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Nanomedicine: Do cancer tumors affect drug release?

"Silicone packages", for the local release of anti-cancer drugs, break down differently in the tumor tissue, and this fact affects their clinical effectiveness. A study conducted at the Technion, MIT and Harvard sheds light on the aforementioned disintegration process and paves the way for improving the treatment of these tumors

Porous silicon particles are used as a platform to transport anticancer drugs (colored in the diagram in glowing green) and release them in breast cancer tumors. The degradation of silicon in the cancerous tumor environment was studied using innovative imaging methods. The researchers followed the breakdown of the substance in the cancerous tissue and revealed its breakdown mechanism, which allows the release of drugs trapped in the porous medium.
Porous silicon particles are used as a platform to transport anticancer drugs (colored in the diagram in glowing green) and release them in breast cancer tumors. The degradation of silicon in the cancerous tumor environment was studied using innovative imaging methods. The researchers followed the breakdown of the substance in the cancerous tissue and revealed its breakdown mechanism, which allows the release of drugs trapped in the porous medium.

"Silicone packages", for the local release of anti-cancer drugs, break down differently in the tumor tissue, and this fact affects their clinical effectiveness. A study conducted at the Technion, MIT and Harvard sheds light on the aforementioned decomposition process and paves the way for improving the treatment of these tumors.

A new article in the prestigious journal Nature Communications reveals that nanoporous silicon, designed for the controlled release of chemotherapy drugs, behaves differently in a cancerous tumor environment compared to healthy tissue. This is a joint study conducted at the Technion, MIT and Harvard Medical School. Professor Esti Segal, who heads the technical group that led the research, explains that "we are showing for the first time that biomaterials in general, and porous silicon in particular, behave differently when they are injected (or implanted) in a cancerous tissue environment. In recent years, we have been able to engineer silicon so that it will serve as a 'packaging' that carries anti-cancer drugs and releases them in a controlled manner, and now we have focused on the mechanism of the disintegration of the silicon in the cancerous target tissue."

Porous Silicon is a general name for a family of silicon-based materials that contain nanometric holes. This material is now known as an effective 'packaging' (platform) for drug transport, due to its unique properties: large surface area (available for loading the drug), biocompatibility and safe and non-toxic breakdown in the body (bio-degradability). In recent years, Professor Segal and PhD student Adi Tzur Belter have developed such 'packages' for transporting anti-cancer drugs. By precisely designing the diameter of the pores in silicon, and controlling their surface chemistry, the group achieved optimal properties for transporting drugs inside the body and releasing them at the target site.
One of the important findings in this study, in which the aforementioned platform was examined in breast cancer tissues, is related to the decomposition process of the silicone. The study proved that the cancerous tumor releases substances that cause accelerated oxidation of that 'packaging' and breaks it down at a faster rate compared to experiments conducted in the laboratory. The article sheds light on the process of breaking down the silicone in the tumor environment, and allows early and intelligent planning of the silicone structure to achieve a controlled release of the drug at the target site.

About Professor Esti Segal:
Professor Segal completed her three degrees in the Faculty of Chemical Engineering at the Technion. In 2007, after a post-doctorate in the Faculty of Chemistry and Biochemistry at the University of California, San Diego (UCSD), she joined the Faculty of Biotechnology and Food Engineering at the Technion. She currently heads the laboratory for functional nanomaterials at the faculty, and last year she won the Henry Taub Award for excellence in academic research and the Yanai Award for excellence in academic education.

Full name of the article:
Mechanism of Erosion of Nanostructured Porous Silicon Drug Carriers in Neoplastic Tissues

11 תגובות

  1. I mean by developing durability -
    Either he will succeed in destroying the box and disrupt the healing or he will develop resistance to the medicine (this is what I think).

  2. safkan
    I'm not sure what I'm supposed to do with a response that says you have no interest in continuing to discuss the issue, but I'll respond a bit anyway.
    The change that the cancer cell goes through in its "adaptation" to chemotherapy is the same as the change that a bacterial cell goes through in its adaptation to antibiotics - the cell undergoes mutations (both cancer cells and bacterial cells are notorious for this ability) and one of the mutations damages exactly the protein that introduced the drug into the cell or exactly the protein that processed the drug in the way it harmed to the cell and thus the cell learns to live and thrive well even under these conditions. All the rest of the cells (those that did not acquire this mutation) die, of course, because the drug kills them, leaving the small percentage that acquired the mutation which now constitutes the entire population. Genetic tests and protein expression tests will prove that this is what happened (and it is even possible to know which specific protein underwent the mutation that made this adaptation possible). And we have a natural choice in live. If you don't want to call it evolution you don't have to, that's what everyone else calls it, but the mechanism is essentially the same as that of a microorganism.
    Gut feeling is nice (seriously) and many times it is a good opening for the beginning of in-depth scientific research on the subject, but of course it does not come to replace scientific research.
    Regarding the topic of this specific article, although I planned to, I still haven't found the time to read the article in question, so I can't express an opinion for the time being. In my understanding, according to what I read here on the website, the capsule that holds the drug breaks down at a different rate than expected in the area of ​​the cancerous tumor, and what the group did was to measure this rate and even repair the capsule so that it would release the substances effectively in the area of ​​the tumor. The capsule is indeed not supposed to react with the body's cells at all, including the cancer cells, so I doubt they will "develop resistance" to it (although who knows) and I assume that what Shigael meant is indeed resistance to the drug itself, although I don't really know what he meant.

  3. to Maya

    beginning. My response was delayed because I was busy. I didn't want to send my response on your matter before I send responses on Andrea Rossi's Ikat nuclear reactor. The matter of Kur Ikat is too important for my comments on him to be ignored.

    On the merits.
    I apologize for the mistake and the deception on my part. I had to count to 10 before I sent a response (regarding the tiny capsules for local instillation of chemotherapy agents). I was probably too tired and impatient, so my reaction was wrong.

    I usually don't immediately send a response if I'm not sure about it, I save it on my tablet to think again. I messed up this time.

    About the facts (regarding the change in the resistance of the cancerous tissue to prolonged biochemical treatment) - I trust you that the facts are not a matter for debate. I learned something from you. "Prolonged treatment" here includes "repeated treatment".

    I do not blindly trust you regarding your claim that the resistance of the cancer tumor to biochemical treatment is due to the cancer undergoing an evolutionary change. Evolutionary change seems to me to be a "joker card" that is pulled out as an "impressive explanation" when there is a process of action change that has no "other clear explanation".

    I can think of other (non-evolutionary) processes that may bring about an acquired change in the behavior of cancerous tissue (during a prolonged chemotherapy process). Not only that - my gut feeling _most_ of the resistance of the cancerous tissue is not through evolutionary change. I won't go into explaining why I have a gut feeling; I have good reasons (in my opinion) but I have no desire to continue the debate.

    Note:
    The solution that the researchers are looking for is not changing drugs, but changing the _method of infusing drugs_ (changing the method of infusing by changing the tiny capsules that infuse the drugs). The material from which the capsules are made is not (probably) a medicinal substance - therefore there is a good chance of changing the capsules (so that the cancerous tissue cannot attack them).

    I have no further interest in discussing the matter. It might take me too long.

  4. hello skeptic,
    I can't open my computer and if I change the nick on this computer it won't let me send a message, so it's Maya, hello.
    I have to ask: what makes you answer with such confidence to people when it comes to topics that you clearly have no idea about?
    "Cancer is not a microorganism capable of evolutionary development" - are you serious? What do you think makes microorganisms so unique that they can evolve in an evolutionary way? Hint: nothing. A cancer cell is indeed a human cell (in the case of cancer in a person), but it is still a cell that reproduces, undergoes mutations and is under selection. Conclusion - it is subject to an evolutionary process, like any other biological organism.
    "That's why his ability to develop resistance is very low if at all." I'll ask again, are you serious? It is no longer related to an in-depth understanding of the field, all that is needed is an acquaintance or two cancer patients (and unfortunately, such are not hard to find) whose cancer has developed resistance to chemotherapy. What do you think it means? By the way, the mechanism by which cancer cells develop resistance to drugs is the same as the mechanism by which bacteria develop resistance to antibiotics. Do you know what this mechanism is called in one word? evolution.
    I really find it disturbing when people answer with such confidence about subjects they have no understanding of at all. This is because there are people who come to this site to learn and a confident answer tends to make people think there is something wrong with them. There's no problem with it when you know what you're talking about, but when that's not the case, it's problematic. This is the reason why I, personally, enter discussions either of topics that are directly related to my research topics or areas that are close enough that it is clear to me that I am well versed in them, or of topics that just interest me and I don't understand them that much, but then I make sure that everything I say ends with a question mark. Because I don't know. It's okay to say you don't know. You don't have to be an expert in everything. But confusing people like that is irresponsible.

  5. Yigal

    Cancer is not a microorganism that is able to develop in an evolutionary way, therefore its ability to develop resistance is very low if at all. Cancer is a "normal" cell (of the animal in which it develops) whose "self-destruction" mechanism has gone wrong and therefore it reproduces wildly, the wild reproduction is at the expense of the healthy tissues next to it).

    In fact, most drugs to eliminate cancer use the fact that the properties of a cancer cell are somewhat different from the properties of a normal cell. The drugs carry out a selective attack on cells while taking advantage of the difference in the properties I mentioned: the drugs are built in such a way that they will destroy mainly cancer cells and destroy as few healthy cells as possible. This selection does not always work successfully. So the new technique tries another method for selective attack, maybe it will succeed or maybe it won't.

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