Anti-CD47 A New Upcoming Immunotherapy Agent

CD47 is a protein that is present on the surface of many types of cancer cells. It acts as a “don’t eat me” signal, sending a signal to immune cells such as macrophages not to engulf and destroy the cancer cell.

Research into CD47 as a target for cancer immunotherapy has shown promising results. One approach involves using antibodies to block the CD47 protein, allowing immune cells to recognize and attack the cancer cells. This approach is sometimes called the “don’t eat me” signal-blocking strategy.

Preclinical studies have shown that blocking CD47 can stimulate an immune response against cancer cells, resulting in the destruction of tumor cells. In animal studies, CD47 blockade has been shown to shrink tumors and even lead to complete regression of some types of cancer.

Intratumoral injection of anti-CD47 antibodies is a novel approach to cancer immunotherapy that aims to enhance the immune response against cancer cells by blocking the “don’t eat me” signal that is sent by CD47 protein.

In this approach, anti-CD47 antibodies are injected directly into tumors, rather than being delivered systemically. The idea behind this approach is that by injecting the antibodies directly into the tumor, higher concentrations of the antibody can be delivered to the cancer cells, while minimizing the risk of systemic toxicity.

Preclinical studies have shown that intratumoral injection of anti-CD47 antibodies can enhance the activity of immune cells, leading to the destruction of cancer cells within the tumor. This approach has been shown to be effective in various types of cancer, including breast cancer, ovarian cancer, and bladder cancer.

Early-phase clinical trials of intratumoral anti-CD47 therapy are ongoing, and initial results have been promising. For example, a phase 1 clinical trial of intratumoral anti-CD47 therapy in patients with advanced solid tumors found that the therapy was well-tolerated and resulted in some tumor shrinkage.

Overall, intratumoral anti-CD47 therapy represents a promising approach to cancer immunotherapy, and may offer a new way to enhance the immune response against cancer cells. However, more research is needed to fully understand the safety and effectiveness of this approach, and to determine which types of cancer and patient populations may benefit most from this therapy.

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HOW DOES CONSUMPTION OF FATS AND SUGAR AFFECT THE BODY AND BRAIN?

The brain requires the substances that make up the food we consume daily to function properly, due to the formation and restoration of brain tissue. The relationship between nutrition and brain function is crucial, as deficiencies can lead to aging and damage learning processes. Therefore, maintaining a healthy diet free of sugar and saturated fats is crucial for the proper functioning of our body.

Sugar is as addictive as saturated fats, which have been found to enter the intestine, causing the brain to react by increasing the desire to consume it, leading to obesity and metabolic disorders. The connection between the gut and the brain intensifies the mental craving for sugar, which promotes the proliferation and survival of cancer cells and alters the intestinal microbiota.

We must also consider that gut bacteria are important for regulating metabolism, appetite, and fat storage, so we must take care of them and avoid excessive consumption of highly processed foods rich in sugar and fats, such as processed meats like sausages or cheese. These foods are having a devastating impact on human health.

Moreover, it is important to consume fats as they are more natural and necessary for the proper functioning of the body. We cannot eliminate fat consumption, as this can be harmful to brain health. Previously, it was believed that fat consumption was bad, but this concept is outdated. In fact, without fat, we could not live, while without sugar we could. Fats help the brain, while trans fats do not. Trans fats are found in foods that have been subjected to hydrogenation at high temperatures, such as fast foods, industrial pastries, and other processed and fried products. This process serves to make the food last longer and preserve its taste, but it is a risk to human health, and of course, to the brain.

We can conclude that cancer has been increasing and can only be controlled if people adopt a healthy lifestyle and a change in their diet.

 

Reference:

Losada, C. (2018, 15^th June). La clave para la salud de nuestro cerebro

está en comer grasas. alimente.elconfidencial.com. https://www.alimente.elconfidencial.com/bienestar/2018-06-05/alimentos-ricos-grasas-cerebro_1565810/

Rabb, M. (2022, 28^th September). Craving Fatty Food? New Study Says

Your Gut is Talking. How to Answer. The Beet. https://thebeet.com/fat-gut-brain-connection-study/?utm_source=tsmclip

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Intratumoral Bee Venom for Cancer

There is some research exploring the potential of melittin, a component of bee venom, as a treatment for cancer when injected directly into tumors, a technique called intratumoral injection.

In laboratory studies, melittin has been shown to induce cancer cell death and inhibit the growth of various types of cancer cells, including breast, prostate, and bladder cancer cells. Some studies have also found that intratumoral injection of melittin can help to shrink tumors in animal models of cancer.

There have also been some early-phase clinical trials evaluating the safety and effectiveness of melittin injections in human cancer patients. One such trial, for example, found that intratumoral injection of melittin in patients with advanced solid tumors was well-tolerated and resulted in some tumor shrinkage.

However, it’s important to note that these are still early-stage studies, and more research is needed to determine the safety and effectiveness of melittin injections as a cancer treatment in humans. It’s also important to remember that bee venom can be dangerous and can cause allergic reactions in some people, so this approach should only be pursued under the supervision of a qualified healthcare provider.

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Sitagliptin and Cancer Immunotherapy

Sitagliptin is a drug that is commonly used to treat type 2 diabetes. It works by inhibiting the enzyme dipeptidyl peptidase-4 (DPP-4), which can lead to increased levels of the hormone glucagon-like peptide-1 (GLP-1), which stimulates insulin secretion and can improve glucose control.

While sitagliptin is not typically used as a cancer treatment, there is some research suggesting that it may have potential as an immunotherapy agent for cancer. In preclinical studies, sitagliptin has been shown to enhance the anti-tumor immune response and increase the infiltration of immune cells into the tumor microenvironment.

PD-1 (programmed cell death protein 1) is another protein that is expressed on the surface of T cells and acts as a negative regulator of the immune response. Antibodies that block PD-1 or its ligand, PD-L1, have been shown to be effective in the treatment of several types of cancer.

There is some research suggesting that sitagliptin may enhance the activity of both CTLA-4 and PD-1 blockade in cancer immunotherapy. For example, a study published in the journal Cancer Immunology Research in 2018 showed that treatment with sitagliptin enhanced the anti-tumor immune response and improved the efficacy of PD-1 blockade in mouse models of lung cancer.

The researchers suggested that sitagliptin may enhance the activity of CTLA-4 and PD-1 blockade by modulating the immune system and increasing the infiltration of immune cells into the tumor microenvironment. In addition, sitagliptin has been shown to increase the expression of PD-L1 on cancer cells, which may sensitize them to PD-1 blockade.

While these findings are promising, more research is needed to fully understand the potential benefits of sitagliptin in combination with CTLA-4 and PD-1 blockade, and to determine the most effective doses and formulations for use in cancer patients. Clinical trials evaluating the use of sitagliptin in combination with immune checkpoint inhibitors are currently underway.

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Clostridium butyricum and Cancer Immunotherapy

Clostridium butyricum is a type of bacteria that is found in the human gut microbiome. It is known for its ability to produce short-chain fatty acids (SCFAs), such as butyrate, which can have anti-inflammatory effects and play a role in the regulation of the immune system.

Studies have suggested that Clostridium butyricum may enhance the efficacy of cancer immunotherapy by modulating the immune system and promoting the anti-tumor immune response. For example, a study published in the journal Science Translational Medicine in 2015 showed that treatment with Clostridium butyricum enhanced the anti-tumor activity of adoptive T cell therapy in mouse models of melanoma.

The mechanisms by which Clostridium butyricum may impact cancer immunotherapy are not fully understood, but it is thought to enhance the production of SCFAs, which can modulate the immune system and reduce inflammation. In addition, Clostridium butyricum has been shown to increase the number and activity of immune cells, such as natural killer cells and T cells, which play a critical role in the anti-tumor immune response.

While the research into Clostridium butyricum and cancer immunotherapy is still in its early stages, these findings suggest that Clostridium butyricum may have potential as a therapeutic target for enhancing the efficacy of cancer immunotherapy. However, more research is needed to fully understand the role of Clostridium butyricum in cancer and to identify the most effective ways to manipulate the gut microbiome to enhance cancer treatment.

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Akkermansia and Cancer Immunotherapy

Akkermansia, a genus of bacteria that is part of the human gut microbiome, has been shown to have potential health benefits and may play a role in the prevention and treatment of certain types of cancer.

Studies have suggested that higher levels of Akkermansia are associated with a reduced risk of colorectal cancer, and that Akkermansia may enhance the efficacy of cancer immunotherapy. For example, a study published in the journal Nature Communications in 2018 showed that treatment with a combination of a checkpoint inhibitor and a probiotic containing Akkermansia muciniphila enhanced the anti-tumor immune response in mouse models of melanoma and colorectal cancer.

The mechanisms by which Akkermansia may impact cancer risk or treatment response are not fully understood, but it is thought to modulate the immune system, reduce inflammation, and improve gut barrier function. In addition, Akkermansia has been shown to enhance the production of short-chain fatty acids (SCFAs), which are known to have anti-cancer effects.

While the research into Akkermansia and cancer is still in its early stages, these findings suggest that Akkermansia may have potential as a therapeutic target for cancer prevention and treatment. However, more research is needed to fully understand the role of Akkermansia in cancer and to identify the most effective ways to manipulate the gut microbiome to enhance cancer treatment.

Until two years ago, there were no Akkermansia supplements; thankfully, there are now.

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Blocking DNA Repair to Enhance Immunotherapy

Blocking DNA repair to enhance immunotherapy is an emerging approach to cancer treatment that aims to increase the effectiveness of immunotherapy by inhibiting the ability of cancer cells to repair DNA damage caused by immune-mediated cell death.

The immune system recognizes cancer by the differences it has from normal cells, due to mutations, However, cancer cells also have the ability to repair DNA damage that reduces mutations, which can reduce the effectiveness of immunotherapy.

By inhibiting DNA repair pathways, it is possible to increase the accumulation of DNA damage in cancer cells, which can enhance the effectiveness of immunotherapy. For example, preclinical studies have shown that combining immunotherapy with inhibitors of DNA repair pathways, such as PARP inhibitors or ATR inhibitors, can result in enhanced tumor regression and prolonged survival in mouse models of cancer. Patients who have mutations in the DNA repair, known as Mismatch Repair Deficiency (dMMR) have a better response to immunotherapy. Unfortunately, these are the minority of patients. There are other DNA repair genes, such as ATM, ATR, RAD-3 and CHEK2. Mutations in DNA repair genes leads to increased mutations and can be associated with and improved response to immunotherapy. Patients who don’t have mutations in these genes can achieve improved responses to immunotherapy by blocking some of these DNA repair mechanisms. This allows a better response, closer to what was seen in people who naturally have mutations, like those in the MSK dostarlimab study for rectal cancer, reported to be 100% cured in 14/14 patients.

Several clinical trials are currently underway to evaluate the efficacy and safety of combining immunotherapy with DNA repair inhibitors in various types of cancer. While the results of these trials are still preliminary, they suggest that this approach has the potential to improve the response rate and duration of response to immunotherapy, particularly in patients with tumors that are resistant to conventional therapies.

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VITAMIN D3

There are many questions regarding whether supplementing Vitamin D can cause a decrease in cancer incidence and whether you should take this vitamin. One normally produces Vitamin D when exposed to sunlight, but we can also find it in foods such as fish, mushrooms, milk, and some cereals.

Vitamin D can downregulate growth hormones and suppress proliferation in many cancers. Vitamin D receptors are widely expressed throughout the body, and experimental evidence suggests that vitamin D has antineoplastic activity. Vitamin D binding to its receptor results in transcriptional activation and repression of target genes producing apoptosis, antiproliferative effects, autophagic cell death and angiogenesis, and immunomodulatory effects that contribute to reduced metastatic disease and fatal cancer.

It has been shown that vitamin D is able not only to potentiate the effects of traditional cancer therapy as gemcitabine, cisplatin, doxorubicin, and proton therapy but can even contribute to overcoming the molecular mechanisms of drug resistance; it can act at various levels through the regulation of growth of cancer stem cells and the epithelial-mesenchymal transition and the modulation of miRNA gene expression.

This antitumor action is probably because it influences intracellular calcium oscillations capable of influencing cell mechanisms of growth and apoptosis. In recent years, vitamin D has modulated the inflammatory state of the tumor microenvironment by affecting immunological infiltrations.

Harvard researchers set out in 2011 a large study with 25,871 people with randomized vitamin D supplementation. The results showed that the rate of fatal or metastatic cancer was 17% lower in those taking vitamin D supplements and 38% in people with a healthy weight.

Although it has been proven that Vitamin D3 can reduce the risk of advanced cancer, metastasis, and fatal cancer, it is not associated with cancer prevention.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7353389/#:~:text=Conversely%2C%20several%20molecular%20studies%20are,activation%20of%20different%20molecular%20pathways.

https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2773074#:~:text=Vitamin%20D%20may%20decrease%20tumor,leading%20to%20reduced%20cancer%20mortality.&text=Higher%20serum%2025%2Dhydroxyvitamin%20D,longer%20survival%20in%20cancer%20patients.

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Intratumoral anti-CD47 Immunotherapy

CD47 is a protein that is overexpressed on the surface of many cancer cells, and it interacts with the immune system to inhibit phagocytosis, or the process by which immune cells engulf and destroy cancer cells. This interaction between CD47 and immune cells, including macrophages, can contribute to tumor growth and resistance to immunotherapy.

Intratumoral CD47 blockade is an emerging approach to cancer therapy that involves delivering CD47-blocking agents directly into the tumor site. The goal of this approach is to enhance the phagocytosis of cancer cells by macrophages, thereby reducing tumor growth and enhancing the effectiveness of immunotherapy.

Preclinical studies have shown that intratumoral CD47 blockade can result in tumor regression and improved survival in mouse models of cancer. For example, a study published in the journal Nature in 2016 showed that intratumoral injection of a CD47-blocking antibody enhanced the phagocytosis of cancer cells by macrophages and resulted in the regression of multiple types of tumors, including breast cancer, ovarian cancer, and lymphoma.

Clinical trials evaluating intratumoral CD47 blockade are currently underway in various types of cancer, including solid tumors and hematological malignancies. While the results of these trials are still preliminary, they suggest that intratumoral CD47 blockade has the potential to be an effective cancer therapy, particularly in combination with other immunotherapeutic agents.

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Exposure to Antibiotics Before Immune Checkpoint Inhibitor Therapy and Overall Survival in Elderly Patients with Cancer

Exposure to antibiotics during the first year after starting immune checkpoint inhibitor therapy has been found to be associated with worse survival among patients with cancer aged 65 years or older.

After conducting multiple studies, it was found that 59% of patients that received antibiotics during the first year and 19% during the 60 days after starting immune checkpoint inhibitors, researchers have observed that exposure to antibiotics, specifically fluoroquinolones, before immune checkpoint inhibitor therapy was associated with worse overall survival among older adults with cancer. Interventions targeted at altering the gut microbiome to increase immunogenicity may help improve outcomes for patients receiving immune checkpoint inhibitors with prior antibiotic exposure.

Lawson Eng, MD, SM, from the Division of Medical Oncology and Hematology, Princess Margaret Cancer Centre, University Health Network, Toronto, is the corresponding author of the article in the Journal of Clinical Oncology.

Disclosure: The study was supported by ICES, which is funded by an annual grant from the Ministry of Health and Long-Term Care of Ontario, the ASCO/Conquer Cancer Foundation Young Investigator Award, and others. For full disclosure information on the study authors, visit ascopubs.org.

 

 

 

Reference:

Antibiotic Exposure Before Immune Checkpoint Inhibitor Treatment and

Overall Survival in Older Patients With Cancer – The ASCO Post. (s. f.). https://ascopost.com/news/march-2023/antibiotic-exposure-before-immune-checkpoint-inhibitor-treatment-and-overall-survival-in-older-patients-with-cancer/?utm_source=TAP-EN-030823-Trending_LUNG

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Do you know about the injectable gel that cures metastasis in a “cold” cancer model?

The hydrogel drug (Imigel) is an immunoadjuvant drug for treating cancer.
Image-guided therapy in mice turned a “cold” tumor, one that is resistant to immunotherapy, into a “hot” immunotherapy-sensitive tumor, allowing immune cells to target and attack the tumor both locally and systemically. The image-guided therapy converted a “cold” tumor, one
that is resistant to immunotherapy, into a “hot” immunotherapy-sensitive tumor, allowing immune cells to target and attack the tumor both locally and systemically.

This finding was named “Image-guided intratumoral cancer vaccine for treating metastatic immunotherapy-resistant cancer with and without cryoablation.” The researchers wanted to discover a mechanism for injecting imiquimod, a topical cancer drug approved by the US Food and Drug Administration, and getting it to rem,main in the tumor for about 5 days, which is the time it can take to activate the immune system. It was also expected to be used to optimize image guidance.

The problem with imiquimod is that it is a small molecule, so it disappears very quickly. One of the elements that has been a challenge for many of our intratumoral injections is the lack of retention of the medicines. Working in collaboration with the interventional radiologist laboratory of MGH Eric Wehrenberg-Klee, MD, and engineering collaborators at the Massachusetts Institute of Technology (MIT), they developed a radiopaque gel that becomes liquid at room temperature but solidifies in the tumor in the body.

Using two metastatic mouse tumor models resistant to checkpoint inhibitors (CPIs), the researchers evaluated 90-day survival after injection with and without cryoablation. Cryoablation has long been shown to have an immune-stimulating effect, meaning they were able to demonstrate that complete regression of a relatively large tumor that they had implanted distally in the site they treated could be obtained, which could be considered as a personalized cancer vaccine. Thus, by taking a clinically approved drug, using materials that are recognized as safe, combining them, and then injecting the material with and without cryoablation, they were able to demonstrate that yes, indeed, we can heat up a cold tumor in many ways simply by improving the retention of drugs that we already have.

“Unfortunately, many people still do not know that interventional radiology exists.” Certainly injecting tumors directly with immunotherapy is the future of cancer treatment. Hydrogels and other agents such as ionic liquids make very promising delivery options to help keep the medication in the tumor site. These techniques are advancing Intratumoral immunotherapy to the next level.

Reference:
Powers, M. P. (2023a, marzo 5). Injectable gel platform cures cancer
metastasis in a «cold» model. IR Quarterly.
http://irq.sirweb.org/sirtoday/injectable-gel-platform-cures-cancermetastasis-in-a-cold/

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Mepazine/Biperiden

Mepazine is a phenothiazine antipsychotic medication. Biperiden is a medication used to treat Parkinson’s disease and is a synthetic acetylcholine antagonist. Both of these drugs inhibit MALT1, which is associated with the CBM signalosome complex. Pilato, et al. published an article in Nature Research; Oct 2018 titled “Targeting the CBM Complex Causes Treg Cells to Prime Tumours for Immune Checkpoint Therapy.” They demonstrated that using Mepazine to inhibit MALT1 could help convert immunologically cold tumors to hot ones. In the animal model, they showed the combination of Mepazine with PD-1 inhibitors causes the development of an anti-cancer immune response with relapse-free tumor control in a model that does not respond to PD-1 therapy alone. This is important, as the majority of cancers do not respond to PD-1 therapy due to a lack of infiltration of attacking immune cells and a predominance of tumor-protecting regulatory immune cells. They also showed that MALT1 inhibition could actually convert regulatory cells into ones that are more tumor-attacking. The big advantage here is that most strategies are to decrease regulatory cells, generally by killing them. This drug may be able to make good use of those regulatory cells in the tumor environment to convert them into attacking the tumor.

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BIFIDOBACTERIUM

Most bacteria species used as probiotics are under the genera Bifidobacterium and Lactobacillus; the genus Bifidobacterium contains approximately 57 subspecies, and it’s the dominant bacterial population in the gastrointestinal tract; the changes in the number of their population are one of the most frequent situations that are present on gastrointestinal diseases like inflammatory bowel disease, colorectal cancer, or/and irritable bowel syndrome. Recently Bifidobacterium spp has caught attention in the cancer field because of its pro-apoptotic effects. Many studies have been made regarding colorectal cancer to demonstrate this effect. Evidence from many studies suggests mechanism probiotics benefit colorectal cancer, including improvement in the host’s immune response, induction of apoptosis, and inhibition of tyrosine kinase signaling pathways, the epidermal growth factor receptor pathway on of them. Some species of Bifidobacterium can decrease carcinogen-induced DNA damage, pre-neoplastic lesions, and tumor in colons of rats, according to previous studies.

Sepideh Bahmani and colleagues conducted a study in 2019 resulting in Bifidobacterium bifidum being effective in combating cancer cells and associated with improved gastrointestinal cancer and concluded that the produced cell-free supernatants could inhibit the growth of cancer cells.

Bifidobacterium and Lactobacillus exert anticancer effects through the production of antioxidative enzymes, binding to reactive oxygen species, chelating heavy metals, neutralizing carcinogens, and they can regulate the cell cycle in cancer cells, inhibiting their proliferation, making them susceptible to apoptosis. The mechanism of action shown in different studies in which Bifidobacterium can act on cancer cell apoptosis resistance is via upregulation and downregulation of effective genes with pro-apoptotic and anti-apoptotic activities.

In a recent study by Zeinab Faghfoori et al., they found that the secretion metabolites of Bifidobacteria spp can induce intrinsic and extrinsic apoptosis pathways in human colorectal cancer cells.

With all the discussion and conclusions of different studies regarding the anti-cancer effect of Bifidobacterium species, we can conclude that, as for now, it is safe to use as a supplement in patients with cancer, especially colorectal cancer. More studies need to be made regarding which species of Bifidobacterium has the most benefits for battling against cancer and if there is a proper dose to achieve this effect.

https://pubmed.ncbi.nlm.nih.gov/31530527/

Faghfoori, Z., Faghfoori, M.H., Saber, A. et al. Anticancer effects of bifidobacteria on colon cancer cell lines. Cancer Cell Int 21, 258 (2021). https://doi.org/10.1186/s12935-021-01971-3

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7219778/

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