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Cancer Therapy - Science topic

Cancer Therapy is a forum to discuss and share information and methods in the area of cancer treatment.
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I am trying to insert a 60 bp shRNA into the pLKO.3G plasmid (variant of pLKO.1), yet nothing is working. 
I digest with EcoRI and PacI, anneal the oligos at 95 for 4 mins then 70 for 10 mins, then cool down to room temperature gradually. And I do quick ligation for 10 mins at room temperature, and transform into HB101 competent cells. However, nothing is growing on the ampicillin plates. Any suggestions?
I followed the protocol they have on Addgene, but it did not work. 
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Raed Hmadi, Ying Ding, I have succeeded to clone shRNA into pLKO.3G. Vanessa Rosa It seems some self-ligation may happen in your cloning. I think pLKO.3G is much easier to self-ligated than pLKO.1, and I don't know why. To avoid this effect, I used CIP to treat the digested pLKO.3G and PNK to treat the annealed oligos.
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what are the main challenges of current miRNA base cancer therapy? and how can we overcome them??
please if you have any alternative methods, used in targeting miRNA, let me know!
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The main challenges of current miRNA base cancer therapy include,
1. Low bioavailability and poor cellular uptake resulting in suboptimal delivery.
2. Off target effects.
3. Long-term safety concerns in humans.
4. The issue of rapid clearance in blood system. For the naked nucleotide-based drugs, the biggest obstacle for their function in vivo is the quick degradation by nuclease and the drug escape from endosome during endocytosis.
To overcome these problems, novel miRNA-formulations including nanoparticles and polymers as well as virus-based approaches could be employed. Target specific delivery could be achieved by direct injection of the synthetic oligonucleotides into solid tumours. This could be a feasible strategy for ocular tumors, brain tumors or sarcomas, and should reduce or eliminate off target effects. You may also try by tagging nanoparticle-miRNA oligonucleotide complexes with antibodies that bind the desired target cell.
You could also make use of sustained-release polymer formulations. Polymers are biodegradable compounds that protect the RNA from degradation and help in sustained delivery to the tissues. Polymers that vary in size, chemistry and pharmacological properties are available. Both invitro and in vivo studies have shown that biodegradable polymer-antisense oligonucleotide combinations achieve sustained delivery and improve tissue biodistribution.
Also, please refer to the article attached below.
Recently, more and more evidence showed that natural products such as paclitaxel, curcumin, resveratrol, genistein or epigallocatechin-3-gallate exert their anti-proliferative and/or pro-apoptotic effects through regulating one or more miRNAs, leading to the inhibition of cancer cell growth, induction of apoptosis or enhancement of conventional cancer therapeutic efficacy.
Best.
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Are there any target therapy for pseudomyxoma peritonii
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Anti-Angiogenic Treatment in Pseudomyxoma Peritonei—Still a Strong Preclinical Rationale:
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there are many side effects of chemo and radio therapy for cancer therapy, moreover, one of the main obstacles is cancer recurrence !!! I would like to know, does genomic engineering approach for cancer therapy gives permanent results or there is still a risk of cancer recurrence
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Frank Mitter thanks for your comment, yes it was very internesting
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Dear Sir/Madam
I am doing research studying the combined effect of two extracts for inhibiting foam cells, not for cancer therapy. Can I use the CompuSyn to investigate the extract interaction whether in addition or synergistic or antagonism. Since the cell we use is not targeted to be killed because macrophage is a normal cell and doing a physiological function to keep the homeostasis.
Can we use the reverse analogism of using CompuSyn in this case?
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If you were interested, also look at this link and the Compusyn software tutorial.
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Many good targets for antibody discovery have been reported, including PD-1/PD-L1, CTLA-4.
If there are some new targets that could be applied in cancer therapy or other diseases?
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Many thanks for Malcolm Nobre .I will learn more about your mentioned. Thank you very much!
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For any no-relapse cancer gene therapy, all cancer cells need to be transfected. Is it possible? Will repeated administration be able to reach all cancer cells? I know different serotypes viral vectors must be used for repeated administration to evade antibody response, but let's not focus on little details. I want to know if its fundamentally possible? Cancer cells have mutated antigens that viruses use to get in, so there can be resistance. Perhaps repeated non-viral transfection in-vivo? What do you think? If not, then why can't repeated transfection reach every cancer cell? It seems to me that due to minuscule size of vectors, spatial availability in-vivo isn't the issue. What do you think?
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Hi John Schloendorn , Thanks a lot for your reply. I might have phrased my question in a wrong manner. 100% transfection efficiency is impossible, let's say it is 20% efficient. Is it possible to still transfect all cancer cells in a patient with repeated administrations each with 20% efficiency, given that the treatment is selective and non-toxic? It seems like non-viral transfection is more stochastic, in a sense that it in principle can transfect any cell, it just happens that it doesn't, so with enough repeated administration it should be able in principle to transfect all cells, right? Thank you very much for your time. Your experience is invaluable on this matter. I am asking for a research proposal I have made, where this issues now stands out.
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Both additive and synergistic activities have been described for chemotherapy drug combinations co-loaded in the same nanoparticle. Such strategies have been aimed at cancer therapy via dual delivery of anticancer drugs bearing complementary anticancer mechanisms. However, how can one discriminate between an additive and a synergistic anticancer performance? I would like to discuss it.
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Julieta María Sanchez thanks for your input!
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I wanted to do a study with 177Lu-PSMA-617, and the only company selling it is MedKoo Bio-science in the US. Which doesn't have any reviews and the webiste looks very old.
is it a trusted company? also the rights to PSMA-617 are with Endocyte so how is it being sold with MedKoo. But if you know a place where i can buy it, i would be grateful!
Open to collaborations too.
Nakul Raval
IGP
Uppsala University
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inflammation NF KB 
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Nice Contribution Rikard G Fred
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As elucidated in article by Mitsunaga, et al (2011) <doi:10.1038/nm.2554>, photoimmunotherapy is a molecular-targeted cancer therapies that utilize photosensitizer molecule conjugated to specific antibody for EGFR (mAbs). The molecule then activated by NIR light irradiation to promote cell death.
It obvious for PIT utilization near body surface, but how about tumour located deep inside, that even endoscope can't reach, does it need a surgery for NIR light irradiation?
Also, is there a paper that explained about molecular mechanisms of these photosensitizer-conjugated antibody in detail?
Thank you.
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OVID-19 case,
Coronavirus
Research gate
I consider that I have a remedy for coronavirus. As I withal found the treatment for cancer, where do I commence and what do I do next want to forfend one's Technology. Moreover, to take it forward to a lab that Will avail to run the tribulations. Furthermore, withal get the opportune recommendation from one's vigilance and information.
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"In conclusion, high-dose intravenous ascorbate represents a promising and inexpensive anticancer therapeutic option that should be further explored in clinical trials. Given its low toxicity and low financial cost, ascorbate could become an important weapon in our arsenal against cancer, either acting as a single agent with predictive biomarkers or used in combination as an adjuvant therapy."
Targeting cancer vulnerabilities with high-dose vitamin C
Bryan Ngo, Justin M. Van Riper, Lewis C. Cantley & Jihye Yun
Nature Reviews Cancer volume 19, pages 271–282 (April 2019)
Invitation: Start a clinical trial.
There are currently 15 clinical trials. See details of those trials here: https://www.nature.com/articles/s41568-019-0135-7/tables/1
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Joe Graymer
Gamal Abdul Hamid Luis Rodrigo Wolfgang Doerr , check this out:
Alessandro Magrì et al. High-dose vitamin C enhances cancer immunotherapy, Science Translational Medicine (2020)
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In trying to getting more effective neoantigens for cancer therapy, I have some questions as followings.
1. T-cell activation is considered to be more important than B-cell activation. Which type of T-cell is more impotrtantbetween CD8+ T-cell and CD4+ T-cell? And what is the reason?
2. If a neoantigen have an activity for B-cell activation (i.e. for antibody production), does it have also the activity for T-cell activation?
If not, it is considered there are no correlation between them. Is it right?
Your answers would be very appreciated.
from DM
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1. Between CD4 or CD8, most would say CD8. First, CD8 recognize MHCI presented antigens, which all cells can present, thus they can have direct cancer cell activity. Also, most CD8s are cytotoxic, and can kill targets. CD4 is restricted to MHC II presented antigens and mostly are helper Ts. They direct immune response, but may not interact directly with targets as easily as CD8s.
2. B cell activation and antibody production isn't exactly without T cell help. Unless the antigen is strong enough to induce B cells to isotype switch without CD4 T cells... antibody production is still dependent on CD4 T cell recognition of antigen.
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Many efforts have been done by the researchers to culture the fungus extracted from Taxus plants in different mediums but the success rate was less. Hence, the Taxus plants remains the only source for paclitaxel extracts which is important for preparation of Taxol used in diagnosing cancer patients.
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Please see the following RG link.
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Can we consider photodynamic therapy of cancer (PDT) as an alternative method of conventinal cancer therapies like surgery, radiotherapy, chemotherapy ?? or it is just a complementary modality that can be combined with these therapies?
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Hello Issawi, PDT depends on how and where the cancer is too. If the patiente has a big tumor, probably the doctor will operate and PDT can be used as a complementary tecnique, but if cancer is on surface and not so deeper, PDT can be used as an alternative method.
I hope it has helped you.
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Their is need to understand the safety and efficacy of exercise therapy on cancer treatment–induced cardiovascular toxicity and tumor progression and metastasis in oncology practice, this can be achieved by having a fundamental knowledge of exercise prescription, dosing and personalization with regards to cancer treatment and according to global best practices.
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Dear Sir/Madam, I invited as a guest editor from high quality journals to handle special issues. If anyone can prepare a review similar to my review papers, particularly about a natural product in cancer prevention with focus on the structure activity relationship and mechanism of action, please kindly let me know to send an official letter. At this stage you should just send the title, authors and affiliation and abstract. Please kindly let me know as soon as you can. The suggested deadline for sending review is about 3 month. Best wishes, Suggeted topic: Genotoxicity of different agents and possble protection. Reducing side effects of radiotherapy and chomotherapy. Next generation of cancer therapy; Natural products. Natural products as novel therapeutic compounds. Radiation protection.
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What is names of the journals
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Non steroidal anti-inflammatory drugs (NSAIDs) are emerging as promising antineoplastic drugs. The use of NSAIDs, primarily aspirin, decreases the risks of several cancers, especially colon cancer, through the inhibition of cyclooxygenase enzyme.
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Please go through the following PDF attachment.
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Treatment for Cancer nowaydays like surgery and chemotherapy is really expensive for majority Cancer pasien in Indonesia, exspecially at Borneo. Can Cancer be cured with any methods that not too expensive but effective and efficient? 
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I have previously responded to a similar question on this platform. Please see the below given RG link.
Thanks!
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Specifically as a polivitaminic compound, and as an anti-tumoral agent.
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Hi,
i am currently looking for an experiment alternative to southern blot. I heard that pcr based assays give results quickly ( let's say within few hours). I want to perform sybr green relied pcr to detect copy number of my interested gene in the human genome like in southern blot. however, I couldn't find a proper protocol. If you address a protocol or share your experience, I will appreciate.
Thanks.
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Agree with the author above. If there are multiple copies of GOI scattered around genome, Southern blot may not resolve all of them, and qPCR may also be inconclusive. You may need to do NGS using long read platform to convulsively determine the copy number. qPCR is handy for an estimate.
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Can anyone help me in finding scientific research articles that confirm the effectiveness of camel milk (and urine) in the treatment of cancer? It seems that Western medicine is interested mainly in treatments that come in the form of a neatly packaged, commercially viable pill, and anything else is almost considered 'folk medicine'. I have asked a Western medical oncologist about the use of camel milk in the treatment of cancer, the response was that he wasn't even aware of such a thing. Any help would be much appreciated, thankyou.
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Hi,
I am having some difficulty finding papers which used nanoparticles to treat pancreatic cancer using 3D pancreatic cancer cells. please is anyone able to recommend some papers to me?
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Look also at the articles citing this paper on Pubmed. There are 14 papers citing this research. Probably you should refine your search strategy using various combinations of search terms. It took 30 sec. to find the above papers. Searching for papers also needs some experience which comes with time.
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Tumors in animal models, mostly mice, are usually very “young” and immature. We inject cancerous cells in matrigell and start administering nanoparticles within the next few days or a week. In the case of human, cancer grows sometimes for many years, so cancer vascular system is much more developed and matured. Can we then compare passive (EPR) targeting in mice and humans? Are there any indisputable published data which proves EPR (based on nano size only) effect in humans?
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The EPR effect is extremely heterogeneous in humans and it works in rodents but not in humans! We cannot expect to find a “one size fits all” answer. It seems to me fighting against cancer should be as a multidisciplinary approach, first having data from personalized medicine (P7), individually, for of each patient , then using nano targeting therapy techniques ( passive or active) accompanied by enhancing the own body immune system within the treatment i.e.a combination treatment might be more effective.
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In this article fig. 1. The Author has made a decision tree with 24 nodes. Each node is specified for a specific cancer tissue of origin and the couple of MicroRNA which can identify these cancer tissues of origin. My question is, if I isolate miRNAs at the node14(hsa-miR-21, let-7e), node21(hsa-miR-205, 152), node24 (hsa-miR182, 34a, 148), node10(hsa-miR-194, 382, 210), will it be enough to identify cancerous tissue originated from the lung.
Why am I asking this question, because, I want to identify cancerous tissue, which has migrated to different region but originated in the lung. So if I take miRNAs from those specified nodes, will it be enough to identify lung cancer tissue, which has migrated to different region but originated in the lung.
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microRNAs have to provide potential signature model for various cancers and other diseases. While miRNA in terms of sequencing is difficult , though being done provides huge number of miRNA in a specific cancer as you have exemplified some in your discussion. Few important learning points:
1- Specific sets of miRNAs usually express or otherwise together and they are termed miRNA families.
2-Some miRNA have the potential to act as pan cancer biomarkers but still no specificity is provided.
3-Some biomarkers are like positive or negative acute phase reactant and may rise or fall with non-cancerous disease.
4-There is some but as i experienced little correlation between blood and tissue based miRNAs
5- The science of miRNAs is still emerging and a lot more has to be learnt i guess before they are available, if available for clinical use.
6-Also need to have complete data about pre, pri and miRNA and he cleaving proteins like DROSHA, DICER and factors incorporated in RISC complex.
The whole picture is yet to appear and but hope is there that someday they may be appearing as both for diagnostic use and therapeutic targets like Riversin (spelling ?) for treating hepatitis C.
So potential is there but more research is needed to quantify and deal associated aspects of miRNA
Sorry, that I could not help you straight as i interpret the knowledge about this subject is still evolving.
Kind regards
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Although cancer immunotherapy can be quite effective, it has a variety of drawbacks.
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Hi Everyone,
I am planning a study to test the effectiveness of a cancer therapy on reducing tumor volume in a 4T1 mouse model. In addition, I would like to see the effect of my treatment on the metastatic spread of the tumors into the lungs. I recently came across a paper where they were able to analyze this with Q-RT-PCR which allows them to detect small metastases that cannot be seen with the traditional counting method by looking at the upregulation of genes that are specific to the cancer cell. In their study, they used human HER2. I dont think this would work for me since 4T1 cells are triple negative. Can anyone else suggest another marker which I could use for this? The link to the original manuscript is below.
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Thank you for your thoughtful responses. I have also been looking into some options and have seen some evidence that Ki67 may be a good candidate. Does anyone have any insights into this?
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I am curious to find more about this
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Aceria pongamiae a species of mite causes gall formation on the leaves of Millettia pinnata (= Pongamia pinnata).
Please have a look at these links and PDF attachment.
Good luck!
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I'm trying to study NAD+ metabolism in cancer cells. I'd like to study the levels of NAD+, nicotinamide and nicotinamide mononucleotide (NMN). Assay kits for ATP and NAD+ are available but I haven't found any for NMN or nicotinamide. Any suggestions?
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Would be possible to implant a prostate PC-3 tumor cell in a gluteus of a mice (or rat) so that it will grow somewhat laterally respect to the animal normal contour?
If that would be possible, a Radiotherapy 6 MV highly collimated single beam could hit the tumor (of about 1 cm3 size) but not vital organs of the animal. If that would be a wrong way, is there a better localization of the tumor Xenograft to obtain the desired result ? Thanks in advance for the help!
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We inject PC-3 cells into the hind flank of mice when doing xenografts (http://altogenlabs.com/xenograft-models/prostate-cancer-xenograft/pc-3-xenograft-model/). Based on your experimental conditions I think you could also do such an injection and proceed with the radiation protocol as you've stated it. If you're trying to not damage vital organs then the hind flank is one of the more "distant" locations from such organs.
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Can the 4T1 metastatic breast cancer model - which is a syngeneic xenograft model based on 4T1-12B - be used as a model to study the anticancer effects of plant based compounds without injecting into a balb/c mice?
Can one culture it directly in flasks, apply plant based extracts and study the effects of plants on the cells?
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I'm not sure which thread is the original one, but I'll re-emphasize my answer here; in vitro cell lines of murine origin will be better for compatibility purposes when translating in vitro cytotoxicity results into drug dosages for 4T1 xenografts (see our examples here: http://altogenlabs.com/xenograft-models/breast-cancer-xenograft/4t1-xenograft-model/). However, because 4T1 is of murine origin, the in vivo results may differ significantly from a study done on a human cell line like MCF-7.
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Can the 4T1 metastatic breast cancer model - which is a syngeneic xenograft model based on 4T1-12B - be used as a model to study the anticancer effects of plant based compounds without injecting into a balb/c mice? Can one culture it directly in flasks, apply plant based extracts and study the effects of plants on the cells?
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Usually it is best to perform in vitro studies of drugs to see their cytotoxicity on a given cell line, translate that concentration into a dosage for in vivo xenograft studies, and use xenografts with the same cell line. In context of 4T1, it has been done many times, and we've run xenografts with it (http://altogenlabs.com/xenograft-models/breast-cancer-xenograft/4t1-xenograft-model/) having a pre-determined concentration of drug/therapeutic along with in vitro results to compare with.
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Like, advances in nanomaterials for cancer treatment, gene therapy, etc...
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Just like we can elucidate bacterial growth by calculus.
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Dear Friends,
I have published a paper recently.
it shows the attitude of stem cells researchers.
All the best!
Mahdi.
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is the nanoparticle with smaller size (about 5 nm) suitable for cancer therapy?
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thank you dear Qaysar M Al-Hashemi
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the silver nanoparticle has a high toxicity with very low bio-compatibility. how i can apply this nanoparticle for cancer therapy purpose?
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thank you dear Qaysar M Al-Hashemi
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After rapamycin, TORC1 and TORC2 specific inhibitors were introduced in the phase of clinical trial for the treatment of angiomyolipomas (TSC / no-TSC). I was expecting some better results from the new drugs that inhibit TORC2 (involved in the organization of actin). I thought in fact, after the first brilliant results with the use of rapamycin, that residual disease could be in part due to the permanence of spindle muscle cells perhaps also for a modulation from epithelioid to spindle cell (with immunophenotypic characteristics of the "perivascular epithelioid cell-PEC"). I imagined that inhibitors of TORC2 could solve this problem (if my idea was correct). Currently our hypothesis of a phenotypic modulation of PEC (in the visceral lesions of TSC) has been accepted. The PEC is modulated by a smooth muscle cell (with progesterone receptors) up to a huge epithelioid cell (HMB-45 positive) in which are obvious metabolic and autophagic alterations.
I would like to know if you know what the immunophenotype of residual lesions of angiomyolipomas after treatment with mTOR inhibitors is. In particular, if the spindle cells are positive for the progesterone receptors. I think it would also be important, as well as the understanding of the mechanisms of regression, to assess the ability to run hormone therapy after mTOR inhibitors.
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I could not find any specific work on PP242 and Tuberous Sclerosis and / or lymphangioleiomyomatosis. Can someone tell me something about ?
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So recently I have come across these two completely contradictory methods for treating cancer, one solely relying on application of D2R agonists (such as quinpirole) for treatment of lung cancer and the other one (that is recently published) claims the application of D2R antagonists (such as aspimozide and haloperidol) for treatment of pancreatic cancer. It is quite confusing to me how can two totally paradoxic methods have the same effect on the cancerous cells. Can someone guide me on which method is actually useful. 
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This is the way I understand it.
The same chemical that excites a receptor at a low dosage may be considered to block it at a high dosage, potentially. This only works out if the chemical/drug in question has a dopaminergic effect, but less than that produced by the docking of the 'real' dopamine.
If the individual has LOW dopamine, our chemical that fits into the (previously empty) receptor excites it and produces a dopaminergic effect.
If our individual has HIGH dopamine receptor activity, then our chemical can snug into the receptor and prevent dopamine from docking. This decreases the dopaminergic effect, since this chemical has a weaker dopamine-releasing effect than dopamine would have.
Thus a chemical can have opposite effects depending on its dosage.
A second mechanism that may occur is where high doses may desensitize the receptor, leading to an inhibition effect over time. Here's a paper that discusses this in the context of dopamine:
Hope this was helpful!
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A micelles is designed for cancer therapy. For in vivo study what type of injection in mice with 4T1 xenograft tumor is better (i.v or i.p) and why?
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Hi Farnaz, I think it depends on factors such as how stable your micelle is in vivo and whether it is targeted.
If it is a standard phospholipid micelle, then IP injected particles will probably never reach the circulation because they have to cross numerous boundaries before they reach the circulation.
If injected IV, it has a better chance to reach highly vascularized tumors. But again if it is not tumor targeted, it can cause collateral damage because phospholipid micelles are processed like any natural lipid particles, that is through the liver and kidneys.
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Although thousands of scientists and specialists around the world are working on different types of cancer to find certain treatment for them, There is no definite way to cure that and we lose our relatives and friends every day. So what is the most important and challenging property of cancer that stands in front of us?
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Cancer has been around since the dinosaurs and, being caused by haywire genes, the risk is hardwired into all of us. The longer we live, the more likely something might go wrong, in any number of ways. For cancer is a living thing – ever-evolving to survive.
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Cancer Immunotherapy:
Do You have anything to say?
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In our Anti-PD-L1 immune checkpoint inhibitor trial we are seeing 30% of patients with complete response, in oesophageal adenocarcinoma, We are still going to see heterogeneous responses, more work needs to be done to understand why.
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Most cancers are detected when they cause symptoms that lead to medical evaluation. Unfortunately, in too many cases this results in diagnosis of cancers that are locally invasive or already metastatic and hence no longer curable with surgical resection or radiation treatment. Medical therapies, which might be curative in the setting of minimal tumor burden, typically provide more limited benefit in more advanced cancers, given the emergence of drug resistance.
http://science.sciencemag.org/content/sci/359/6378/866.full.pdf
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Liquid biopsy detection is promising method to detect cancer at early stage. Following the progresses of developing the sensitive methods to detect the cancer-related DNA or proteins in the blood, early detection for cancer becomes realistic.
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The autophagic network is important for cancer initiation, progression, and response to therapy. What activates the autophagy?. Is there a relation between the daily fasting of 8-12 hours and autophagy in cancer treatment?
Nature Cell Biology | VOL 20 | MARCH 2018 | 243–251
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Given the “autophagy-addiction” of tumor cells, the glutamine concentration in the tumor microenvironment greatly influences on the activity of autophagy-inducing signal pathways. It is notable to keep in mind the function of sestrin2 (leucine sensor molecule) for the regulation of mTOR signal pathway (Oncotarget. 2017 Oct 4;8(52):90132-90143, Cell Death Dis. 2017 Jun 1;8(6):e2842, Science. 2016 Jan 1;351(6268):43-8.)
Autophagic cell death with JNK signal activation is expected to exhibit the anti-tumor effect, which is explained in details in the review manuscript entitled“Therapeutic strategies of drug repositioning targeting autophagy to induce cancer cell death: from pathophysiology to treatment.”(Journal of Hematology & Oncology. 2017;10:67) For instance, a recent study described the chemical screening of 680 neurochemical compounds using patient-derived glioblastoma neural stem cells (GNS) and the subsequent identification of dopamine receptor D4 (DRD4) antagonists as selective inhibitors of GNS growth and inducers of normal neural stem cell differentiation and LC-3 puncta formation.
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Is loading Anti-Angiogenic Factors on drug delivery systems effective in the process of killing cancerous cells? Would it limit the delivery of nutrients to the tumor?
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It is needless to say that anti-VEGF agent exhibit the therapeutic effect. It has been widely accepted in the clinical settings that bevacizumab, the monoclonal antibody against human VEGF, is effective for the treatment for the patients with metastatic colon cancer. There are two important points you have to keep in mind.
Firstly, the neoangiogenesis of the tumor tissue depends only on VEGF, whereas that becomes to depend on not only VEGF but also other cytokines such as FGF-2, TGF-beta, and PIGF at the later stage of solid tumor.
Secondly, what determines the distribution of the therapeutic agent and oxygen concentrations does not depend on the amount of the intra-tumor blood. Those depend on the distribution of the blood vessels in the tumor microenvironment. The temporal and spatial intra-tumoral heterogeneity of the blood vessels makes it challenging to improve the drug delivery system.
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Could you please share your approach and experience if you are using any platform for personalized cancer treatment?
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Dear Navid,
Molecular diagnosis using IHC and PCR are progressing rapidly.
oncoDNA is also a new approach...
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Hello Dear colleges;
I) As we know that cancer cells grow up in a hypoxic conditions; "less oxygen, more growth". Morever; Angiogenesis maintain blood flow to the growing tumor tissues, providing nutrients and O2 for helping cancer cells to build up (even that we know that cancer cells don't like O2).
In other words, more cells more demand causing more hypoxia!!!!??? (how this work!!!).
First questions:
1) How these cells becomes hypoxic even thought of the presence of new vessels blood that supply oxygen??
2) is that means that tumours neglect and uncared for O2??!!!
II) During aerobic Glycolysis, tumours produce Lactate and H+ which leads to microenvironment acidosis (Warburg Effect).
3) Why cancer cells like to use fermentation process with which we've just got 2ATP per Glucose molecule rather than oxidative phosphorylation (36-38ATP per 1mole Glucose); EVEN the frenquency of oxygen supply!!! For Note, some studies mention that in some type of cancers the mitochondria is functionnal)!!
In addition, some studies say that: for a simple adaptation to intermittent hypoxia in pre-malignant lesions, they altered the glucose metabolism!!
Thank you for your consideration and help :)
Sincerely,
Fouzia
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In the first place new vessels formed through angiogenesis brought up by the tumor, are functionally ineffective for keeping up with the need of nutrients and O2.
So that major areas of the tumor are in hypoxic and acidic areas. These areas contain glycolytic cells. There are areas with better supply of O2 and cells in this other areas remain in OX-PHOS metabolism. There are in these oxigenated areas cells that take up lactic acid from ECM and metabolize it via OX-PHOS.
Tumors are metabolically heterogeneous coexisting three different cells: glycolytic, oxidative and lactic oxidative.
This said, the energy ecuation of glycolysis vs oxidative metabolism is 2 vs 38 ATP. But malignant cells consume around 10 to 20 times more glucose which compensates for any insufficient production of ATP.
OX-PHOS creates ROS while fermentation does not. Tumor cells are in continuos fight against an increased ROS production. Glycolysis is one if the responses to decrease ROS.
Finally glycolytic metabolism allows a major deviation of netabolites in order to create building blocks for structures like membranes and nuckeic acids. It permits an important deviation toward PPP (pentoses pathway) necessary for building nucleic acids.
The problem is very complex and not fully understood, but slowly we are finding out the advantages of glycolytic metabolusm for tumors.
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I am working on apoptosis and need to find mouse cell lines that express DR4 or DR5 receptors so sensitive to TRAIL (TNF-related apoptosis-inducing ligand ).
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Hi Ilya
Can you tell me the source where I can get the 4T1.2 cell line.
Thanks
Nidhi
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Since TSGs/oncogenes could have cellular context dependent function (previous question) is the tumor microenvironment a better alternative for cancer therapy ?
Deleting oncogenes by CRISPR/Cas9 gene editing is an option being considered for cancer therapeutics .
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Targeting the cancer microenvironment is a good instrument against cancer. The simplest way to do it is by targeting extracellular acicity with drugs as simple as omeprazol or even sodium bicarbonate. Neutralizing extracellular acidity slows down tumor migration.
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Activating a tumor suppressor/inhibiting an oncogene within a tumor by a drug may alter tumor cellular state. Tumor cells may adapt and give survival cues to the tumor microenvironment. So drug has to target signaling by tumor microenvironment to tumor cells. So not one drug but two, targeting tumor cell +tumor microenvironment.
Cellular States in Cancer: Visualization-Oscillating pendulum
Cellular states preceding and following tumorigenesis are  like- an oscillating pendulum that  overshoots mean position once (equivalent to cellular state i.e benign tumor after primary mutational hit-State A). The pendulum tries to  come back to mean balance position (equivalent to restoring homeostasis in cell after primary mutational hit). Due to  loss of elasticity of pendulum string (equivalent to secondary hit due to tumor microenvironment interactions) status quo of extreme position maintained, (which is  equivalent to malignant tumor-State B ).
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Dear Sengupta;
Main theme of this analogy is phase transition
Thanks
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I need to know if you can induce gene expression by injecting it into the mouse. There are plenty of examples of using the system in cell culture but I wasn't able to find anything about using it in animals. Thank you.
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As of a couple of weeks ago, no. They were offering a discount on the system if we were going to try...but that's not super helpful unfortunately.
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Please contact me if you are working on translational development of CAR T-cells and are interested in exploring potential collaboration opportunities.
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Hello folks! I guess my question might not be quite clear. I am seeking some rare mechanisms that could allow cancer therapeutics take effect outside of the cells. For example, (Maybe) breaking down the membrane intactness (in other words permeabilize the cells like TritonX). Most of the times to my knowledge, drugs need to be internalised by cells and subsequently release to effect the cancer cells' metabolism. That is quite boring, isn't it? So solving this puzzle will offer me a big help as this would give me some hints to design my project as I am intended to make a anticancer drug that may be applied to cancer therapy via such pathways.
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Decades ago, L-asparaginase has been pronounced largely inefficient against solid tumors, besides occasional responses noticed in melanomas and some lymphomas. Now we know that it may be effective against solid tumors with low level of asparagine synthetase (ASNS), such low-ASNS subsets of ovarian cancers.
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Dr Solary, how the corruption and the nepotism in Biomedical research in France, you are both Research Director of IGR and ARC -!!, affects the advancement in Science ? in the field of MDS/AML pathophysiology project.
ARC history is already a strong element in the analysis of this question.
You know that I can provide concrete data to you and to your colleagues to concretize the question and identify solutions;
Scientists, patients, donors, the citizen need to know how this system works - you are the Director!, for the good of human health and the democracy.
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@Jyoti, you do not need to comment. Dr Solary and the surrounding system will comment.
To remind, “Ethical axioms are found and tested not very differently from the axioms of science. Truth is what stands the test of experience.”― Albert Einstein
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Accumulating evidence demonstrates that intestinal bacteria influence oncogenesis, tumor progression, and response to therapy. Thus, selectively manipulating the gut microbiota may represent a feasible means to (i) limit the incidence of specific tumors in the general population and/or (ii) improve the activity of various anticancer agents . Although the first possibility has been investigated in several models of oncogenesis with promising results, the actual oncopreventive effects of anti-, pre-, pro-, and postbiotics in humans remain to be established.
Also, it is indirect evidence of "cancer is an adaptation mechanism"
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 DEPTHCANCER Gut microbes shape response to cancer immunotherapy Science  03 Nov 20l                 Summary
  1. Jocelyn Kaiser
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This week, two studies offer a raft of evidence from cancer patients suggesting that the gut microbiome—the community of bacteria, viruses, and other bugs living in our digestive tracts—helps determine whether tumors shrink when treated with a powerful new type of cancer drug. Patients who took antibiotics for routine reasons before or soon after starting a type of immunotherapy known as a PD-1 inhibitor relapsed and died sooner than those who were antibiotic-free. And when mice received fecal transplants from patients who responded to the drugs, they did better on PD-1 blockers than did mice given nonresponder feces. Researchers are now planning a clinical trial to test whether manipulating the gut microbiome could help more cancer patients respond to PD-1 blockers.
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Accumulating evidence demonstrates that intestinal bacteria influence oncogenesis, tumor progression, and response to therapy. Thus, selectively manipulating the gut microbiota may represent a feasible means to (i) limit the incidence of specific tumors in the general population and/or (ii) improve the activity of various anticancer agents . Although the first possibility has been investigated in several models of oncogenesis with promising results, the actual oncopreventive effects of anti-, pre-, pro-, and postbiotics in humans remain to be established. Also, it is indirect evidence of "cancer is an adaptation mechanism"
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As there is a lot of buzz about Immunotherapy, which is mainly antigen-based, In Dendritic Cell therapy or T cell therapy, we need to stimulate cells by a specific Tumor antigen.
My question is related to tumor microenvironment what percentage of cells expressing the antigen in the tumor?
Tumor microenvironment has its mechanisms to escape immune response in which antigen loss is also critical.
Why Can we not use direct antigen for tumor Immunotherapy, if we can then how effective it is?
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Dear Prashant,
Back to your original discussion, yes antigen loss and tumor micro-environment are both major roadblocks for immunotherapy. A good example is that thus far, direct antigen cancer vaccines targeting single tumor antigens (MAGE, WT1, NY-ESO1, have not shown dramatic therapeutic efficacy.  https://www.ncbi.nlm.nih.gov/pubmed/27058246
Even with engineered CAR T cells, it has been observed that antigen-negative relapse happens in about 30% of patients. https://www.jci.org/articles/view/87366
The reason why Checkpoint inhibitors work effectively in a subset of patients (along with several other reasons being studied) could be that checkpoint inhibition releases the brakes on a polyclonal immune response and therefore the immune system is targeting several antigens, not just the 1 or 2 that cancer vaccines use. This is suggested in observations where relapse after checkpoint inhibition occurs in tumors which have lost B2M and therefore have lost the ability to present antigen.  http://www.nejm.org/doi/full/10.1056/NEJMoa1604958#t=article
Therefore, certain cancer immunotherapies (CAR T cells, checkpoint blockade etc) have already proven to be effective in clinical trials, but relapse does occur due to antigen loss, and thus they can still be improved.
It will be interesting to see what clinical trials show in the next few years combining immunotherapies with other drugs that have synergistic mechanisms of actions.
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In particular, what are the resolution limits of radiation planning as applied to cancer therapy? Do these limits depend only on the equipment, or are we starting to see some limitations due to the ways in which the inverse problem of mathematical optimization is solved?
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The most outstanding limit, I would say, is related to the trade-offs we still need to take between accuracy and speed in the radiation transportation calculations, such as the Papanikolau approximation in convolution/superposition methods (see for instance Phys Med Biol 44, R99). The optimization of fluences and beam shapes in IMRT/VMAT aren't much of a problema nowadays.
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Is anyone experienced with assays to distinguish non-homologous end joining from homologous recombination in DNA repair?
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there is a kind of report- plasmid produced by university of rochester(Gorbunova) to discover the pathway of hr and nhej 
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Trials of anti-cancer compounds (for instance Erlotinib) in mice usually deliver the compound by intraperitoneal injection (IP). An exception seems to be Trametinib, which in all reports I have seen was delivered orally (with food or by oral gavage). Does anyone have experience with delivering Trametinib by intraperitoneal injection, or know of reports where this was done, or know a reason why this is not done?
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Intraperitoneal Tametinib in mouse as in human,  represents  a rapid  absorptiont's view .
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Cancer cells are resistant to radiotherapy, chemotherapy, hormonal or immunotherapy, they evade immune surveillance, have multiple mutations, short doubling time.blaah blaah..my question is how it is possible to take so many steps by a cells/group of cells in a short period of time or what make them to do so?
Whether we are familiar with elephant or just seeing tail as elephant?
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Undoubtedly we need to treat cancer.  My personal opinion is that many factors are responsible for this delay in efficiently treating cancer.  Cancer or virus, the cell system is exposed to a signaling hijacker.  As we still do not know how a signal is coordinated at the cellular level, we will still keep searching in the dark.  This is the reason that the majority of drug screening systems stop at the phase II or III.  
To my opinion the health system at the international level needs to be reviewed and that includes not only the public but also the private Co.  The human health has been transformed to a huge market system.  The question is what brings better money the “hope” or the “healing”.
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I am working on new developments in production of leuprolide depot.
Most products in the market are based on PLGA. I could not find any trade name with liposomal API. Could you please help me in this respect?
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As of March 3rd 2017, still not on the market.
For a list of liposomal drug products on the market have a look at this article:
Pharmaceutical liposomal drug delivery: a review of new delivery
systems and a look at the regulatory landscape.
Claudia Zylberberg and Sandro Matosevic
Drug Deliv, 2016; 23(9): 3319–3329.
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Hi
What is meant by targeted cancer therapies, and what advantages
do they offer?
Best wishes
Mohammad Amin
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Targeted therapies block the spread of cancer by interfering with specific molecules ("molecular targets") that are involved in the spread of cancer. Targeted cancer therapies are also called "molecularly targeted drugs," "molecularly targeted therapies,"  or "precision medicines".
For more information refer to the NIH cancer treatment fact sheet
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which compounds have recently been added to either Borono-phenylalanine(BPA) or sodium borocaptate (BSH) to increase tumor selectivity and boron distribution on the tumor for any type of cancer
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Examples are boron-hyaluronic acid (BHA), thiododecaborated α, α- cycloalkylamino acids, boron phosphate (BPO4) nanoparticles, dodecaborate-containing L-amino acids, and core-polymerized, boron-conjugated micelles.
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There are so many studies which explains the interaction of anticancer drugs with the mismatch DNA base pairs (AA, GG, CC etc). During de novo mutations, once a mutation is introduced, the corrupted DNA contains regular base pairing. Thus, interaction of anticancer drug like 6-Mercaptopurine with mismatched base pairs cannot play a significant role in cancer treatment. Hence, how this kind of studies can be implemented in cancer therapy?
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Dear Radhika
Most Important genes in Miss Match Repair in normal cells is: MLH1, MSH2, MSH6, PMS2, and MSH3 for repair base changed in normal cells.
some time we can use from macro molecule that can cohesion to DNA in cancer cells, and inhibit amplifications, gene expression and DNA replication as cancer treatment. 
Good luck
Amin
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In flow cytometry analysis of propidium iodide (PI) stained nuclei, if the cell arrest occurs in G0/G1 phase which are the most important enzymes involved in this phase?
Is there a cascade enzyme activity involved in this process? 
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Accumulation of cells in G0/G1 (cell arrest) is due to apoptotic mechanism. However to distinguish between intrinsic and extrensic pathways you need to measure caspases enzymes activity ( casp 3, 7, 8, 9) as well as detection of BCl 2 family proteins. Also as an indicator for apoptosis mechanisms, you can detect the expression of the cyclin-dependent kinase inhibitor (p21 protein).
Good luck
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i m searching for papers that have an injection dose of stem cells that used to treat colon cancer ..
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i think using mesenchymal cells may enhance tumour progress if they act as immune supressants
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In designing study about long QT with anticancer drugs.
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Dear Bandar,
This question is really quite open and does not lend itself to an immediate or meaningful answer.
I clearly do believe you are best served by a careful reading of current ICH E14 guidelines and recently added Q&A.
Happy New Year
Best
Per
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I would like to evaluate the effectiveness of a specific imaginative relaxation technique in a sample of cancer patients. My plan is to measure physiological parameters (e.g. surface electromyography, heart rate, respiration rate, skin surface temperature, or heart rate variability) as an addition to the subjective psychometric evaluation. 
Does anyone know studies that have investigated the effect of relaxation techniques on said physiological parameters in (cancer) patients?
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Hi David,
You might also look here - Hidderley M, Holt M. A pilot randomized trial assessing the effects of autogenic training in early stage cancer patients in relation to psychological status and immune system responses. Eur J Oncol Nurs 2004;8(1):61-65.
Best wishes,
Ruth
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After CLL relapse, what might we expect to observe in the genetics of the recurrent cancer?
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At patient may harbor the same karyotype but it is common to find some other additional cytogenetic lesions. Furthermore, the TP53 abnormalities (deletion or mutation) become more common at relapsed in particular among fludarabine-refractory patients.
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Dear Researchers,
There will be an impact in the binding of G-quadruplex DNA with the anticancer drugs due to different PH and temperature environment in our body. During the simulation how these PH and temperature should be treated with. (how to choose the proper environment). I have done a simulation  under the neutral PH (7.4) and acidic (5.5) environment, since in most of the literature these level have been used towards the cancer therapy. But I am so confused about choosing the temperature environments. In addition to the neutral temperature (300 K), what will be the most effective temperature environment should be considered towards the cancer therapy? Suggestions will be highly appreciated.
With regards,
R. Radhika
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PH is the power of hydrogen, in other words concentration of hydrogen i.e in the normal temperature 300k when PH value around 7, which mean that neutral. Mostly you proceed simulation neutral ph is good, some time temperature will go high, Ph goes to low, the hydrogen bond has not been formed, that situation may comes. My point of view, u perform the system at both low and high ph, and than compare them. Bio physical technique poin of you, i have less idea. go ahead.
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Why has differentiation therapy been explored for Myelodysplastic Syndromes (MDS), but not Myeloproliferative Neoplasms (MPN)?
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Hi Abdulqader
Defects in precursor cell differentiation are prominent in myelodysplastic synbdrome. In fact defective differentiation is an important cause of cytopenias in MDS. Therefore, this syndrome is amenable to differentiation therapy. On the other hand, the main defect in myeloproliferative diseases is abnormal proliferation (uncontrolled). The differentiation and maturation in MPD are often unaffected. Therefore, differentiating agents will have limited effect. The drugs that either inhibit specific proliferative signals (eg ruxolitinib) or those with general cytotoxic effect (eg hydroxycarbamide, busulphan...) are used to control the blood counts. Hope this makes sense. Best wishes
Siva
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A common feature of some advanced cancers is their enhanced capacity to metabolize glucose to lactic acid. Some carcinoma cells express highly glycolytic phenotype depending on the expression of hexokinase II in vitro and in vivo in some animal models.
Alkylating agent 3-BP apparently shows structural similarity to lactate, then the reactive 3-BP may enter cancer cells using the same transporter that exports lactate and then induce cancer cells ATP depletion followed by cell apoptosis.
is there any ongoing or recently finished experimental clinical trial using 3-BP as monotherapy or as a add on drug?
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Dear Dr Vargas,
Sorry to answer your question only after a year. I am the father of the patient, treated with 3BP  by Prof Vogl. I think I can answer most of your questions, but would prefer to do so by private mail.
kind regards,
Harrie Verhoeven
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Which depression model for rats do you prefer? What is the best way to induce depression in rats? We would like to start some projects in this field and we do not have any experience....
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You are most welcome, please let me know how it goes, and i might be able to help you with one of the Books (2010).   Best wishes.
Ghanim.