Cancer Therapy - Science topic

Introduction:

> Cancer remains one of the leading causes of mortality worldwide, accounting for nearly 10 million deaths annually (WHO, 2022). The economic burden is equally staggering, with global cancer care costs surpassing $1.16 trillion per year.

Current treatment modalities such as chemotherapy and radiotherapy—while effective—lack precision and selectivity, often causing significant damage to surrounding healthy tissues and resulting in debilitating side effects. These systemic approaches do not specifically target cancerous cells at the local level, thus limiting treatment efficiency and increasing recovery time.

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Our Conceptual Innovation:

> Through extensive studies on the biological effects of negative pressure on tissues, we observed that:

Controlled negative pressure below a certain threshold encourages tissue regeneration.

However, beyond pressures exceeding systolic blood pressure levels, negative pressure induces:

Vascular stasis

Tissue necrosis

Disintegration of cellular architecture

Detachment and suction of cells into the drainage system.

This mechanism presents a novel opportunity for cancer therapy:

By applying regulated negative pressure locally to tumor sites, it may be possible to selectively detach and remove cancerous cells.

Since malignant cells exhibit weaker adhesion, this approach can also reduce intraoperative metastasis risks by preventing cancer cells from dispersing during treatment.

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Key Features of the Proposed Device:

1️⃣ Dual-Lumen System:

Negative-pressure cannulas to create localized suction at the tumor site.

Positive-pressure microcannulas strategically placed (via ultrasound-guided navigation) to protect adjacent sensitive tissues by creating a pressure barrier.

2️⃣ Dynamic Pressure Gradient:

Establishing a tissue-wide pressure gradient for continuous tissue flushing, selectively removing cancerous cells while sparing healthy structures.

3️⃣ Integrated Safety and Efficacy Measures:

Real-time pressure monitoring to prevent excessive ischemic damage.

Co-infusion of pro-coagulant factors to control hemorrhage and prevent unnecessary blood suction.

Enzymatic agents delivered via positive-pressure channels to degrade extracellular matrices selectively.

4️⃣ Advanced Treatment Modulation:

Localized drug delivery: On-demand administration of chemotherapeutic agents, reducing systemic toxicity.

Thermal regulation: Adjustable temperature control to aid in tumor cell destruction.

Electrostimulation: Application of frequency-specific electrical currents to enhance therapeutic outcomes.

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Operational Considerations:

> Preoperative Planning:

High-resolution 3D imaging (CT/MRI) to map the lesion.

Digital guide fabrication for precise cannula placement.

Intraoperative Navigation:

Real-time imaging for safe, accurate cannula insertion.

Dynamic adjustment of pressure parameters based on tissue feedback.

Potential Integration:

Could be combined with conventional treatments (surgery, radiation, chemotherapy) to improve local control and reduce recurrence rates.

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Why This Approach Could Be a Game-Changer:

> This methodology represents what could be considered the first physiotherapeutic treatment for cancer, using mechanical forces (pressure gradients) to target and eliminate malignant tissue. Unlike traditional systemic therapies, this approach:

Reduces collateral damage to healthy tissues.

Minimizes the risk of metastasis during intervention.

Offers real-time, adaptable treatment protocols tailored to individual patient anatomy.

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Request for Feedback:

> We are currently developing this concept and welcome constructive feedback regarding:

Clinical feasibility and safety considerations.

Potential technical challenges in device engineering.

Integration with existing cancer treatment modalities.

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Intellectual Property Notice:

> This concept and its underlying methodologies are part of our proprietary research.

All intellectual property rights are reserved. We are sharing this for academic discussion and expert feedback.

The mechanism of the new method Cancer Therapy exhibits combination Prolonged medical starvation 42 - 45 days with considerably decreased dosage of cytotoxic drugs which was described in detail in the article: Ponizovskiy M.R., The detailed description mechanisms of the herbs extracts operations in the new method cancer disease treatment via rearrangement of metabolism from pathologic development into normal development, Journal of Clinical Trials, 2012, v. 2, Issue 4, doi:10.4172/2167-0870.1000124. The mechanism of this method of cancer therapy operates via Warburg effect targeting. The purpose of this work is substantiation the supplementary mechanisms of efficient Cancer Therapy via combination “Prolonged medical starvation” with considerably decreased dosage of cytotoxic drugs and also substantiation advantage of this method of cancer therapy in comparison with cancer treatment with great dosage of cytotoxic drugs. There were described the biochemical and biophysical mechanisms of formations resistance to some cytotoxic drugs and recurrence cancer disease after modern methods chemotherapy with large dosage cytotoxic drugs after some disease remission. Also it was described the benefits of use the method “Prolonged medical starvation” with decreased dosage of cytotoxic drugs for cancer treatment. It was substantiated the mechanism operation of this method cancer treatment, which leads to suppression cancer metabolism of Warburg Effect and create depression of cancer disease metabolism without resistance to decreased dosage of anticancer cytotoxic drugs in comparison with intensive anticancer chemotherapy with great dosages of cytotoxic drugs which violate immune and hormonal defensive systems of an organism. The offered method Cancer Therapy should be made by Clinical Trial for introduced into official practical medicine.

Recent Breakthroughs of Nano medicine in Applications of Cancer Therapy and Diagnosis

This question addresses the ongoing challenge of improving cancer therapies by focusing on the development of advanced drug delivery systems that can more accurately target cancer cells, thereby reducing side effects and increasing the effectiveness of treatment. Nanotechnology offers a promising avenue for this research due to its potential to create highly specific, controlled, and responsive drug delivery platforms.

Does anyone know an institute/research facility in Europe running research in the field of cancer therapy and willing to accept a student of Micro- and Nanotechnoligies in Biophysics for Erasmus+ holiday traineeship?

"Recent updates on nano-phyto-formulations based therapeutic intervention for cancer treatment" in Oncology Research.

Discover how nanotechnology and phytochemicals are changing the game in cancer therapy.

Read it here:https://techscience.com/or/online/detail/19431

Lentivirus-Mediated Gene Delivery is a common method for introducing therapeutic genes into cancer cells. One such gene is Tiam1, known for its potential impact on cancer cell behavior.

Write review about Plant Exosomes as Targeted microRNA Delivery Vehicles in Cancer Therapy?

In vitro release of drug loaded PHB nanoparticles was carried out at pH 4. There is a burst release of drug at acidic pH as compared to the neutral pH. Does the crystallinity of PHB plays role in the burst release at pH 4?

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. 

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!

Are there any target therapy for pseudomyxoma peritonii

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

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?

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?

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.

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?

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.

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

inflammation NF KB 

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.

"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)

Read it: https://www.nature.com/articles/s41568-019-0135-7

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

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

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.

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?

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.

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.

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.

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? 

Specifically as a polivitaminic compound, and as an anti-tumoral agent.

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.

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.

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?

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?

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.

Although cancer immunotherapy can be quite effective, it has a variety of drawbacks.

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.

I am curious to find more about this

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?

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!

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?

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?

Like, advances in nanomaterials for cancer treatment, gene therapy, etc...

Different drugs and different conditions have been tried on two cancerous cell lines named A549(epithelial) and U2OS(osteosarcoma). However, when using Rotenone initially diluted in DMSO but then placed onto full DMEM media to form a final concentration of 1uM,the resulting solution is viscous and not fully dissolved making colorimetric assay results unreliable. Any solutions to this? It is a well established drug used in classical studies into mitochondrial function so hoping someone will know.

Just like we can elucidate bacterial growth by calculus.

is the nanoparticle with smaller size (about 5 nm) suitable for cancer therapy?

the silver nanoparticle has a high toxicity with very low bio-compatibility. how i can apply this nanoparticle for cancer therapy purpose?

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.

What conc. Should we add

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. 

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?

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?

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

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

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?

Cancer Immunotherapy:

Do You have anything to say?

Could you please share your approach and experience if you are using any platform for personalized cancer treatment?

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 ).

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 .

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 ).

Please contact me if you are working on translational development of CAR T-cells and are interested in exploring potential collaboration opportunities.

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.

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.

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.

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"

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"

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?

Is anyone experienced with assays to distinguish non-homologous end joining from homologous recombination in DNA repair?

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?

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?

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?

Hi

What is meant by targeted cancer therapies, and what advantages

do they offer?

Best wishes

Mohammad Amin

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

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?

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? 

i m searching for papers that have an injection dose of stem cells that used to treat colon cancer ..

In designing study about long QT with anticancer drugs.