Podcasts about lncap

Light Em UP! Targeted Combination Therapy Kills Cancer Cells in Less than 2 Hours Show Guests: Matthew Gdovin & Tom Roberts, CEO According the National Cancer Society, a staggering 606,000 people died of cancer in the U.S in 2019. When a cancer tumor grows in the body, it creates an acidic environment on the outside of its cells. This acidic environment causes blood vessels to grow and attach to the tumor in an attempt to remove the acid. In something of a biological trick, the tumor then commandeers the blood vessels and uses them as a source of nutrients to help it grow. The current standard of care to treat cancer is to cut (surgery), poison (chemotherapy), or ablate (radiation therapy). Unfortunately, these treatments can cause debilitating unwanted side-effects. Vitanova Biomedical (VNB) is developing an alternative therapy, Light-Activated Acidosis (LAIA), which uses a focused beam of light to activate a targeted drug injected into the tumor. Once activated, this drug causes the cancer cell to become very acid on the inside triggering rapid apoptosis (cell death). LAIA therapy has proven capable of killing up to 95 percent of cancer cells within two hours across five different cancer cell types including breast cancers including the very aggressive triple negative breast cancer (MDA-MB-231), two types of prostate cancers (LNCaP and 22RV1), and a pancreatic cancer (BxPC3). sparing near-by healthy tissue, and potentially causes no debilitating unwanted side effects. Tom Roberts, the company’s CEO, resports that VNB has entered a global strategic partnership with LiteCure Medical Lasers, and was awarded a competitive National Science Foundation SBIR Program Phase I grant to further develop LAIA therapy. Together, these partnerships should help to advance VNB’s LAIA therapy from laboratory bench to an FDA submission….and ultimately provide an effective alternative cancer treatment for multiple cancer types.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.13.249730v1?rss=1 Authors: Finn, P. B., Bhimsaria, D., Ali, A., Eguchi, A., Ansari, A. Z., Dervan, P. B. Abstract: Regulating desired loci in the genome with sequence specific DNA binding molecules is a major goal for the development of precision medicine. Pyrrole imidazole (Py Im) polyamides are synthetic molecules that can be rationally designed to target specific DNA sequences to both disrupt and recruit transcriptional machinery. While in vitro binding has been extensively studied, in vivo effects are often difficult to predict using current models of DNA binding. Determining the impact of genomic architecture and the local chromatin landscape on polyamide DNA sequence specificity remains an unresolved question that impedes their effective deployment in vivo. In this report we identified polyamide DNA interaction sites across the entire genome, by covalently crosslinking and capturing these events in the nuclei of human LNCaP cells. This method, termed COSMIC seq, confirms the ability of hairpin polyamides, with similar architectures but differing at a single ring position, to retain in vitro specificities and display distinct genome-wide binding profiles. These results underpin the development of Py Im polyamides as DNA targeting molecules that mediate their regulatory or remedial functions at desired genomic loci. Copy rights belong to original authors. Visit the link for more info

On this episode, I discuss my recent 5-day fast: how it went, what I learned, and whether I'll be doing it again. In the News & Views segment, we discuss a CNN article about fasting and longevity as well as a NY Times article that indicates intermittent fasting is becoming more widely accepted. You'll learn about a 450-lb man who did not eat food for over a year and reduced his body to a normal size. In the Moment of Paleo, I offer some ideas about when less is more. And After the Bell features a Dr. Jason Fung presentation about fasting as an important health tool. Enjoy the show! Links for this episode:This Episode's HomepageLatest in Paleo on Facebook - News hunters and gatherers post your links here.Full List of Recommended Books & AudiobooksEat, Fast & Live Longer HD - Video DailymotionOccasional fasting could help you live longer - CNN.comPeriodic fasting may lead to longer, healthier lives - AOLFasting Diets Are Gaining Acceptance - The New York TimesDietary restriction improves repopulation but impairs lymphoid differentiation capacity of hematopoietic stem cells in early agingHere's how occasional fasting could actually be good for you - ScienceAlertThe up- and downside of caloric restriction for aging and healthAGINGADVICE.ORGFasting - Wikipedia, the free encyclopediaDaniel Fast - Wikipedia, the free encyclopediaFasting Chart - Beliefnet.comUsing Fasting for Natural Healing | AllAboutFastingFasting: health benefits and risks - Medical News TodayA Periodic Diet that Mimics Fasting Promotes Multi-System Regeneration, Enhanced Cognitive Performance, and Healthspan: Cell MetabolismA History of Modern Research into Fasting, Starvation, and Inanition - SpringerMedically Supervised Water-only Fasting in the Treatment of HypertensionThe Fasting AdvantageHarpersMagazine Fasting - CloudupFasting: health risks - Live Well - NHS ChoicesWhat no one talks about when they extol the benefits of fasting - VoxFive day 'fasting' diet slows down ageing and may add years to life - TelegraphThe three-day fast: Day Four | Josh MitteldorfLifeboat Foundation Bios: Dr. Joshua MitteldorfBursts of fasting may be key to longevity and health - The Columbia Chronicle: Health & TechCould a 5-Day Fasting Diet Prolong Your Life?Effect of diet and exercise on serum insulin, IGF-I, and IGFBP-1 levels and growth of LNCaP cells in vitro (United States) - SpringerA year without food › Dr Karl's Great Moments In Science (ABC Science)The Ancient Secret of Weight LossIs Fasting an Effective Therapy for Weight Loss? - Weight LossThe Aetiology of Obesity Part 4 of 6: The Fast Solution - YouTubeVisit PuraKai to shop for eco-friendly clothing and stand-up paddle boards. Be sure to use coupon code "latest in paleo" for 15% off all clothing purchases.

Autoregulation is a control mechanism common to several proteins of the steroid/thyroid hormone receptor superfamily. In this work the effect of androgens and antiandrogens on the expression of the human androgen receptor (hAR) in prostate and breast cancer cell lines was studied. Northern blot analysis revealed a decrease in hAR steady state RNA levels in LNCaP cells by 3.3 nht of the synthetic androgen mibolerone. Maximal down-regulation of hAR RNA to 30% of control levels occurred 48 h after hormone addition. T47D breast cancer cells showed a similar effect with mibolerone, while hAR expression in normal skin fibroblasts did not respond to androgen treatment. As shown by nuclease Sl analysis, hAR transcripts initiate at three principal start sites, all of which are equally sensitive to androgen. Steroidal as well as nonsteroidal antiandrogens were capable of partially antagonizing androgen-mediated hAR RNA down-regulation in LNCaP and T47D cells, while not exerting a significant effect when administered alone. While hAR RNA stability was increased by hormone, nuclear run-on analysis revealed a 4-fold reduction of hAR gene transcrip tion 98 h after androgen treatment. Although decreased hAR RNA levels did not coincide with a parallel decrease in AR protein levels, analysis of androgen-inducible reporter constructs demonstrated that prolonged androgen administration to ceils results in a progressively impaired sensitivity of the intracellular androgen response mechanism. These results show that prolonged androgen exposure leads, besides its effect on hAR RNA levels, to functional inactivation of the AR. Thus, in viva, posttranslational control of AR activity appears to be a novel mechanism of negative autoregulation of androgen effects on gene expression.

Using gene-specific synthetic oligonucleotides the expression and regulation of kallikrein-like genes in the human prostatic cancer cell line LNCaP were studied. Prostate-specific antigen (PSA) and human glandular kallikrein (hGK-1) together constitute a subfamily of serine proteases exclusively produced in the human prostate. RNA analysis revealed that both genes are expressed in LNCaP cells with PSA basal levels being 2-fold higher than hGK-1 levels. Both mRNAs are induced over a period of 24 h in the presence of 3.3 nM of the synthetic androgen mibolerone. Stimulation of PSA RNA is about 5- fold,whereas hGK-1 stimulation is less pronounced. Nuclear run-on analysis revealed that androgen induction of kallikrein-like genes in LNCaP cells is a rapid event (c3 h) occurring at the level of transcription initiation. Treatment of cells with cycloheximide demonstrates that, while PSA/hGK-1 basal transcription strictly depends on continuous protein synthesis, transcriptional induction by androgen does not. This suggests the direct involvement of the androgen receptor in the induction process independent of additional labile protein factors necessary for kallikrein basal transcription. A binding motif is present in the PSA and hGK-1 promoters, closely resembling the consensus sequence for steroidresponsive elements. The androgen antagonist cyproterone acetate was also able to stimulate transcription of kallikrein-like genes in LNCaP cells. In contrast, androgen-dependent transcriptional suppression of the protooncogene c-myc was strongly counteracted by cyproterone acetate. Thus, antiandrogens act differentially on androgen-regulated prostate-specific (PSA, hGK-1) and growthrelated (c-myc) gene expression in LNCaP cells.