone adjuvant tamoxifen therapy, were genotyped for seventeen common variants within the genes encoding CYP2D6, CYP2C9, CYP2C19 and CYP2B6 using TaqMan and PCR-RFLP technology. Kaplan-Meier and Cox regression analyses were performed to elucidate the impact of genetic variants on RFT. Furthermore, CYP2D6 metabolic activity was determined in a subset of 50 patients by assessing dextromethorphan/dextrorphan urinary excretion ratios. CYP2D6 activity was compared to the CYP2D6 allelic combinations to evaluate the predictive value of the CYP2D6 ...
New and emerging treatments for estrogen receptor-positive breast cancer: focus on everolimus Elisavet Paplomata, Ruth O’ReganDepartment of Hematology and Medical Oncology, Winship Institute of Emory University, Atlanta, GA, USAAbstract: Management of patients with metastatic hormone receptor-positive breast cancer poses a challenge due to the inevitable development of endocrine resistance. Hormone resistance is associated with a complex interaction of the estrogen receptor with growth factors, transmembrane receptors, and intracellular growth cascades. The PI3K/Akt/mTOR pathway plays a major role in hormone resistance and proliferation of breast cancer. Preclinical and clinical data indicate that inhibitors of human epidermal growth factor receptor-2, epidermal growth factor receptor, insulin-like growth factor-1 receptor, and the mammalian target of rapamycin pathway may act synergistically with hormone therapy to circumvent endocrine resistance. Everolimus is currently approved for combination
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The third-generation aromatase inhibitors (AI) anastrozole exemestane and letrozole lower risk of breasts cancer recurrence in comparison to tamoxifen in postmenopausal women with hormone receptor positive breasts cancer. GBR 12935 dihydrochloride manufacture women doctors and sufferers must weigh the potential risks and great things about each therapeutic choice when coming up with decisions about selection of therapy. AIs possess a different risk profile than GBR 12935 dihydrochloride manufacture SERMs. As well as the increased threat of bone tissue fractures and coronary disease AIs may also be connected with bothersome unwanted effects that can result in intolerance and following discontinuation of treatment.[1 13 Cross-trial and direct evaluations have demonstrated that AIs possess similar toxicities especially musculoskeletal and menopausal unwanted effects.[3 10 These observations recommend the relative unwanted effects are most likely because of a course impact from aromatase inhibition. ...
TY - JOUR. T1 - A phase 2 study of carboplatin plus docetaxel in men with metastatic hormone-refractory prostate cancer who are refractory to docetaxel. AU - Ross, Robert W.. AU - Beer, Tomasz (Tom). AU - Jacobus, Susanna. AU - Bubley, Glenn J.. AU - Taplin, Mary Ellen. AU - Ryan, Christopher. AU - Huang, Jiaoti. AU - Oh, William K.. PY - 2008/2/1. Y1 - 2008/2/1. N2 - BACKGROUND. Prostate cancer is the second leading cause of cancer mortality among men in the U.S. To the authors knowledge, there is no proven, effective, second-line therapy for docetaxel-refractory disease. Recent data suggest that platinum salts may be effective when combined with taxanes in metastatic hormone-refractory prostate cancer (HRPC). The authors conducted a phase 2 trial of docetaxel plus carboplatin chemotherapy in this disease setting. METHODS. Eligible men had metastatic HRPC that had progressed during or within 45 days after the completion of docetaxel-based chemotherapy. Patients were treated with intravenous ...
PubMed Central Canada (PMC Canada) provides free access to a stable and permanent online digital archive of full-text, peer-reviewed health and life sciences research publications. It builds on PubMed Central (PMC), the U.S. National Institutes of Health (NIH) free digital archive of biomedical and life sciences journal literature and is a member of the broader PMC International (PMCI) network of e-repositories.
TY - JOUR. T1 - Mutational analysis of triple-negative breast cancers within the International Breast Cancer Study Group (IBCSG) Trial 22-00. AU - Munzone, Elisabetta. AU - Gray, Kathryn P.. AU - Fumagalli, Caterina. AU - Guerini-Rocco, Elena. AU - Láng, István. AU - Ruhstaller, Thomas. AU - Gianni, Lorenzo. AU - Kammler, Roswitha. AU - Viale, Giuseppe. AU - Di Leo, Angelo. AU - Coates, Alan S.. AU - Gelber, Richard D.. AU - Regan, Meredith M.. AU - Goldhirsch, Aron. AU - Barberis, Massimo. AU - Colleoni, Marco. PY - 2018/7/1. Y1 - 2018/7/1. N2 - Purpose: We investigated the occurrence and the prognostic and predictive relationship of a selected number of somatic mutations in triple-negative breast cancer (TNBC) patients having known clinical outcomes treated within the IBCSG Trial 22-00. Methods: A matched case-control sampling selected patients enrolled in the IBCSG Trial 22-00 who had TNBC tumors, based on local assessment. Cases had invasive breast cancer recurrence (at local, regional, or ...
Many women diagnosed with breast cancer, especially younger women, are concerned about their ability to have children after treatment. Some breast cancer treatments can cause temporary infertility or make it harder to get pregnant after treatment ends. Other treatments, especially certain chemotherapy regimens, can cause early menopause and infertility. A meta-analysis suggests that women diagnosed with breast cancer who are treated with a luteinizing hormone-releasing hormone agonist in addition to chemotherapy may be more likely to become pregnant after chemotherapy ends. The research was presented on Sept. 28, 2015 at the 2015 European Cancer Congress and published online on Sept. 7, 2015 by the Annals of Oncology. Read the abstract of "Ovarian suppression using luteinizing hormone-releasing hormone agonists during chemotherapy to preserve ovarian function and fertility of breast cancer patients: a meta-analysis of randomized studies." Luteinizing hormone-releasing hormone agonists are ...

Antineoplastic Agents, Hormonal - DrugBankAntineoplastic Agents, Hormonal - DrugBank

Antineoplastic agents that are used to treat hormone-sensitive tumors. Hormone-sensitive tumors may be hormone-dependent, ... For adjuvant treatment of hormone receptor positive breast cancer , as well as hormonal treatment of advanced breast cancer in ... Toremifene is currently under investigation as a preventative agent for prostate cancer in men with high-grade prostatic ... A hormone-dependent tumor regresses on removal of the hormonal stimulus, by surgery or pharmacological block. Hormone- ...
more infohttps://www.drugbank.ca/categories/DBCAT000063

List of hormonal alkylating antineoplastic agents - WikipediaList of hormonal alkylating antineoplastic agents - Wikipedia

This is a list of dual hormonal and alkylating antineoplastic agents. Estramustine phosphate (Emcyt, Estracyt; Leo 299, NSC- ...
more infohttps://en.wikipedia.org/wiki/List_of_hormonal_alkylating_antineoplastic_agents

Actinex
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        Antineoplastic Agents, Hormonal,  Contraceptives, Oral, Synthetic,  ATC:G03AC05,  ATC:G03DB02,  ATC...Actinex - Antineoplastic Agents, Hormonal, Contraceptives, Oral, Synthetic, ATC:G03AC05, ATC:G03DB02, ATC...

Megestrol is a synthetic progestin and has the same physiologic effects as natural progesterone. The precise mechanism of megestrols antianorexic and anticachetic effects is unknown. Initially developed as a contraceptive, it was first evaluated in breast cancer treatment in 1967 ...
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Decagel
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        Antineoplastic Agents, Hormonal,  Glucocorticoids,  Antiemetics,  Anti-inflammatory Agents, ...Decagel - Antineoplastic Agents, Hormonal, Glucocorticoids, Antiemetics, Anti-inflammatory Agents, ...

Oral, rat LD50: >3 gm/kg. Signs of overdose include retinal toxicity, glaucoma, subcapsular cataract, gastrointestinal bleeding, pancreatitis, aseptic bone necrosis, osteoporosis, myopathies, obesity, edemas, hypertension, proteinuria, diabetes, sleep disturbances, psychiatric syndromes, delayed wound healing, atrophy and fragility of the skin, ecchymosis, and pseudotumor cerebri ...
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Male Infertility Related With Post Infection Inflammatory Syndrome - Full Text View - ClinicalTrials.govMale Infertility Related With Post Infection Inflammatory Syndrome - Full Text View - ClinicalTrials.gov

Antineoplastic Agents, Hormonal. Antineoplastic Agents. To Top. *For Patients and Families. *For Researchers ... Anti-Inflammatory Agents. Glucocorticoids. Hormones. Hormones, Hormone Substitutes, and Hormone Antagonists. Physiological ...
more infohttps://clinicaltrials.gov/ct2/show/NCT01407484?recr=Open&cond=%22Infertility%2C+Male%22&rank=3

Radiation Therapy With or Without Bicalutamide and Goserelin in Treating Patients With Prostate Cancer - Full Text View -...Radiation Therapy With or Without Bicalutamide and Goserelin in Treating Patients With Prostate Cancer - Full Text View -...

Antineoplastic Agents, Hormonal. Antineoplastic Agents. Androgen Antagonists. Hormone Antagonists. Hormones, Hormone ... Intensity Modulated Radiotherapy Plus Adjuvant Hormonal Therapy In Localized T1b-c, T2a, N0, M0 Prostatic Carcinoma. A Phase ...
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Study of Efficacy and Safety in Premenopausal Women With Hormone Receptor Positive, HER2-negative Advanced Breast Cancer - Full...Study of Efficacy and Safety in Premenopausal Women With Hormone Receptor Positive, HER2-negative Advanced Breast Cancer - Full...

Antineoplastic Agents, Hormonal. Selective Estrogen Receptor Modulators. Estrogen Receptor Modulators. Bone Density ... Antineoplastic Agents. Aromatase Inhibitors. Steroid Synthesis Inhibitors. Enzyme Inhibitors. Molecular Mechanisms of ... Patient is currently using other antineoplastic agents. *Patient is pregnant or nursing or physiologically capable of becoming ... Patients who received any prior hormonal anti-cancer therapy for advanced breast cancer, except for ≤ 14 days of tamoxifen or ...
more infohttps://clinicaltrials.gov/show/NCT02278120

SWOG-9346, Hormone Therapy in Treating Men With Stage IV Prostate Cancer - Full Text View - ClinicalTrials.govSWOG-9346, Hormone Therapy in Treating Men With Stage IV Prostate Cancer - Full Text View - ClinicalTrials.gov

Antineoplastic Agents, Hormonal. Antineoplastic Agents. Androgen Antagonists. Hormone Antagonists. Hormones, Hormone ... and prior hormonal therapy (neoadjuvant hormonal therapy vs finasteride vs neither). ... More than 1 year since any prior neoadjuvant or adjuvant hormonal therapy for a duration of no more than 4 months ...
more infohttps://www.clinicaltrials.gov/ct2/show/NCT00002651

Clinical Study on Strategy for Refractory Henoch-Schönlein Purpura - Full Text View - ClinicalTrials.govClinical Study on Strategy for Refractory Henoch-Schönlein Purpura - Full Text View - ClinicalTrials.gov

Anti-Inflammatory Agents. Glucocorticoids. Hormones. Hormones, Hormone Substitutes, and Hormone Antagonists. Physiological ...
more infohttps://www.clinicaltrials.gov/ct2/show/NCT03647852

Stimulus-Responsive Polymeric Nanogels as Smart Drug Delivery Systems.Stimulus-Responsive Polymeric Nanogels as Smart Drug Delivery Systems.

Antineoplastic Agents, Hormonal. Antineoplastic agents that are used to treat hormone-sensitive tumors. Hormone-sensitive ... If you are a legal copyright holder or a designated agent for such and you believe a post on this website falls outside the ... A hormone-dependent tumor regresses on removal of the hormonal stimulus, by surgery or pharmacological block. Hormone- ... particles under 100 nanometers possessing many biomedical applications including DRUG DELIVERY SYSTEMS and CONTRAST AGENTS. The ...
more infohttps://www.bioportfolio.com/resources/pmarticle/2374574/Stimulus-Responsive-Polymeric-Nanogels-as-Smart-Drug-Delivery-Systems.html

CYP2C19 | Cancer Genetics WebCYP2C19 | Cancer Genetics Web

Antineoplastic Agents, Hormonal. *Stereoisomerism. *Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. *Genotype ... Adjuvant endocrine therapy as well as other forms of targeted therapy such as HER2 inhibitors and antiangiogenic agents reduce ... Significant association of CYP2B6 transcript levels in tumors with expression of hormonal receptors was found in the ... our findings provide an immediate cue for clinical studies to evaluate the utility of PPARα ligands as safe agents for the ...
more infohttp://www.cancerindex.org/geneweb/CYP2C19.htm

ACSL3 | Cancer Genetics WebACSL3 | Cancer Genetics Web

Antineoplastic Agents, Hormonal. *Gene Expression Profiling. *FISH. *Cohort Studies. *RTPCR. *long-chain-fatty-acid-CoA ligase ... The aim of the present study was to characterize the androgen receptor (AR) response in hormonal therapy-resistant PC346 cells ... In (early) prostate cancer (PCa) androgens also regulate tumor growth, which is exploited by hormonal therapies in metastatic ... Modulation of androgen receptor signaling in hormonal therapy-resistant prostate cancer cell lines.. PLoS One. 2011; 6(8): ...
more infohttp://www.cancerindex.org/geneweb/ACSL3.htm

Pulmonary lymphangioleiomyomatosis in Korea.Pulmonary lymphangioleiomyomatosis in Korea.

Antineoplastic Agents, Hormonal / therapeutic use. Female. Humans. Korea. Lung / pathology, physiopathology, radiography. Lung ... CONCLUSIONS: As in other countries, in Korea LAM occurs exclusively in women and progresses despite hormonal treatment.. ... 0/Antineoplastic Agents, Hormonal; 10540-29-1/Tamoxifen; 520-85-4/Medroxyprogesterone ...
more infohttp://www.biomedsearch.com/nih/Pulmonary-lymphangioleiomyomatosis-in-Korea/10377208.html

Beliefs about medicine and illness are associated with fear of cancer recurrence in women taking adjuvant endocrine therapy for...Beliefs about medicine and illness are associated with fear of cancer recurrence in women taking adjuvant endocrine therapy for...

Antineoplastic Agents, Hormonal / therapeutic use*. Anxiety / etiology, psychology. Attitude to Health*. Breast Neoplasms / ... 0/Adjuvants, Pharmaceutic; 0/Antineoplastic Agents, Hormonal From MEDLINE®/PubMed®, a database of the U.S. National Library of ...
more infohttp://www.biomedsearch.com/nih/Beliefs-about-medicine-illness-are/23134580.html

Drug Information Portal - U.S. National Library of Medicine - Quick Access to Quality Drug InformationDrug Information Portal - U.S. National Library of Medicine - Quick Access to Quality Drug Information

A hormonal antineoplastic agent. Categories:. * Info Antineoplastic Agents. * Info Aromatase Inhibitors. * Info Enzyme ...
more infohttps://druginfo.nlm.nih.gov/drugportal/rn/107868-30-4

Pharmacogenomic Variation of CYP2D6 and the Choice of Optimal Adjuvant Endocrine Therapy for Postmenopausal Breast Cancer: A...Pharmacogenomic Variation of CYP2D6 and the Choice of Optimal Adjuvant Endocrine Therapy for Postmenopausal Breast Cancer: A...

Antineoplastic Agents, Hormonal / therapeutic use *. Actions. * Search in PubMed * Search in MeSH ... Baatjes KJ, Conradie M, Apffelstaedt JP, Kotze MJ. Baatjes KJ, et al. Anticancer Agents Med Chem. 2017;17(13):1805-1813. doi: ...
more infohttps://pubmed.ncbi.nlm.nih.gov/18445827/

Outcome prediction for estrogen receptor-positive breast cancer based on postneoadjuvant endocrine therapy tumor...Outcome prediction for estrogen receptor-positive breast cancer based on postneoadjuvant endocrine therapy tumor...

Antineoplastic Agents, Hormonal (therapeutic use) *Aromatase Inhibitors (therapeutic use) *Biomarkers, Tumor (analysis) ...
more infohttp://www.curehunter.com/public/pubmed18812550.do

Pyoderma disease: Malacards - Research Articles, Drugs, Genes, Clinical TrialsPyoderma disease: Malacards - Research Articles, Drugs, Genes, Clinical Trials

Antimetabolites, Antineoplastic. Phase 3. 29. Antineoplastic Agents, Hormonal. Phase 3. 30. alanine. Nutraceutical. Phase 3. ... The drugs Infliximab and Anti-Bacterial Agents have been mentioned in the context of this disorder. Affiliated tissues include ...
more infohttps://www.malacards.org/card/pyoderma

Lymphangioma disease: Malacards - Research Articles, Drugs, Genes, Clinical TrialsLymphangioma disease: Malacards - Research Articles, Drugs, Genes, Clinical Trials

Vasodilator Agents. Phase 1, Phase 2. 11. Antineoplastic Agents, Hormonal. Phase 2. ...
more infohttp://www.malacards.org/card/lymphangioma

Prednisone - WikipediaPrednisone - Wikipedia

Antineoplastic Agents, Hormonal (2009). Retrieved 9-11-2010 RIEMER, AD (April 1958). "Application of the newer corticosteroids ...
more infohttps://en.wikipedia.org/wiki/Prednisone

Hormonal Agents - Pharmacology - Merck Veterinary ManualHormonal Agents - Pharmacology - Merck Veterinary Manual

Learn about the veterinary topic of Hormonal Agents. Find specific details on this topic and related topics from the Merck Vet ... of certain lymphomas with prednisone may increase resistance of neoplastic cells to subsequent cycles of antineoplastic ... Hormonal Agents By Lisa G. Barber, DVM, Assistant Professor, Cummings School of Veterinary Medicine, Tufts University ; ... Hormonal therapy for neoplasia commonly involves use of glucocorticoids. Direct antitumor effects are related to their ...
more infohttp://www.merckvetmanual.com/en-pr/pharmacology/antineoplastic-agents/hormonal-agents

GnRH reduces the motility of HK1 cells. (A) Images of t | Open-iGnRH reduces the motility of HK1 cells. (A) Images of t | Open-i

Antineoplastic Agents, Hormonal/pharmacology*. *Cell Movement/drug effects*. *Cell Proliferation/drug effects* ...
more infohttps://openi.nlm.nih.gov/detailedresult.php?img=PMC4581822_MMR-12-04-4909-g04&req=4

Androgen Deprivation Therapy for Prostate Cancer - PubMedAndrogen Deprivation Therapy for Prostate Cancer - PubMed

Antineoplastic Agents, Hormonal / therapeutic use *. Actions. * Search in PubMed * Search in MeSH ...
more infohttps://pubmed.ncbi.nlm.nih.gov/16014598/

Meta-analysis of trials comparing anastrozole and tamoxifen for adjuvant treatment of postmenopausal women with early breast...Meta-analysis of trials comparing anastrozole and tamoxifen for adjuvant treatment of postmenopausal women with early breast...

Antineoplastic Agents, Hormonal /therapeutic use; Aromatase Inhibitors /pharmacokinetics /pharmacology /therapeutic use; Breast ... This review found that anastrozole was more effective than tamoxifen in adjuvant hormonal treatment of early breast cancer in ... To be eligible, studies needed to be randomised controlled trials (RCTs) that compared anastrozole with another agent in the ... Anastrozole appeared to be more effective than tamoxifen in the adjuvant hormonal treatment of early breast cancer. Until ...
more infohttps://www.crd.york.ac.uk/CRDWeb/ShowRecord.asp?AccessionNumber=12009100376&AccessionNumber=12009100376

MiR-100 impairs CSC properties by down-regulating Plk1A | Open-iMiR-100 impairs CSC properties by down-regulating Plk1A | Open-i

Antineoplastic Agents, Hormonal/pharmacology. *Cell Cycle Proteins/genetics/metabolism. *Cell Line, Tumor ... It induces the expression of a functional estrogen receptor (ER) and renders basal-like BrCSCs responsive to hormonal therapy. ... It induces the expression of a functional estrogen receptor (ER) and renders basal-like BrCSCs responsive to hormonal therapy. ... By promoting cell differentiation, miR-100 sensitizes basal-like breast cancer stem cells to hormonal therapy. ...
more infohttps://openi.nlm.nih.gov/detailedresult.php?img=PMC4385854_oncotarget-06-2315-g005&req=4
  • A hormone-dependent tumor regresses on removal of the hormonal stimulus, by surgery or pharmacological block. (drugbank.ca)
  • Moreover, miR-100 favors BrCSC differentiation, converting a basal like phenotype into luminal.It induces the expression of a functional estrogen receptor (ER) and renders basal-like BrCSCs responsive to hormonal therapy.Our findings indicate a new possible therapeutic strategy, which could make aggressive breast cancers responsive to standard treatments. (nih.gov)
  • However, evidence from several sources suggests that treatment of certain lymphomas with prednisone may increase resistance of neoplastic cells to subsequent cycles of antineoplastic chemotherapy through induction of MDR-1-related P-glycoprotein expression. (merckvetmanual.com)
  • This analysis provided no support for the hypothesis that the agents studied provide any clinical benefit for renal cancer patients although they increase the risk of toxic effects. (biomedcentral.com)