Thursday, April 18, 2024

What Kills Prostate Cancer Cells

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What Should Patients Know About Msks Approach To Treating Prostate Cancer

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At MSK, we manage prostate cancer in a very comprehensive way, tailored to each patients disease. There is no one specific therapy that is best for everyone.

Our initial assessment includes a carefully evaluated biopsy and a very detailed MRI to show the location of the disease, the integrity or soundness of the capsule surrounding the prostate, and the amount of disease. We will often obtain next-generation imaging and do genomic testing. Then, based on that information and with input from the urologist, the radiation oncologist, and the medical oncologist we can provide a comprehensive recommendation.

The radiotherapy we do here at MSK is state-of-the-art and unparalleled. We are one of the few centers in the world to do MRI-based treatment planning and one of the few centers in the US to offer MRI-guided treatment. When we give brachytherapy, we use computer software that provides us with real-time information about the quality and accuracy of the seed implant during the procedure. It requires a great deal of collaboration with our medical physics team to try to get the most accurate positioning of the prostate during the actual three or four minutes of the treatment.

We make adjustments while the patient is still under anesthesia, so that when the procedure is completed, we have been able to achieve ideal placement of the radiation seeds. This translates into improved outcomes.

How Will I Know That My Hormone Therapy Is Working

Doctors cannot predict how long hormone therapy will be effective in suppressing the growth of any individual mans prostate cancer. Therefore, men who take hormone therapy for more than a few months are regularly tested to determine the level of PSA in their blood. An increase in PSA level may indicate that a mans cancer has started growing again. A PSA level that continues to increase while hormone therapy is successfully keeping androgen levels extremely low is an indicator that a mans prostate cancer has become resistant to the hormone therapy that is currently being used.

Grape Seed Extract Kills Prostate Cancer Cells

Grape seed has been known to have medicinal properties for ages. It has been used in traditional medicines in many cultures for treating various ailments. Recent studies have established that it can be linked to treating cancer. You might be aware of the usage of grape seed extract for prostate cancer treatment. Lets delve into this topic briefly.

Grapeseed is a gift of nature. Nature has got tons of cancer fighters. Many fruits and vegetables have some kind of chemopreventive agent. Speaking of grape seed extract , it contains lots of antioxidants. The interest of consumers has peaked due to the fact that the antioxidants in the grape seed are superior to even Vitamin C and Vitamin E. Besides, why the demand for grape seed for cancer prevention is increasing can be attributed to the high content of antioxidants in the form of proanthocyanidins.

In addition to prostate cancer, GSE has also demonstrated the ability to suppress the growth of tumour cells in human breast, lung, and gastric cancer cell lines. The proanthocyanidins contained in GSE have a wide range of chemical defence properties against free radicals and oxidative stress.

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How Does Hormone Therapy Work Against Prostate Cancer

Early in their development, prostate cancers need androgens to grow. Hormone therapies, which are treatments that decrease androgen levels or block androgen action, can inhibit the growth of such prostate cancers, which are therefore called castration sensitive, androgen dependent, or androgen sensitive.

Most prostate cancers eventually stop responding to hormone therapy and become castration resistant. That is, they continue to grow even when androgen levels in the body are extremely low or undetectable. In the past, these tumors were also called hormone resistant, androgen independent, or hormone refractory however, these terms are rarely used now because the tumors are not truly independent of androgens for their growth. In fact, some newer hormone therapies have become available that can be used to treat tumors that have become castration resistant.

Magnolia Kills Prostate Cancer Cells

natural insecticide kills advanced prostate cancer cells

Magnolol, a substance taken from the root and bark of the magnolia tree, is a potent killer of prostate cancer cells, according to a study in the Journal of Cellular Biochemistry. Because it does not damage healthy cells, magnolol could be a promising new therapy for prostate cancer, as well as other types of cancers.

Next to skin cancer, prostate cancer is the most common cancer in men. More than 27,000 men die from the disease each year, according to the American Cancer Society. Although treatments such as surgery and hormone therapy are available, many come with significant side effects. Researchers are on the hunt for new treatments that kill cancer cells without harming healthy tissue.

One of these potential new therapies is magnolol, a compound isolated from the root and bark of the magnolia tree. Magnolol has been used in China and Japan for thousands of years to treat a variety of conditions, ranging from inflammation to ulcers. Recent research suggests that it also slows the growth and triggers the death of cancer cells.

The researchers then took their investigation a step further, looking at the pathways by which magnolol affected prostate cancer cells. It is very important to understand how magnolol acts as an anticancer agent, says lead author Yong Lee, PhD, Professor in the Department of Surgery and Pharmacology at the University of Pittsburgh. If we understand the mechanisms of killing , we can improve the efficacy of the drug and avoid side effects.

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What Else Should You Consider

Remember, you have options, and itâs important to choose the one that works best for you. When choosing a treatment, think about:

  • The risks. Talk to your doctor about the pros and cons of each type of therapy.
  • The side effects. Consider whether or not youâre willing to deal with how the treatment might make you feel.
  • Whether or not you need it. Not all men with prostate cancer need to be treated right away.
  • Your age and overall health. For older men or those with other serious health conditions, treatment may be less appealing than watchful waiting.

Show Sources

American Cancer Society: âCan Prostate Cancer be Found Early?â âConsidering Prostate Cancer Treatment Options,â âHormone Therapy for Prostate Cancer,â âHow is Prostate Cancer Treated,â âProstate Cancer,â âWhat is Prostate Cancer?â âCryotherapy for Prostate Cancer,â âRadiation Therapy for Prostate Cancer,â âSurgery for Prostate Cancer,â âVaccine Treatment for Prostate Cancer.â

National Cancer Institute: âProstate Cancer Treatment.â

Prostate Cancer Foundation: âOther Treatment Options,â âProstatectomy ,â âRadiation Therapy,â âSide Effects,â âTreatment Options.â

UpToDate: âBone metastases in advanced prostate cancer: Management.â

Cancer.Net: âProstate Cancer: Types of Treatment.â

Prostate Cancer And Tumor Suppressors

After skin cancer, prostate cancer is the most common cancer in men in the United States, where, in 2017, an estimated 161,360 people discovered that they had the disease.

In the vast majority of cases, prostate cancer is diagnosed before the disease has started to spread. While the cancer is in this localized state, it is much easier to treat, and the 5-year survival rate is close to 100 percent.

However, once the cancer has become metastatic that is, it has spread and set up new tumors in other parts of the body it is much harder to treat.

For men diagnosed with metastatic or advanced prostate cancer, the average 5-year survival rate is 29 percent.

In their study paper, the authors note that a hallmark of advanced prostate cancer is that two tumor suppressor genes PTEN and p53 do not work properly because they are mutated.

When tumor suppressor genes work properly, they slow down cell division , repair broken DNA, and trigger programmed cell death.

Faulty tumor suppressor genes, on the other hand, fail to carry out these functions and give rise to faulty cells that can grow uncontrollably and cause cancer.

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Common Component Of Fruits Vegetables Kills Prostate Cancer Cells

University of Georgia
A new study finds that pectin, a type of fiber found in fruits and vegetables and used in making jams and other foods, kills prostate cancer cells. The study found that exposing prostate cancer cells to pectin under laboratory conditions reduced the number of cells by up to 40 percent.

A new University of Georgia study finds that pectin, a type of fiber found in fruits and vegetables and used in making jams and other foods, kills prostate cancer cells.

The study, published in the August issue of the journal Glycobiology, found that exposing prostate cancer cells to pectin under laboratory conditions reduced the number of cells by up to 40 percent. UGA Cancer Center researcher Debra Mohnen and her colleagues at UGA, along with Vijay Kumar, chief of research and development at the VA Medical Center in Augusta, found that the cells literally self-destructed in a process known as apoptosis. Pectin even killed cells that arent sensitive to hormone therapy and therefore are difficult to treat with current medications.

What this paper shows is that if you take human prostate cancer cells and add pectin, you can induce programmed cell death, said Mohnen, a professor of biochemistry and molecular biology. If you do the same with non-cancerous cells, cell death doesnt occur.

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Possible Risks And Side Effects Of Brachytherapy

How Does Prostate Cancer Kill Us?

Radiation precautions: If you get permanent brachytherapy, the seeds will give off small amounts of radiation for several weeks or months. Even though the radiation doesnt travel far, your doctor may advise you to stay away from pregnant women and small children during this time. If you plan on traveling, you might want to get a doctors note regarding your treatment, as low levels of radiation can sometimes be picked up by detection systems at airports.

There’s also a small risk that some of the seeds might move . You may be asked to strain your urine for the first week or so to catch any seeds that might come out. You may be asked to take other precautions as well, such as wearing a condom during sex. Be sure to follow any instructions your doctor gives you. There have also been reports of the seeds moving through the bloodstream to other parts of the body, such as the lungs. As far as doctors can tell, this is uncommon and doesnt seem to cause any ill effects.

These precautions arent needed after HDR brachytherapy, because the radiation doesnt stay in the body after treatment.

Bowel problems: Brachytherapy can sometimes irritate the rectum and cause a condition called radiation proctitis. Bowel problems such as rectal pain, burning, and/or diarrhea can occur, but serious long-term problems are uncommon.

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What Is Intermittent Adt

Researchers have investigated whether a technique called intermittent androgen deprivation can delay the development of hormone resistance. With intermittent androgen deprivation, hormone therapy is given in cycles with breaks between drug administrations, rather than continuously. An additional potential benefit of this approach is that the temporary break from the side effects of hormone therapy may improve a mans quality of life.

Randomized clinical trials have shown similar overall survival with continuous ADT or intermittent ADT among men with metastatic or recurrent prostate cancer, with a reduction in some side effects for intermittent ADT .

Deguelin Stopped Cancer Progression

Prof. Trotman and colleagues suggest that, of the 3 million men in the U.S. who have prostate cancer, roughly 100,000 carry cancers with co-mutation of .

This prompted them to look for drugs that might work specifically against prostate cancers that carry mutated PTEN and p53.

However, because several studies have shown that loss only of p53 does not give rise to prostate cancer, they decided to focus on PTEN.

The researchers began the study by running a series of experiments using cells with and without PTEN.

They found that deguelin had the capacity to kill both types of cell, but the dose required to kill cells with PTEN was 500 times higher than the dose required to kill cells without PTEN .

They also discovered that the drug had a much stronger effect on the cells without PTEN because their mitochondria were consuming ATP instead of producing it.

Thats the exact opposite, Prof. Trotman says, of what mitochondria are supposed to be doing. Mitochondria are supposed to generate ATP for the rest of the cell.

Finally, when they then tested deguelin in their mouse model of lethal metastatic prostate cancer, the researchers found that it stopped the cancer progressing.

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Production Of A Chimeric Protein To Deliver Polyic Selectively To Psma

Once we had verified that the single chain antibody ScFvJ591 could specifically target PSMA-overexpressing cells, we designed a chimeric protein in which ScFvJ591 was fused with the two dsRNA-binding domains of the human dsRNA-dependent protein kinase, PKR .2A). The 48kDa chimeric protein, dsRB-SCP , was expressed in E. coli, purified on nickel sepharose as a partially unfolded protein, refolded on the column, eluted and submitted to ion exchange, as described in the experimental procedures .

Design, expression and purification of dsRB-SCP

A. Schematic representation of dsRB-SCP. B. Expression and purification of dsRB-SCP: L: Cleared lysate, M: Molecular weight marker, E1: Eluate following IMAC , E2: Purified dsRB-SCP eluted from IEX . C. Binding of dsRB-SCP to dsRNA. dsRB-SCP was preincubated with 500 bp long dsRNA in binding buffer at pH 8.3 or pH 5, and electrophoresed on a 2% agarose gel. M: 100 bp DNA molecular weight marker. Dashed lines indicate where the pictures of the gels were cut and reorganized.

New Drug Kills Off Prostate Cancer Cells

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Disclaimer: Results are not guaranteed*** and may vary from person to person***.

Thanks to a new RNA-based experimental drug that was developed at the Duke University Medical Center, there may be a new treatment available in the fight against prostate cancer on the horizon.

The new drug, which has yet to be officially named and is the first of its kind, works by tricking its way into prostate cancer cells. Once inside these dangerous cells, the drug then takes action and starts destroying them. The benefit is that while the drug is wiping out the malignant cells while leaving the healthy cells alone.

The drug targets one type of genetic material ribonucleic acid which allows it to enter the prostate cancer cells, and another, called silencing RNA, in order to stop the functioning of a protein that keeps the cells alive.

In tests involving the drug, researchers looked at mice with prostate cancer and gave them the therapy. They used two test groups, one that received the drug and one that did not. The researchers injected the one group of mice with the drug once every two days, with a total of 10 injections in 20 days.

The drug managed to shrink the size of the animals tumors in half. In the mice that didnt get the drug, the tumors kept on growing. The best part? The mice showed no signs of experiencing any side effects from taking the drug.

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Sanguinarine Decreases Survivin Protein Stability By Enhancing Protein Degradation

We then studied how sanguinarine decreases survivin expression. First we examined the effects of sanguinarine on survivin expression at the transcriptional level. LNCaP cells were transfected with a survivin promoter luciferase reporter construct, pLuc-1430, following increasing doses of sanguinarine treatment for 24 h. As shown in Figure 4A, sanguinarine did not affect promoter reporter luciferase activity, suggesting that sanguinarine did not affect survivin expression at the transcriptional level. This experiment was repeated in C4-2 and DU145 cells, and the data remained consistent . We then used real-time PCR to determine the effect of sanguinarine on the level of survivin mRNA. Consistent with luciferase data, sanguinarine did not affect survivin mRNA expression . These data indicate that downregulation of survivin expression by sanguinarine is not at the transcriptional level.

Good Prostate Cancer Care

Your MDT will be able to recommend what they feel are the best treatment options, but ultimately the decision is yours.

You should be able to talk with a named specialist nurse about treatment options and possible side effects to help you make a decision.

You should also be told about any clinical trials you may be eligible for.

If you have side effects from treatment, you should be referred to specialist services to help stop or ease these side effects.

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Stereotactic Body Radiation Therapy Or Stereotactic Ablative Radiation Therapy

Guided by advanced imaging techniques, SBRT delivers large doses of radiation over a short period of time to a precise area. SBRT is commonly referred to by the names of the machines used to deliver the radiation. SBRT can offer some patients with localized prostate cancer the convenience of fewer treatments while maintaining treatment effectiveness and safety. SBRT may also be used to treat metastases for some patients to reduce tumor mass and potentially enhance survival.

Powerful Bystander Effects Induced By Dsrb

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We next tested whether the recruited immune cells could evoke an immune-cell-mediated bystander effect. We treated LNCaP-Luc/GFP cells, which stably express luciferase, with a low dose of dsRB-SCP/polyIC, followed by co-incubation with PBMCs. Luciferase activity served to measure the viability of the LNCaP-Luc/GFP cells. At the low doses used here, luciferase activity was barely affected when PBMCs were absent. In contrast, when PBMCs were added, the LNCaP-Luc/GFP cells were eradicated .5A). These results suggest that dsRB-SCP/polyIC induces a powerful bystander effect, mediated by immune cells among the PBMCs.

dsRB-SCP/polyIC induces direct and PBMC-mediated bystander effects

To evaluate whether dsRB-SCP/polyIC also induces a direct bystander effect, LNCaP cells were co-incubated with PC3-Luc/GFP cells, which do not express PSMA. dsRB-SCP/polyIC treatment resulted in the killing of up to 60% of the PC3-Luc/GFP cells .5B). Since PC3-Luc/GFP cells are not targeted by dsRB-SCP/polyIC ,5B), we infer that the death of these cells is the result of a direct bystander effect elicited by the dsRB-SCP/polyIC-targeted LNCaP cells. The addition of human PBMCs to this co-culture system led to a significant increase in the killing rate of the PC3-Luc/GFP cells ,5B), indicating that the direct and indirect bystander effects both operate under these conditions.

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