Amazon scorpion venom could be as effective as chemotherapy

 Researchers at University of Sao Paulo in Brazil were working with a species of Amazon rainforest scorpion. They identified a molecule in its venom called BamazScplp1, that shows strong activity against human breast cancer cells. In tests the peptides effect on cancer cells was comparable to that of standard chemotherapy. 

    How this works is that BamazScplp1 exhibited cytotoxic effects which basically means it killed the cancer cells. The main mechanism was thought to be necrosis rather than just slowing or triggering classical apoptosis. Researchers use a technique called heterologous expression which produces the peptide in lab rather that extracting Vermon from real scorpions. 

    This is important because breast cancer remains a major cause of death among women worldwide. The fact that natural molecule from scorpion venom can match effectiveness of chemotherapy is a strong proof that natural toxins might be produced into cancer drugs for the future.

Sources:

Amazon scorpion venom shows stunning power against breast cancer. (2025, November 25). ScienceDaily. https://www.sciencedaily.com/releases/2025/11/251117095658.htm

Koumoundouros, T. (2025, June 26). Amazonian scorpion venom can kill breast cancer cells, scientists say. ScienceAlert. https://www.sciencealert.com/amazonian-scorpion-venom-can-kill-breast-cancer-cells-scientists-say

P53 in breast cancer and its role in chemotherapy efficacy

The TP53 gene is one of the most common genes seen in breast cancer tumor cells which codes for the P53 protein. For years scientists have known about the frequency of P53 seen in breast cancer cells, but only recently have they begun to explore the role of mutations in this protein and how they affect the overall effectiveness of chemotherapy.

The first paper I read was written in 1998 and it studied 40 tumors; 29 of which were linked to BRCA1 and 11 of which were linked to BRCA2. The scientists examined the tumors for mutations in various genes linked to breast cancer development, one of which being the TP53 gene. One of the most staggering statistics gathered from this study was the fact that P53 mutations were seen in 80% of the tumors, affecting 83% of BRCA1-linked tumors and 73% of BRCA2-linked tumors. Mutations of P53 most commonly resulted in the upregulation of the protein which was most likely the result of a change in the cell cycle checkpoints. The paper concluded that even though P53 may not be mutated in every case, different components of the P53-dependent cell cycle could have been altered which may have a direct effect on the tumors.

The second paper I read was written by French scientists in 2013, and the study was prompted because the scientists realized that even though previous findings showed an obvious central role of P53 in cancer, the status of TP53 has never been studied as a way to manage breast cancer. Mutations of the TP53 gene are the most common across all breast cancer sub-types, seen in 30% of tumors. In breast cancer patients, tumors are determined to be ER(+) or ER(-), meaning they are either receptive (+) or nonreceptive (-) to estrogen. The paper suggested that having a tumor that is ER(-) with TP53 mutations is the best case scenario for patients, because the accumulation of genetic mutations and abnormalities in these tumors lead to a better response to chemotherapy compared to ER(+) TP53 wild type tumors.

After reading these two articles, it is clear that there is much more research needed in this field for any hope of finding a way to completely eliminate these tumors. The largest challenge when treating breast cancers is the fact that there are so many types of tumors which can range in their response to chemotherapy. I believe these studies are huge leaps forward for the field of oncology, but more studies need to be conducted on P53 as well as any other genes thought to play a role in any stage of tumorigenesis. I think for now studies should focus on P53 due to its widespread activity in breast cancer because it may hold the secrets to the main pathways that allow for tumor growth. If we can find even one pathway responsible for tumor growth, we may be able to break the pathway and cure cancers that were difficult to near impossible to treat before.

Links to articles:

Molecular genetic characterization of BRCA1- and BRCA2-linked hereditary ovarian cancers:
https://cancerres.aacrjournals.org/content/canres/58/15/3193.full.pdf

p53 in breast cancer subtypes and new insights into response to chemotherapy:
https://reader.elsevier.com/reader/sd/pii/S0960977613001409?token=928B8AEBFB15502B20406BA94D56BD2D5DFDEB8F1AE42F99BBCC1C8D495CC458BC5BB9A7324D713715B1B69FE7332585

Gene-Altering Leukemia Treatment

An article in the New York Times discusses the recent recommendation on approval of a gene-altering Leukemia treatment.  The recommendation came from the FDA panel and it would allow allow the genetic alteration of a patients cells to fight their own cancer.  If the FDA accepts the recommendation, it will be the first gene therapy to reach the market in the United States.  Novartis is the drug company that will likely be first; they target the treatment of Leukemia but are currently working on other types of cancer.  Emily Whitehead was the first child to revive the treatment, as a clinical trial, and it saved her life; Whitehead grew very ill and came close to death but she emerged cancer free.  This is one of the main reasons there has been hesitation with this therapy.  In some cases the patients suffer from life-threatning illness; however, this treatment can be an alternative to the toxic treatments like chemotherapy.  There are still questions about the short-term side affects as well as the chances these cells can cause secondary cancer later in life.  In the current studies the cancer has not reappeared but the study will continue continue until fifteen years from treatment.  This could be a huge breakthrough on curing cancer, this is so important because cancer is hard to fight and the current toxic treatments further break down the immune system making it hared to patients to stay healthy.  This is a huge step in the right direction and will most likely be approved by the FDA.

Promotion of Apoptosis in Cancer Cells

Healthy cells have an even balance of apoptosis promoter proteins and anti-apoptosis promoter proteins. However, damaged cells usually possess a higher ratio of apoptosis promoting proteins. This allows for the destruction and degradation of cells that are not functioning properly. Unfortunately, cancer cells do not work this way. The genetic alterations found in cancer cells show an increased production in anti-apoptotic proteins. The result is a damaged cell that is virtually invincible and will continue to divide and produce more identical cells that are damaged. As stated in the article, there are six known anti-apoptotic proteins. The main anti-apoptotic proteins found in cancer are Bcl-1, Bcl-2, and Mcl-1. Currently, cancer treatments include, chemotherapy, radiation, and immuno-therapy. These treatments promote the toxin NOXA in cells, specifically cancer cells, and promote apoptosis of the cell. However, the anti-apoptotic proteins oppose the effects of the toxin and allow the cell to survive. This is observed in patients with chronic lymphocytic leukemia who show resistance to chemotherapy.

            Based on the results of a study conducted at University of California Riverside scientists should focus on the Bfl-1 protein. This protein is more abundant in humans particularly. According to Maurizio Pellecchia, this protein is the main protein in humans and not Mcl-1. Mcl-1 predominates in mice.

            This article is very interesting because if scientists can figure out a way to completely inhibit the anti-apoptotic proteins in cancer cells it would be a great treatment. The cancer cells would have no choice but to self-destruct. Furthermore, the healthy cells would be unaffected by the cancer treatments. Other forms of cancer treatment, such as chemotherapy and radiation, destroy healthy cells as well as cancer cells. When cancer cells are targeted, the healthy cells will be unchanged.

 

Gene Testing that lets Breast Cancer Patients Skip Chemo

      A new study performed by doctors in Europe have shown that not all breast cancer patients have to go through chemo therapy. The study shows that about half of woman with early stage breast cancer who would receive chemotherapy, actually don't need it and would have little to no risk of the cancer coming back.

      The study uses a genetic test called MammaPrint to look at 70 different genes involved in breast cancer growth. If 50 genes were active and 20 genes were inactive, the patient was considered high risk for cancer spread. If the patient had 20 active genes and 50 inactive genes, the patient was considered low risk for cancer spread.

     This test will be good for patients who fall into an area of uncertainty, mostly for patients who show high clinical risk but low genomic risk. The study included women with the most common type of breast cancer in its early stages that tested negative for a receptor called her2. The studied involved 6,693 women at 112 hospitals in 9 European countries. All patients had the usual initial treatments of surgery, hormonal therapy, and radiation. Then genomic testing was performed to see if the patient had a high or low risk for recurrence. Clinical features were also looked at such as tumor size and number of positive lymph nodes.

     Patients who had a high clinical risk but low genomic risk were of most interest in the study. 1,550 patients in this study fell into that category. These were assigned at random to be treated based on their clinical risk or genomic risk. Some patients received chemotherapy and others did not. The patients were then watched for the spread of cancer.

     After 5 years 94.4% of women who did not receive chemotherapy did not have distance spread of cancer and 95.9% of women who received chemotherapy had no distant spread. Based on this study, researchers conclude that it is safe for women with high clinical risk and low genomic risk to skip chemotherapy. An editorial the went along with this study noted that the study was not large enough and that more research needed to be done to say it is actually safe for women to skip chemotherapy.

     I found this article really interesting because it was talking about this use of genetics in the help of treating cancer. Women could now have the option to skip chemotherapy all together without enduring the harmful side effects of chemotherapy such as weight loss, hair loss, nausea/vomiting, infection, and other effects. This is a huge step in the treatment of breast cancer and in the future hopefully in the treatments of other types of cancer.

For more information on genetic testing in breast cancer please visit:

http://www.breastcancer.org/symptoms/testing/genetic

Gene Study of Liver Tumor Reveals Versatile DNA

Researchers have been working on sequencing a single human liver tumor.  The tumor was only slighter larger than one inch in diameter, yet it contained 100 million distinct mutations within the coding region of its genetic sequence.  This is thousands of times more than originally believed.  Each of these mutations is capable of altering proteins in the tumor, affecting the ability to treat tumors.

These results show even the smallest of tumors have extremely high genetic diversity in their genetic sequences.  This diversity explains why chemotherapy does not always work in treating tumors.  Cells with mutations that are resistant to standard treatment methods, go on to reproduce more cells with these mutations, causing treatment to be futile in some circumstances.  

This is a great discovery, however it is rather unfortunate.  We often believe we are making great medical advances, however this study shows we might have much more work ahead of us to effectively treat tumors.  It is known that patient’s survival rates decrease substantially as genetic diversity in a tumor increases.  It seems the medical field will need to make huge advances to find a way to properly eliminate these genetically varying cells to find a successful cure in the treatment of tumors.

For more findings from the study click here.

For the original article click here.

Predicting Chemotherapy Treatment of Ovarian Cancer Patients

    The leading cause of gynecological cancer in women is ovarian cancer, as it takes about 152,000 women's life's each year. Compared against other deadly cancers for women, this is the fifth most common cancer. Ovarian Cancer, like most other cancers, is treated with chemotherapy, however all patients undergo various experiences with this treatment. For many, the chemotherapy treatments kills patients. Many patients are fairly healthy when they choose to undergo this vigorous treatment and before it can completely kill the cancer, it takes the patients life either spiritually or literally.
    Fortunately, science has found a light into predicting how a patient may react to chemotherapy. This knowledge will aid patients decisions regarding their treatment path. Thus increasing the survival rate. The study of this topic was researched among 200 patients at Queen’s University by Doctor Madhuri Koti (visit the article here). He specifically was looking for biomarkers which would indicate the individuals biological state or condition. Meanwhile,  a larger experiment is being observed by Terry Fox Research Institution in Canada to validate Dr. Koti’s findings. It is expected that such biomarkers may suggest other methods of therapy, for example pelvic radiotherapy.
    I find this article extremely important as it searches for the proper ovarian cancer treatment for each patient uniquely. In an illness that takes such a numerous number of lives yearly, it is rare to find scientist studying the affects that treatments will have on different individuals rather than simply looking for the universal cure. I think this is a smart method of tackling cancer as everyone is different, therefore can handle various therapy’s in their own manor. Initially, I was attracted to this article because my grandmother passed away during chemotherapy treatment for her ovarian cancer. Although, it is too late to find the proper treatment for her, this is a hereditary illness; consequently, it is vital I follow the newest methods of treatment.

A Way to Outsmart Cancer that is Outsmarting Us?

A recent study at Dartmouth-Hitchcock's Norris Cotton Cancer Center has shown a certain form of breast cancer developing its own resistance to anti-cancer therapies. The ERBB2 gene (also known as HER2) is a human epidermal growth factor receptor that if mutated, leads to different forms of cancer (lung, gastrointestinal, testicular, etc.), but most commonly, the most aggressive forms of breast cancer. 25% of all forms of breast cancer rely on ERBB2 to proliferate and survive. It is currently the focus of 30% of all breast cancer studies due to it being associated with recurrence and poor prognosis.

A pie chart of ERBB2 cancers as described by Gary A. Palmer, MD, JD, MBA MPH at the American Society of Clinical Oncology.

ERBB2 positive breast cancer cells are developing resistance to anti-ERBB2 drugs after one or two rounds of treatment. The researchers at the Norris Cotton Cancer Center have so far showed that ERBB4 (also known as HER4) may be beneficial to breaking through the ERBB2 forms of cancer. Once the ERBB2 positive breast cancers go through treatment, they turn to and rely on ERBB4 for survival. Using the ERBB4 protein, researchers can develop a new line of cancer treatment to perform after the failed rounds of ERBB2 targeted therapy. This new method is called a cancer driver, which includes targeted therapies and less side effects than chemotherapy (yay!!)

We still have a long road ahead of us in cancer research and treatment development, but we have already made great strides. Knowing how things evolve through time, it is no surprise to me that cancer cells are evolving to survive anti-cancer therapies that are still relatively new to human medicine. If this cancer driver really succeeds, it can potentially open several doors to new and effective cancer treatments and maybe one day, a cure.

Original Article: Receptor tyrosine kinase ERBB4 mediates acquired resistance to ERBB2 inhibitors in breast cancer cells

Acid Ceramidase Inhibitor Potential Cancer Drug

     Recent research at UC Irvine School of Medicine and the Italian Institute of Technology has led scientists to describe the first class of acid ceramidase (AC) inhibitors that may aid in the efficacy of chemotherapies. AC has been found to be upregulated in melanoma, lung and prostate cancers. This has made the enzyme a recent target for novel synthetic inhibitor compounds. AC is encoded by the ASAH1 gene and plays an important role in the regulation of cell fate. Commonly, mutations in this gene are associated with spinal muscular atrophy and Farber disease, which is a lysosomal storage disorder.
    In a recent study at UC Irvine, researches presented a potent and systematically active small molecule inhibitor of intracellular AC. Using in vivo studies, the scientists found that inhibiting the AC with their inhibitor compound alters the balance between pro-aging/death and pro-life chemical signals, while favoring the pro-aging/death chemicals.
    The team hopes that in the future their compound will someday be used as a "chemosensitizer", which is a drug that enhances the killing power of anti-tumoral drugs.

    I found this article interesting because cancer is such a prevalent issue. As one of the hottest topics for research, it is interesting to read about the different approaches for new treatment methods that are being developed. This particular method seems to have definite potential and I hope to see more about it in the news in the future. However, it also seems like there could be some serious side-effects if it is making the chemotherapy and other anti-tumoral drugs more powerful.

Article: http://www.sciencedaily.com/releases/2014/11/141120183627.htm

Gene Mutation Makes Tumors Vulnerable to Chemotherapy

Most cancer patients have a mutation in a gene called p53 which allows tumors to continue to grow even after chemotherapy. A new study from MIT biologists have discovered that tumor cells with the mutated p53 can be affected by the chemotherapy in a stronger way by blocking a certain gene called MK2. The study was conducted on mice and revealed that tumors lacking both p53 and MK2 became much smaller when the drug cisplatin was applied. Tumors with functional MK2 continued to grow after cisplatin was applied. The results reveal that giving cancer patients both a combination of a DNA damaging drug and an MK2 inhibitor would be extremely effective against the growth in tumors. The p53 gene is a tumor suppressor protein that controls cell divison. Before cell division undergoes, the p53 gene repairs the DNA if neccessary. At times the damage is too much and the p53 gene forces cell death, or apoptosis, tumors that lack p53 do not have this happen. "Our data suggested if you block the MK2 pathway, tumor cells wouldn't recognize that they had DNA damage and they would keep trying to divide despite having DNA damage, and they would end up committing suicide," Yaffe states. Using the mice researchers discovered that before treatment, tumors lacking both MK2 and p53 grow much faster than tumors that have just MK2. Therefore, treating tumors with an MK2 inhibitor alon would do more harm than good alowing the tumor to continue to grow. The combination of cisplatin and MK2 inhibitors is different from any other chemotherapy combinations that have been approved by the Food and Drug Administration. The researchers also recieved similar results in cancer cells grown in the lab from bone, cervical and other tumors.

http://www.medicalnewstoday.com/releases/268877.php
http://www.cancer.org/treatment/treatmentsandsideeffects/treatmenttypes/chemotherapy/chemotherapyprinciplesanin-depthdiscussionofthetechniquesanditsroleintreatment/chemotherapy-principles-types-of-chemo-drugs

Genes Can Predict the Relapse After Chemotherapy

This research, found in an article from ScienceDaily , was done in an attempt to see the linkage between genes and being able to predict how well chemotherapy would work on a given patient. The data from the researchers from the National Taiwan Universsity College of Medicine and the National Cancer Institute were used. Sixty human cancer cells and their pattern of activation were tested to see their response to 99 different anti-cancer drugs. Out of all those, eight genes were found to be involved in invasion and had a correlation in the relative activation and chemotherapy outcome. The five drugs that had the most impact were paclitaxel, docetaxel, erlotinib, everolimus, and dasatinib.

The research indicated that patients with lung and breast cancer who were plaved in the low-risk group, based on their genes, spent a longer time being relapse free. Professor Pan-Chyr Yang believes that this discovery is crucial to improving cancer treatment in patients. It also would be beneficial in individualizing cancer treatments, and can hopefully one day be applied to other forms of cancer other than lung and breast.

I believe that personalized chemotherapy can be a great new way to treat cancer. Cancer is not the same in every person and it only makes sense if they are all treated differently. Choosing a personalized chemotherapy does come with it's costs, and it might not be affordable to all, as is explained in the following article. I do also worry about the financial and time consuming aspects of the research itself, however I suspect it will all be worth it.

Mutant Cells

Researchers at USC have found new cells called "checkpoint mutants" that may prove to be more detrimental for cancer patients. Chemotherapy treatment stops the replication process for a majority of cancer cells. However, these "checkpoint mutants" continue to unwind DNA strands and create abnormal ones that are similar to cancer cells. This discovery was found after their researchers did some testing on yeast cells. In their test, the scientists used chemotherapy on fission yeast cells while they were going through the DNA replication process. The chemotherapy starves the cells of nucleotides needed to make new DNA strands. The mutant cells, however, tried to replicate even though they were lacking this essential component. "These mutant cells keep trying to replicate their DNA, unwinding the strands, until the DNA strands reach a "collapse point" where they break-arguably the worst kind of damage that can be done to a cell."

The researchers here hope that their new found information will help for future chemotherapy treatments. Hopefully, they will be able to tell why these cells essentially resist these treatments. Also, maybe a new treatment method for cancer can be administered that will be able to destroy these mutant cells. Overall, I think that this new found information will be very helpful in trying to find a way to better treat those affected by cancer.

Mutant Cells The Keep Trying To Replicate Their DNA Increase Cancer Risk

According to new research from USC certain mutated cells were found to continuously trying to replicate even after medicine robbed them of all raw material to do so. For the first time scientists were able to see that even when chemotherapy drugs shut down the DNA replication process of most cancer cells, "checkpoint mutants" kept unwinding the DNA and creating more damaged DNA strands. These damaged strands could then result in abnormalities seen in cancer cells. Up until now it was believed that these checkpoint mutants stopped replicating because of DNA damage and instead just fell apart. But this new discovery suggests that instead the replication process continues and adds to the damage.

A team from USC used a common chemotherapy drug in order to put stress on fission yeast cells while undergoing the DNA replication process. This drug deprives the cells of nucleotides which are necessary to build the DNA strands. It was believed that with the loss of nucleotides the cell would stop trying to replicate their DNA but instead it was found that the checkpoint mutants ignore this signal. They keep trying to replicate their DNA by unwinding the strands until they break, which is the worst possible damage that can be done to a cell. Because of this extreme damage it is thought that an increased cancer risk comes from this. What they are still trying to determine is what happens to the mutant cells that survive this process.

This research could lead to how checkpoint-defensive human cancer cells preserve their DNA and somehow resist chemotherapy. With cancer being such a traumatic and overwhelming disease, any information and improvement in this could make incredible differences.

New gene causes chemotherapy resistance in ovarian cancers

A new gene has been discovered that makes women with ovarian cancer  three times more resistant to the standard chemotherapy treatment using platinum-based drugs such as carboplatin and paclitaxel than women without this gene mutation. This harbors bold new meanings for women who are diagnosed with the cancer because once a woman is diagnosed, she must then get further tested to see if the modern platinum-based chemotherapy treatments will even help against her ovarian cancer.

Although this may seem like just bad news, it actually can bring better choices for women with this genetic mutation, they can opt to have surgical intervention before they begin their chemo which would be the best course of action in their case. In addition, if they are identified with this gene mutation they can decide to completely bypass the majorly used platinum-based chemo drugs and  look for other alternatives right away, saving them precious time and useless harm to their body.

image link: healblog.net

article link: http://healthland.time.com/2011/12/05/a-genetic-test-identifies-chemo-resistant-ovarian-cancers/#more-48311