Hormone-related cancers account for almost 30% of all cancer cases in the United States. Data from animal experiments and from epidemiological and endocrinological studies in humans support the hypothesis that the individual hormones which control normal growth of target organs can also create the proper conditions for enoplastic transformation. The concept that hormones can cause, i.e., increase the incidence of, human cancer is most developed for the four hormone-related cancers which are numerically the most important, namely, breast, prostate, endometrium, and ovary. Even for these sites, large gaps remain in our knowledge of the responsible hormones and the conditions which create the optimal opportunity for carcinogenesis. Although scanty, the available epidemiological evidence also suggests a hormonal role in the pathogenesis of testis cancer, thyroid cancer, and osteosarcoma. We believe that the primary prevention of all these cancers will probably depend on modification of the factors ...
... On-line free medical diagnosis assistant. Ranked list of possible diseases from either several symptoms or a full patient history. A similarity measure between symptoms and diseases is provided.
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.. ...
Proliferation is an important part of cancer development and progression. This is manifested by the expression and / or altered activity of proteins related to the cell cycle. The constitutive activation of many signal transduction pathways also stimulates cell growth. Once tumors appear, growth and metastasis can be supported by the overproduction of appropriate hormones (in hormone-dependent cancers), by promoting angiogenesis, by the transition from epithelium to mesenchymal, by triggering autophagy and by take the signals of the surrounding stromal cells. Cancer therapy, which involves cytotoxic drugs, destroys cells that have a high basal level of proliferation and regeneration. While this type of therapy targets tumor cells, it affects non-tumor cells that proliferate rapidly. The objective of this study is to program through CRISPR-Cas9 a sequence to genetically inhibit the proliferation pathway of the rapamycin Diana protein in mammalian cells (mTOR) to alter and block the proliferation ...
The efforts of many laboratories have contributed to our current understanding of the GR cistrome and transcriptome in mammalian epithelial cells (38-42). For example, GR [and other nuclear receptors (NRs)] interact with DNA in multifaceted complexes composed of coregulators (43, 44), transcription factors (22, 45), and more recently appreciated, other NRs (11-15, 21, 46). Thus far, the interplay between GR and other NRs is most evident in hormone-dependent cancers, such as prostate and breast cancer. Data from this study and others suggest that GR and ER influence each others chromatin accessibility, as well as subsequent hormone-dependent transcriptional activity (3, 13-15).. Because GR is known to activate TNBC cell survival gene expression pathways (5, 6, 10-12) and high tumor GR expression is associated with poor ER− patient outcome (3, 4), we were struck by the observation that high GR expression was conversely associated with a significantly improved outcome in ER+ breast cancer. ...
Fibroblast growth factors (FGF) are small polypeptide growth factors. Many FGFs bind to the heparan-like glycosaminoglycans of the extracellular matrix (ECM; ref. 1). From this reservoir, FGFs may act directly on target cells by binding to specific receptor tyrosine kinases and this binding induces receptor dimerization and activation, ultimately resulting in the activation of various signal transduction cascades (2, 3). Some FGFs are potent angiogenic factors, and most of them play important roles in embryonic development and wound healing (4, 5).. FGF signaling seems to play a role in tumor growth and angiogenesis, and autocrine FGF signaling may be particularly important in the progression of steroid hormone-dependent cancers to a hormone-independent state (6). FGFs secreted by tumors act, on the one hand, in an autocrine manner promoting tumor growth, and, on the other hand, in a paracrine manner on endothelial cells, thereby promoting tumor angiogenesis (7). Both FGF-2 and VEGF are known to ...
development of hormone-dependent cancers4.. Xenoestrogens increase the size of our fat cells, promoting obesity in exposed people4. A literature review identifying connections between exposures to these POPs and type 2 diabetes was found, proving the "obesogen" theory that these chemicals make us fat and may lead to chronic disease. The review also identified support for the "developmental obesogen" hypothesis, which suggests that chemical exposures in utero may increase the risk of obesity in childhood and later in life by altering fat cell and the hormones that regulate appetite and eating behaviors. When pregnant women are exposed to POPs their children are more likely to get diabetes type 2 and obesity, particularly when they consume a diet high in calories, carbohydrates, or high-fat diet later in life5.. Despite the fact that food is a major source of exposure to these known reproductive ...
Maeda T, Irokawa M, Arakawa H, Kuraoka E, Nozawa T, Tateoka R, Itoh Y, Nakanishi T, and Tamai I. Uptake transporter organic anion transporting polypeptide 1B3 contributes to the growth of estrogen-dependent breast cancer. J Steroid Biochem Mol Biol 2010 Oct; 122(4) [http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6T8X-50G6962-1-C&_cdi=5098&_user=16764&_pii=S0960076010002888&_origin=search&_coverDate=10%2F31%2F2010&_sk=998779995&view=c&wchp=dGLbVlW-zSkzS&md5=4e61be9c7a06b0a1c489bad90ac1d2c4&ie=/sdarticle.pdf 180-5](10/7/10 ...
The genetic mechanisms of prostate cancer recurrence during hormonal therapy are largely unknown. So far, data from conventional karyotype analysis on hormone-refractory prostate carcinomas have not been published, mainly because of the difficulties in obtaining fresh hormone-refractory prostate carcinoma samples and getting metaphases from them. Here, we have studied chromosomal changes in 12 locally recurrent, hormone-refractory prostate carcinomas using karyotyping and CGH that revealed genetic aberrations in all tumors. Loss of the Y chromosome was the most common (89%) finding, and tetraploidy or near-tetraploidy was detected in all tumors. Also non-random translocations were found in 56% of the tumors. The present study indicates that clonal chromosomal aberrations in hormone-refractory prostate carcinomas are more common than in untreated primary tumors, and also, further studies on the frequency and significance of translocations in prostate carcinoma progression during hormonal therapy are
Patients who meet eligibility criteria and are enrolled will undergo whole-body imaging with 18F-choline PET/CT at 3 time points during the course of treatment that is indicated for castrate resistant prostate cancer. The 1st PET/CT scan is performed at baseline before treatment initiation. The 2nd and 3rd scans are performed at two other treatment-releated timepoints or at approximately 1 month and 3 months after treatment initiation. Change in lesion 18F-choline uptake from baseline measured at each time point will be determined. Cancer 18F-choline uptake will be evaluated as a marker of therapeutic response in comparison to PSA response and symptom scores. Treatment-related changes in tumor 18F-choline uptake occur will be studied after the second and third PET scans to determine the acuity by which changes in tumor 18F-choline uptake can be expected following specific treatments for castrate-resistant prostate cancer. The study evaluates a diagnostic intervention and the treatments ...
The purpose of this study is to evaluate the efficacy, tolerability and safety of a multi-targeted therapy in patients with hormone-refractory prostate
While some foods and cooking methods may encourage the development of cancer, others act as deterents. Red meat, animal fat and salt have been implicated as contributing to risk. The American Cancer Society recommends a diet high in plant-based foods and low in fat and meats. Betacarotene and vitamins found in fruits and vegetables have been shown to lower cancer risk. Isoflavinoids, found in soybeans, reduces the risk of hormone-related cancers. Fiber from plant foods aids in elimination of toxic wastes in the body and may also positively affect the risk of hormone-sensitive cancers ...
We carried out a fine-mapping study in the HNF1B gene at 17q12 in two study populations and identified a second locus associated with prostate cancer risk, approximately 26 kb centromeric to the first known locus (rs4430796); these loci are separated by a recombination hot spot. We confirmed the ass …
On HEALTH REPORT: Research in younger women finds that those ate the most red meat were twice as likely to get hormone-related cancers.
Fiber (Positively) Affects Hormone-Related Health: The March 2017 issue of the Journal of Diabetes describes that "low circulating levels of sex hormone-binding globulin (SHBG) have been shown to be a direct and strong risk factor for type 2 diabetes, cardiovascular disease, and hormone-dependent cancers". The publication goes on to report that a high fiber, low glycemic diet was associated with higher SHBG levels in a group of over 11,000 women. Another study published in the very same month revealed an inverse association between fiber rich food and breast cancer incidence. Whats more, a trial from January 2017 reveals that dietary fiber may mitigate the risk of breast cancer incurred by alcohol consumption. Taken together, this collection of evidence may provide a proactive way for women to avoid some of the most prevalent diseases of the modern age.. Fiber for Better Blood Sugar and Metabolic Health: Several new studies offer a unique method of adding more fiber to ones diet: replacing ...
Prostate Cancer Most common non cutaneous malignancy in men Second leading cancer killer of men Prostate Breast 180,400 cases/yr 182,000 cases/yr 36% of new ca cases 32% of new ca cases 40,400 deaths 46,000 deaths 1/6 chance of dvlp. 1/8 chance of dvlp. Hormone dependence hormone dependence
TY - JOUR. T1 - Impaired trafficking of connexins in androgen-independent human prostate cancer cell lines and its mitigation by α-catenin. AU - Govindarajan, Rajgopal. AU - Zhao, Sumin. AU - Song, Xiao Hong. AU - Guo, Rong Jun. AU - Wheelock, Margaret. AU - Johnson, Keith R.. AU - Mehta, Parmender P. PY - 2002/12/20. Y1 - 2002/12/20. N2 - Gap junctions, composed of connexins, provide a pathway of direct intercellular communication for the diffusion of small molecules between cells. Evidence suggests that connexins act as tumor suppressors. We showed previously that expression of connexin-43 and connexin-32 in an indolent prostate cancer cell line, LNCaP, resulted in gap junction formation and growth inhibition. To elucidate the role of connexins in the progression of prostate cancer from a hormone-dependent to -independent state, we introduced connexin-43 and connexin-32 into an invasive, androgen-independent cell line, PC-3. Expression of these proteins in PC-3 cells resulted in intracellular ...
TY - JOUR. T1 - FKBP51 and Cyp40 are positive regulators of androgen-dependent prostate cancer cell growth and the targets of FK506 and cyclosporin A. AU - Periyasamy, S.. AU - Hinds, T.. AU - Shemshedini, L.. AU - Shou, Weinian. AU - Sanchez, E. R.. PY - 2010/3. Y1 - 2010/3. N2 - Prostate cancer (PCa) growth is dependent on androgens and on the androgen receptor (AR), which acts by modulating gene transcription. Tetratricopeptide repeat (TPR) proteins (FKBP52, FKBP51 and Cyp40) interact with AR in PCa cells, suggesting roles in AR-mediated gene transcription and cell growth. We report here that FKBP51 and Cyp40, but not FKBP52, are significantly elevated in PCa tissues and in androgen-dependent (AD) and androgen-independent (AI) cell lines. Overexpression of FKBP51 in AD LNCaP cells increased AR transcriptional activity in the presence and absence of androgen, whereas siRNA knockdown of FKBP51 dramatically decreased AD gene transcription and proliferation. Knockdown of Cyp40 also inhibited ...
Intermittent administration of Taxotere® (docetaxel) appears to provide as much benefit, with fewer side effects, than continuous administration of Taxotere among patients with hormone-refractory prostate cancer. These results were recently presented at the 23rd annual meeting of the European Association of Urology.. Prostate cancer is one of the most common types of cancer diagnosed in men in the United States. One frequent approach to treatment of prostate cancer is androgen deprivation therapy (ADT), also referred to as hormone therapy. Prostate cancer is stimulated to grow from exposure to the circulating male hormone testosterone. ADT reduces the production of testosterone in the male body, reducing its growth stimulatory effects on cancer cells.. Unfortunately, prostate cancer cells can become resistant to the effects of hormone therapy, a condition referred to as hormone refractory prostate cancer (HRPC) or androgen-independent prostate cancer (AIPC). Men with AIPC are often treated with ...
The estrogenic soy isoflavone, genistein, stimulates growth of estrogen-dependent human breast cancer (MCF-7) cells in vivo. Genistin is the glycoside form of genistein and the predominant form found in plants. It is generally believed that genistin is metabolized to the aglycone genistein in the lower gut. However, it is unclear if the rate of metabolism of genistin to genistein is sufficient to produce a level of genistein capable of stimulating estrogen-dependent breast cancer cell growth. Our hypothesis was that dietary genistin would stimulate tumor growth similar to that observed with genistein in athymic mice. To test this hypothesis, genistin or genistein was fed to athymic mice containing xenografted estrogen-dependent breast tumors (MCF-7). Mice were fed either genistein at 750 p.p.m. (parts per milllion) or genistin at 1200 p.p.m., which provides equal molar concentrations of aglycone equivalents in both diets. Tumor size was measured weekly for 11 weeks. At completion of the study, ...
Adenocarcinoma of the prostate is the most prevalent tumor in men, a major cause of morbidity and mortality mainly because of the hormone refractory component. Hormone refractory prostate cancer...
Docetaxel-based therapy has been shown to prolong survival as first-line therapy for patients with hormone refractory prostate cancer (HRPC), and has become the standard of care. The beneficial effects of any therapy in HRPC may be diverse and include reduction in tumor bulk (when measurable), reduction in prostate-specific antigen PSA, reduction in symptoms (particularly pain), or stabilization of disease. Clear reductions in tumor bulk or PSA may provide objective evidence of a treatment effect, and stabilization of disease may be just as clinically meaningful in patients who are actively progressing prior to starting therapy. Pemetrexed has shown a broad array of activity in many diseases that until now were thought to be non-responsive to chemotherapy in the second-line setting.. This trial is designed to further assess the efficacy, safety, tolerability, and pharmacogenetics of pemetrexed as a single agent in subjects with HRPC whose disease has progressed following one prior taxane-based ...
BACKGROUND: The alpha-emitter radium-223 ((223)Ra) is a bone-seeking radionuclide studied as a new treatment for patients with bone metastases from hormone-refractory prostate cancer. We aimed to study mature outcomes from a randomised, multicentre, phase II study of (223)Ra.. METHODS: Patients with hormone-refractory prostate cancer and bone pain needing external-beam radiotherapy were assigned to four intravenous injections of (223)Ra (50 kBq/kg, 33 patients) or placebo (31 patients), given every 4 weeks. Primary endpoints were change in bone-alkaline phosphatase (ALP) concentration and time to skeletal-related events (SREs). Secondary endpoints included toxic effects, time to prostate-specific-antigen (PSA) progression, and overall survival. All tests were done at a 5% significance level, based on intention to treat.. FINDINGS: Median relative change in bone-ALP during treatment was -65.6% (95% CI -69.5 to -57.7) and 9.3% (3.8-60.9) in the (223)Ra group and placebo groups, respectively ...
Prostate cancer is one of the leading causes of cancer death in men. Androgen ablation, the most commonly-used therapy for progressive prostate cancer, is ineffective once the cancer cells become androgen-independent. The regulatory mechanisms that cause this transition (from androgen-dependent to androgen-independent) remain unknown. In this study, based on the microarray data comparing global gene expression patterns in the prostate tissue between androgen-dependent and -independent prostate cancer patients, we indentify a set of transcription factors and microRNAs that potentially cause such difference, using a model-based computational approach. From 335 position weight matrices in the TRANSFAC database and 564 microRNAs in the microRNA registry, our model identify 5 transcription factors and 7 microRNAs to be potentially responsible for the level of androgen dependency. Of these transcription factors and microRNAs, the estimated function of all the 5 transcription factors are predicted to be
Punit Saraon, Natasha Musrap, Daniela Cretu, George S. Karagiannis, Ihor Batruch, Chris Smith, Andrei P. Drabovich, Dominique Trudel, Theodorus van der Kwast, Colm Morrissey, Keith A. Jarvi, Eleftherios P. Diamandis, Proteomic Profiling of Androgen-independent Prostate Cancer Cell Lines Reveals a Role for Protein S during the Development of High Grade and Castration-resistant Prostate Cancer, Journal of Biological Chemistry, 2012, 287, 41, ...
The purpose of this study is to find the recommended doses of dasatinib and docetaxel given in combination to men with metastatic hormone refractory pro
A new drug has improved overall survival among patients with hormone resistant prostate cancer. The endothelin A antagonist ZD4054 was investigated in a placebo-controlled trial among 300 patients whose hormone-resistant prostate cancer had metastasized to bone ...
Thalidomide and its analogues have generated excitement for the treatment of inflammatory and autoimmune diseases as well as cancers. We have identified a thalidomide analogue (5HPP-33) with potent in vitro activity against a variety of tumor cell lines (both solid tumor and lymphoma). The IC50 values of the antiproliferative activities on these cell lines ranged from 1.7 μmol/L (LNCaP) to 11.1 μmol/L (Hs Sultan; Table 1). Interestingly, comparison of the IC50s of 5HPP-33 on the prostate cancer cell lines suggests that 5HPP-33 is effective against prostate cancer cell lines irrespective of their p53 status (LNCaP, wild-type p53; PC-3 and DU-145, mutant p53). In addition, the antiproliferative activities of 5HPP-33 on many cancer cell lines were independent of their hormone dependencies. Both androgen-dependent (LNCaP) and androgen-independent (PC-3 and DU-145) prostate cancer cell lines and estrogen-dependent (MCF-7) and estrogen-independent (MDA-MB-231) breast cancer cell lines were equally ...
The progression of all cancers is characterized by increased-cell proliferation and decreased-apoptosis. The androgen-independent prostate cancer (AIPC) is the terminal stage of the disease. Many chemokines and cytokines are suspects to cause this increased tumor cell survival that ultimately leads to resistance to therapy and demise of the host. The AIPC cells, but not androgen-responsive cells, constitutively express abundant amount of the pro-inflammatory chemokine, Interleukin-8 (IL-8). The mechanism of IL-8 mediated survival and therapeutic resistance in AIPC cells is unclear at present. The purpose of this report is to show the pervasive role of IL-8 in malignant progression of androgen-independent prostate cancer (AIPC) and to provide a potential new therapeutic avenue, using RNA interference. The functional consequence of IL-8 depletion in AIPC cells was investigated by RNA interference in two IL-8 secreting AIPC cell lines, PC-3 and DU145. The non-IL-8 secreting LNCaP and LAPC-4 cells served as
The progression of all cancers is characterized by increased-cell proliferation and decreased-apoptosis. The androgen-independent prostate cancer (AIPC) is the terminal stage of the disease. Many chemokines and cytokines are suspects to cause this increased tumor cell survival that ultimately leads to resistance to therapy and demise of the host. The AIPC cells, but not androgen-responsive cells, constitutively express abundant amount of the pro-inflammatory chemokine, Interleukin-8 (IL-8). The mechanism of IL-8 mediated survival and therapeutic resistance in AIPC cells is unclear at present. The purpose of this report is to show the pervasive role of IL-8 in malignant progression of androgen-independent prostate cancer (AIPC) and to provide a potential new therapeutic avenue, using RNA interference. The functional consequence of IL-8 depletion in AIPC cells was investigated by RNA interference in two IL-8 secreting AIPC cell lines, PC-3 and DU145. The non-IL-8 secreting LNCaP and LAPC-4 cells served as
This trial assessed efficacy and tolerability of satraplatin together with bevacizumab works in treating patients with metastatic prostate cancer previously
To assess the tumor targeting, safety, and efficacy of monoclonal antibody 131I-labeled CC49 in patients with androgen-independent prostate cancer, 16 patients received 75 mCi/m2 of the radiolabeled antibody after 7 days of IFN-gamma pretreatment. Sequential tumor biopsies in three patients showed a median 5-fold (range, 2-6-fold) increase in the proportion of cells staining positively for the TAG-72 antigen, whereas one showed a decrease in staining. Fourteen patients received 131I-labeled CC49, whereas 2 showed a disease-related decrease in performance status, precluding antibody treatment. The antibody localized to sites of metastatic androgen-independent prostate cancer in 86% (12 of 14; 95% confidence interval, 57-95%) of cases. Both osseous and extraosseous sites were visualized, and in six (42%) patients, more areas were visible when the radioimmunoconjugate was used than were apparent when conventional scanning techniques were used. The localization of the conjugate in the marrow cavity ...
Sabarubicin (MEN-10755), a new synthetic anthracycline analogue, was evaluated for safety and efficacy in a multicentre phase II study in patients with advanced hormone refractory prostate cancer (HRPC). Thirty seven patients were included, of which 34 were evaluable for PSA response according to Bu …
Removes ADP-ribose from asparatate and glutamate residues in proteins bearing a single ADP-ribose moiety. Inactive towards proteins bearing poly-ADP-ribose. Deacetylates O-acetyl-ADP ribose, a signaling molecule generated by the deacetylation of acetylated lysine residues in histones and other proteins. Plays a role in estrogen signaling. Binds to androgen receptor (AR) and amplifies the transactivation function of AR in response to androgen. May play an important role in carcinogenesis and/or progression of hormone-dependent cancers by feed-forward mechanism that activates ESR1 transactivation. Could be an ESR1 coactivator, providing a positive feedback regulatory loop for ESR1 signal transduction. Could be involved in invasive growth by down-regulating CDH1 in endometrial cancer cells. Enhances ESR1-mediated transcription activity.
CAUTION: Consult a healthcare professional prior to use if taking prescription drugs, or if you have been treated for breast cancer or any other hormone-dependent cancer. Do not use if pregnant or nursing. Discontinue use and consult a healthcare professional if you have a liver disorder or develop symptoms of liver trouble, such as abdominal pain, dark urine, or jaundice. May impair your ability to drive or operate heavy equipment. Due to additive sedative effect, avoid using with alcohol. For further instructions please read the enclosed insert.. Our black cohosh extract is standardized to be equivalent to 40 mg black cohosh root and rhizome.. Remifemin® and associated logo designs with butterfly are registered trademarks of, and RemiSure™ is a trademark of Schaper & Brummer GmbH & Co. KG.. Product of Germany. ...
Sometimes, the silencing of a gene is as important as its activation. Nonetheless, up to now, most studies on hormone-mediated gene regulation have focused on researching the factors that influence the activation of certain genes. Little attention has been paid to gene silencing.. But researchers at the Centre for Genomic Regulation (CRG) have discovered that there is a mechanism of active repression in hormone-dependent breast cancer cells that acts on genes related with cell proliferation and death.. "Up to now, the emphasis has focused more on the fact that steroid hormones can augment the activity of certain genes, and little was known about the mechanisms by which these hormones can also repress or silence genes," says Guillermo Vicent, main author of the study and researcher in the Chromatin and Gene Expression Group led by Dr. Miguel Beato.. In a study published in The EMBO Journal, Vicent and his team show that in the cell lines derived from breast cancer, some 1,000 genes are activated ...
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Global Hormone Refractory Prostate Cancer (HRPCA) Market Research Report 2020-2026, this title divided by product type, applications, industry vertica
Since 1995, when the first Hsp90 inhibitor was shown to demonstrate antitumor efficacy in mouse xenograft tumor models, there has been considerable effort focused on the development of Hsp90 inhibitors for the treatment of cancer. To date, there have been minor differences reported between N-terminal or C-terminal Hsp90 inhibitors. We recently reported that the novobiocin analogue, F-4 induces client protein degradation with minimal Hsp90 induction in androgen dependent and independent prostate cancer cells [18]. These were some of the first pieces of evidence that showed C-terminal inhibitors to possess a unique pharmacology when compared to N-terminal inhibitors. A hallmark of N-terminal Hsp90 inhibition is the induction of Hsps (Hsp27, Hsp70 and to a lesser extent Hsp90) mediated through HSF-1 transcriptional activation of the heat shock response element (HSE). This is of significant concern because clinical resistance has been attributed to the induction of pro-survival Hsps [11, 41, 42]. As ...
Adenovirus constructs. AdTSTA-FL was constructed as previously described (13, 14). The AdTSTA-sr39tk was constructed with the AdEasy system (15). The head-to-head orientation of activator (BCVP2) and reporter (SR39tk) in the single plasmid was constructed by replacing FL with SR39tk in PBCVP2G5-L (16). The BCVP2G5-sr39tk fragment generated by NotI and SalI digestion of PBCVP2G5-sr39tk was inserted into pShuttle, which was used in bacterial recombination to generate the full-length virus. The virus was grown on 293 cells, purified on a CsCl gradient, and titered by plaque formation assays on 293 monolayers. The level of replication competent adenovirus contamination in the viral stocks was evaluated by plaque formation on A549 cells. No plaque was detected at 108-fold higher viral stock dilution compared with assays on 293 cells.. Prostate cell lines and luciferase activity assay. The human prostate cancer cell lines LNCaP, CWR22Rv1, DU145, and PC-3 were grown in RPMI 1640 supplemented with 10% ...
To determine the time to progression produced by the combination of Novantrone (mitoxantrone) and Erbitux (cetuximab) versus Novantrone alone in metastatic
Topic summary contributed by volunteer(s): Randy All animal products contain steroid hormones, and the presence of hormones in food has been connected with several human health problems. For example, steroid hormones in milk may contribute to the acne epidemic. The sex steroid hormones in meat may alter a mans testicular development in utero as well as affect female fertility. Breast cancer is sensitive to growth promoting steroid hormones like estrogen. The dramatic increase of hormone dependent cancers, including breast, ovarian, endometrial, and prostate cancer in Japan, for example, has been speculatively linked to anabolic steroids in the beef supply. Due to the possibility of dietary hormones, including steroids, being a factor in hormone-related cancers, we should consider monitoring the levels of steroids and other hormones in dairy and meat-containing foods. There may be natural alternatives to anabolic steroids. For example, a lotion made out of cilantro seeds had some ...
Description: Hormonal carcinogenesis is an important and controversial area of current research. In addition to accelerating existing cancers, can hormones play the role of primary carcinogens? How do genetic factors influence hormone-related cancer risk? Hormones, Genes, and Cancer addresses these questions. Over the past few decades, cancer research has focused on external environmental causes(e.g., tobacco smoke, viruses, asbestos). With the advent of new genetic sequencing techniques, we are just now beginning to understand how the bodys internal environment(i.e., the hormones and growth factors that determine normal development) influences cancer etiology and prevention. From molecular insights to clinical analyses, this volume provides state-of-the-art information on the complex interactions between hormones and genes and cancer. The epidemiology and molecular endocrinology of prostate, breast, uterine, ovarian and testicular cancer are detailed in this timely treatise ...
The overall aim of this thesis is to illuminate and describe bodily changes and problems in incurable cancer, with focus on prostate cancer, from the patients perspective. The thesis consists of four papers, each of which illuminates various aspects of the phenomenon studied. The study population consisted of 24 participants, three women with different cancer diagnoses in the palliative phase, and 21 men with hormone refractory prostate cancer (HRPC) and skeletal metastases. Data are based on interviews (papers I-IV) and a quality of life questionnaire (paper I). The study design is cross-sectional (papers I-III) and longitudinal (paper IV). Qualitative description, descriptive statistics, phenomenological hermeneutics, and analysis of discourse were used to analyze data.. The findings of study I show that the dominating symptoms for the men with HRPC (n=20) were pain and fatigue, and three different variants of each problem were described. The men said that changes in their sex life were not ...
Nature Genetics has published a study that represented a fundamental step ahead in the improvement of drugs effectiveness for breast cancer treatment. The research has been performed at the European Institute of Oncology (EIO) by Saverio Minucci and Giancarlo Pruneri, both professors at the University of Milan -funded by the Italian Association for Cancer Research (AIRC) - in collaboration with the groups of Dr Luca Magnani (Imperial College, London) and Prof Antonino Neri (Policlinico Hospital and University of Milan). Researchers unraveled a genetic alteration responsible for drug resistance in hormone-responsive breast cancer, which represents two thirds of all breast tumor cases, and launched a molecular test to identify this mutation in patients.. "One of the main issues in using anti-cancer drugs -state Dr Minucci and Dr Pruneri- is represented by the appearance of tumor cells resistant to treatment. Identifying cancer resistance mechanisms represents a key objective of anti-cancer ...
1gs4: Structural basis for the glucocorticoid response in a mutant human androgen receptor (AR(ccr)) derived from an androgen-independent prostate cancer.
This book focuses on the functional significance of targeting apoptosis for the treatment of prostate cancer. New concepts on the challenges relating to the development of resistance by androgen-independent tumors are introduced, in terms of the contribution of anoikis and cross-talk of androgens with key growth factor signaling pathways. This volume also provides insightful discussion on the exploitation of the apoptotic and angiogenic synergism towards complete eradication of prostate tumors. Last but not least, it includes reflections on the drug development challenge based on the analysis of data from existing clinical trials. ...
The analysis of the molecular mechanisms underlying androgen-independent prostate cancer has been greatly facilitated by the generation of mouse models that can recapitulate key features of hormone refractory disease. Work in our laboratories has used mouse models that contain null mutant alleles of two key regulatory genes known to be inactivated in human prostate cancer progression, Nkx3.1 and Pten ( 11, 12). The Nkx3.1 homeobox gene encodes a transcriptional regulator that is expressed from the earliest stages of prostate organogenesis and is essential for proper branching morphogenesis of the prostate and expression of secretory proteins ( 13). Homozygous Nkx3.1 mutant mice are healthy and viable but develop a prostate epithelial hyperplasia that leads to the development of low-grade prostatic intraepithelial neoplasia (PIN) with increasing age ( 13). The Pten tumor suppressor encodes a lipid phosphatase that negatively regulates the phosphoinositide-3 kinase/Akt pathway and, thus is ...
In approximately two-thirds of cases, ER-positive breast cancer is characterized by the sustained expression of the ER-α (ESR1), making this receptor the most frequently utilized biomarker and therapeutic target for ER-positive disease.. Genetic mutations fuelling ESR1 expression in ER-positive breast cancer have been studied extensively, therefore, in this study the team aimed to look beyond genetic mutations. Utilizing epigenetics, the team observed a significant number of somatic mutations in a set of regulatory elements that have previously been demonstrated to regulate ESR1 expression in 7% of ER-positive breast cancers.. Lead author Mathieu Lupien (Princess Margaret Cancer Centre) commented: "By investigating acquired mutations found outside of genes through the power of epigenetics, we have identified that functional regulatory components can be altered to impact the expression of genes to promote breast cancer development.". Lupien believes that this research highlights the importance ...