Commonly prescribed drug could boost cancer survival rate - Statins

One of UK’s most prescribed drugs could reduce death rate of common blood cancer

Researchers discovered that patients who took a statin had a 61 per cent reduced risk of dying from their cancer

Rebecca Whittaker

Wednesday 23 April 2025 14:06 BST

1 min read   The Independent

Statin use has been linked to a lower risk of dying from blood cancer (PA)
Medicine stock© PA Archive

• A study has found that statin use is linked to a significantly reduced risk of death in patients with chronic lymphocytic leukaemia (CLL) and small lymphocytic lymphoma (SLL).

• Researchers analysed data from 1,467 patients across four international trials and found that those taking statins had a 61 per cent lower risk of dying from their cancer.

• The study also showed a 38 per cent reduction in all-cause mortality and a 26 per cent reduced risk of disease progression in statin users.

• While the study highlights a strong association, further research is needed to determine if statins directly improve cancer outcomes.

• Future research will involve laboratory studies to understand how statins affect cancer biology and clinical trials to assess the direct impact of statin use on CLL and SLL patients.

One of the most prescribed drugs in the UK could reduce the risk of dying from blood cancer by more than 60 per cent, a study has revealed.

Statin, a cholesterol-lowering medication taken by more than 7 million people in the UK, lowers the risk of heart disease, which can lead to heart attacks or strokes.

But it’s also been suggested that it can reduce the death rates of several cancers, including chronic lymphocytic leukaemia (CLL) and small lymphocytic lymphoma (SLL), according to a study published today in the journal Blood Advances.

These are both types of slow-growing cancers. CLL starts in the blood-forming cells of the bone marrow and is a common form of leukaemia. SLL affects the same type of cells but starts in lymphoid tissues such as the spleen instead of in the blood-forming cells.

Researchers analysed data from 1,467 patents with CLL or SLL who participated in four international trials conducted between 2012 and 2019.

Each patient was either newly diagnosed, their blood cancer had come back or had not responded to prior treatment.

These trials saw patients randomly assigned ibrutinib, a targeted cancer drug, either alone or in combination with other anti-cancer drugs, or to a drug regimen that did not include ibrutinib.

A total of 424 patients (29 per cent) were taking a statin at the time they started treatment across the four clinical trials, which looked at how long patients lived after starting treatment. They were followed up after five years for overall survival and 22 months for progression-free survival.

Researchers discovered that patients who took a statin had a 61 per cent reduced risk of dying from their cancer, a 38 per cent reduction in death of any cause and a 26 per cent reduced risk of disease progression.

Researchers adjusted their analysis for variables including each patient’s diagnosis, age, sex, weight, disease severity, length of time since their diagnosis, number of co-existing illnesses, use of other medications for heart conditions or high blood pressure, and the specific anti-cancer treatment regimen received.

“Our results highlight a strong link between statin use and improved survival in this patient population,” said the study’s principal investigator, Ahmad Abuhelwa, PhD, an assistant professor of pharmacy practice and pharmacotherapeutics at the University of Sharjah in the United Arab Emirates.

He added: “These findings don’t allow us to say for certain that statins directly improve cancer outcomes.

“However, the fact that this association remained strong even after accounting for multiple factors makes it an important area for future research.”

As next steps, he recommended conducting laboratory studies to better understand how statins may influence cancer biology, as well as prospective clinical trials in which patients with CLL or SLL are randomly assigned to take a statin or not.

One of UK’s most prescribed drugs could reduce death rate of common blood cancer | The Independent

05 May 21 Stunning therapy lands knock-out blow to cancer

 A cancer treatment in which a patient’s own cells are engineered to hunt down and wipe out their disease ...

4 May 2021

Fiona Macrae for the Daily Mail

© Provided by Daily Mail MailOnline logo

While it sounds like the stuff of science fiction, a cancer treatment in which a patient’s own cells are engineered to hunt down and wipe out their disease — and then linger in the body to stop the cancer returning — is helping to save patients’ lives.

The results of the treatment, known as CAR T-cell therapy, have been astonishing. 

Patients who had exhausted all other options and been told they had just months to live have gone into remission. Others have even been cured by the one-off dose.

In trials, all signs of cancer disappeared in more than 80 per cent of patients with acute lymphoblastic leukaemia — the most common cancer in children — after receiving CAR T-cells.

Success stories include Emily Whitehead, now 16, who in 2012 became the first child in the world to take part in a CAR T-cell trial.

© Provided by Daily Mail

Emily, who only had weeks to live when her leukaemia became resistant to conventional therapies, had the revolutionary treatment at the Children’s Hospital of Philadelphia in the U.S. when she was six years old. She is still cancer-free today.

First given in the NHS two years ago to children with a rare blood cancer, CAR T-cell therapy is now used to treat four forms of the disease — and more could follow.

It is also being trialled in a number of other blood cancers, such as myeloma, non-Hodgkin lymphoma and chronic lymphocytic leukaemia, and could be available soon for these patients.

Early research suggests it can also tackle solid tumours. A new study showed that a new generation of CAR T-cells with more advanced genetic engineering could help treat mesothelioma, ovarian cancer and the deadly brain cancer glioblastoma in mice, without side-effects, reported the journal Science Translational Medicine.

The current uses of CAR T-cell therapy are ‘just the tip of the iceberg’, says Dr Andrew Furness, a consultant medical oncologist at the Royal Marsden Hospital in London. ‘Doctors and scientists are working tirelessly to expand its reach to many more patients.’

CAR T-cell therapy (or chimeric antigen receptor T-cell therapy) is a form of immunotherapy, using the power of a patient’s immune system to fight the disease. 

There are several types that work in different ways to help the immune system recognise and attack cancer cells.

With CAR T-cell therapy, immune cells called T-cells are engineered to seek out and destroy cancer cells.

The process of making these weaponised T-cells is lengthy, complex and expensive. 

It begins with hooking the patient up to a machine (similar to a dialysis machine used for kidney patients) that takes a sample of their blood and separates out their T-cells, before returning the rest of the blood to their body.

The machine repeats the process until it has collected 200ml of T-cells, which can take six hours.

In a lab, these T-cells are then engineered to hunt down and destroy the patient’s cancer. This is done using an inactivated virus to insert genetic material instructing the cells to make a protein called a chimeric antigen receptor (CAR) that recognises a specific protein on the patient’s cancer cells.

Certain cancers over-produce certain proteins and the treatments target these. Acute lymphoblastic leukaemia (ALL) cells make too much CD19, for example, and so ALL patients will have their T-cells engineered to lock on to this protein. 

The supercharged T-cells are then multiplied in the lab, before an infusion of 200 million cells is delivered to the patient via a drip, which takes just two minutes.

The cells should then home in on, and kill, cancer cells that have the protein they’ve been engineered to recognise. In some cases the cancer is undetectable within a month, although this can take longer.

Excitingly, the CAR T-cells should remain in the body as a ‘living drug’ to prevent the cancer returning.

It's given me a second chance- now we're having twins!

In January 2019, when his non-Hodgkin lymphoma became resistant to standard treatment, Thomas Romain, 29, a recruitment consultant who lives in Croydon with wife Emma, 29, and daughter Olivia, three, was offered CAR T-cell therapy. He says:

It all started when I developed excruciating itching on my arms and legs in February 2018. It rapidly spread to the rest of my body, and I also started having extreme night sweats and developed a cough.

At first, I put it down to allergies or exhaustion from looking after Olivia, who was still a baby. But after six months of this and with the symptoms persisting, my GP referred me for blood tests and an X-ray.

In the July, I was diagnosed with non-Hodgkin lymphoma, a type of blood cancer, and told that I also had a 14cm tumour in my chest. The itching was possibly a reaction to the cancer in my blood.

Being just 26 and a new dad, this hit Emma and me like a brick. But we were unable to take time to deal with the terrible news because the tumour was aggressive and they had to move quickly.

I started high-strength chemotherapy later that week, along with oral steroids to stop the tumour growing. I finished treatment in November 2018 and scan results showed that the tumour in my chest hadn’t shrunk much. My consultant told me bluntly that this was bad news. If it isn’t eliminated at this stage, it will almost certainly grow again and spread — even if I had additional chemo.

As a last resort, he referred me to the Royal Marsden Hospital in London, knowing they had a trial of a new treatment called CAR T-cell. They explained that it would help my body fight the cancer itself, and even prevent it returning.

Finally, I had some hope. Studies suggested it improved survival for patients like me from 9 per cent to 75 per cent.

The researchers, who I met in December 2018, didn’t pull any punches: they told me about the potential side-effects, such as nausea and seizures, or worse.

By this point, Emma and I were engaged and Olivia was growing up fast. It was a no-brainer to proceed in the trial. Two weeks later, I had my T-cells extracted. A machine was attached by tubes to both arms. One tube removes blood and takes it into the machine to extract the T-cells. Blood is then returned via the tube in the other arm.

Although it was painless, it took about three hours and the process was quite energy-draining.

A month later I went back to have the CAR T-cells put in. This took only a few minutes and was painless. But after a week I became ill with something called cytokine release syndrome — basically a massive overreaction by my immune system.

I was kept in intensive care for several days with low blood pressure and fever while I received treatment. Apparently, the reaction was a sign the treatment was working, so although I felt terrible, with confusion and fever, for instance, I saw this as a necessary step in the process.

I stayed in hospital for five weeks, being monitored in case the side-effects got any worse — but thankfully I improved.

I had regular scans to monitor the tumour, and three months after the infusion, a scan showed the cancer was completely gone. Hearing that, we felt simply euphoric.

For the first year I had scans every three months. Now it’s just once a year as the risk of relapse has dropped dramatically.

I feel incredibly lucky to be given a second chance at life. Emma and I wed last month and expect twins in August.

MATTHEW BARBOUR

The whole process costs around £250,000 for each patient. From the collection of T-cells to the transfusion of the engineered cells back to the patient takes about a month. 

CAR T-cell therapy on the NHS was first given the go-ahead in September 2018, when the drug Kymriah was approved as a last resort for children and young adults with ALL.

There are around 600 cases of this aggressive blood cancer a year in the UK, mostly in children, and around 10 per cent will relapse despite up to three years of treatment, which can include bone marrow transplants.

A month later, Yescarta was given the green light for diffuse large B-cell lymphoma and primary mediastinal large B-cell lymphoma, cancers of the lymphatic system. Up to 200 patients a year, whose cancer has stopped responding to treatments, are suitable for the new drug.

This January, CAR T-cells became available on the NHS for a third type of cancer, mantle cell lymphoma. Another fast-growing cancer of the lymphatic system, this affects around 600 Britons a year, of which 100 could be eligible for treatment with Tecartus.

Commenting on the new treatment in December 2018, Sir Simon Stevens, chief executive of NHS England, said: ‘The NHS is at the forefront of providing a new wave of personalised treatments that are individually tailored to patients. CAR T-cell therapy is one of the most promising new treatments in a generation for lymphoma and leukaemia.’

CAR T-cells for several more blood cancers are likely to be licensed for use in the next couple of years, says Dr Emma Nicholson, a consultant haematologist at the Royal Marsden Hospital. Work is also ongoing to make CAR T-cell therapy even more effective.

‘There is lots of work on making CAR T-cells better able to persist, better able to expand up to high numbers in the body and better able to kill,’ says Dr Furness, who is also a researcher at the Institute of Cancer Research in London.

Other possibilities include giving CAR T-cell therapy earlier. While it is currently used only as a last resort treatment, because it is so new, if the therapy continues to prove effective, then giving it sooner could spare patients gruelling treatments such as bone marrow transplants and multiple rounds of chemotherapy.

Dr Nicholson predicts that in some cases, such as patients who are judged to be a high risk of relapsing with conventional treatment, CAR T-cell therapy could be their sole treatment. Another possibility is the development of off-the-shelf CAR T-cell treatments, using donor T-cells. Rather than having to wait a month for processing the patients’ own T-cells, these could be used immediately. This approach is already in trials for a number of blood cancers.

However, like all treatments, CAR T-cells are not without risk. Side-effects include dizziness, fever, headaches, confusion, speech changes and seizures.

More rarely, it can cause organ failure and, in extremely rare cases, swelling of the brain. While most side-effects are temporary, they can be fatal and 2 to 3 per cent of patients in trials have died.

Patients are also at higher risk of infections for the first year or so and are given preventative antibiotics and antiviral drugs.

CAR T-cell therapy is currently used only to treat blood cancers rather than solid tumours such as breast and bowel cancer.

‘There are a number of reasons for this,’ says Dr Astero Klampatsa, a CAR T-cell researcher at the Institute of Cancer Research.

‘Solid cancers are made up from a large number of cancer cells, and the protein that CAR T-cells target might not be present on all of them, therefore CAR T-cells cannot kill the whole cancer.

‘Also, solid cancers are acidic and low in oxygen and nutrients, so CAR T-cells find it hard to survive and function properly. Crucially, within the solid tumour there are various cells that act against CAR T-cells, undermining their proper function.

‘It is too early to say whether CAR T-cells will be successful on solid tumours, but research to overcome the problems is already underway,’ Dr Klampatsa added.

Dr Nicholson is optimistic, saying it is likely to be ‘only a matter of time’ before the treatment is as effective against solid tumours as it is on blood cancers.

But even if effective, will the treatment’s hefty price-tag prevent widespread use in the NHS?

Indeed, the three drugs that are already in use haven’t yet been deemed cost-effective enough for routine NHS use. They are being prescribed through the Cancer Drugs Fund — a scheme that fast-tracks the use of new cancer drugs — and used for a subset of desperately ill patients as a last resort.

However, competition between different manufacturers should lower the cost, says Dr Nicholson, so as more CAR T-cell drugs become available, the overall cost of each should come down.

And while a price tag of £250,000 per patient may seem expensive, it could work out cheaper than the total cost of years of conventional treatment (a bone marrow transplant, for example, can cost up to £200,000) and hospital stays.

‘These are expensive therapies but potentially transformative,’ says Dr Furness. ‘These might avoid financial toxicity as well as treatment-related toxicity [long-term side-effects] if you could give them at the start of treatment.

‘For that to be your only cancer therapy would be fantastic.’

https://www.msn.com/en-gb/health/medical/stunning-therapy-lands-knock-out-blow-to-cancer/ar-BB1gjZJC?ocid=msedgntp

Curcumin Starves Cancer Cells to Death - by Life Extension

Cancer cells require tremendous energy to promote their rapid growth. A new study shows how curcumin can selectively starve tumor cells.

Winter 2018-2019 Special Edition

By Kirk Stokel

(Previously published here on 7 October 2019)

Over 4,500 published studies describe the anti-cancer effects of curcumin.

Researchers are intrigued by a promising discovery that curcumin selectively starves tumor cells to death.1

Curcumin does this by depriving cancer cells of the ability to make and use ATP, the energy currency within cells.2

Since most cancer cells generate ATP in a different way than healthy cells, curcumin selectively kills tumor cells with no impact on healthy tissues.

These newly uncovered energy-disrupting properties of curcumin further support the preventive potential of this botanical compound.

Cutting Cancer’s Energy Supply

Cancer cells require tremendous energy to promote their rapid, uncontrolled growth, and they have developed numerous methods to support that energy demand.

In particular, cancer cells have an unusual, oxygen-free mechanism of extracting energy from glucose to produce ATP (adenosine triphosphate). This process helps most cancer cells survive in the low-oxygen environments they generate as they grow rapidly.2

Scientists conducted a study to determine if this process can be reversed in cancer cells.

Since many different types of cancer use the same metabolic trick to extract energy, the researchers studied curcumin’s impact on a variety of tumor lines, including leukemia, breast, melanoma (skin), and colon cancers.2

This study shed new light on curcumin’s ability to starve cancer into submission by interfering with how tumors cells use energy.

Let’s look at the findings one at a time.

Curcumin Blocks ATP Production

First, the researchers found that curcumin can sharply reduce how much energy is available to the cancer cells.2

This study showed that curcumin was able to:

1) Reduce levels of ATP-synthase (the enzyme that creates ATP) in all four tumor cell lines in culture,

2) Reduce cellular levels of ATP in three of the four cell lines, and

3) Lower the ratio of high-energy ATP to lower-energy AMP in all four cell lines.

Curcumin Slows Tumor Growth

Next, researchers implanted aggressive skin cancer (melanoma) cells into live mice. Half the mice were treated with curcumin and the other half served as the control group.2

Just 2 days into the study, the curcumin-treated mice were demonstrating significantly slower tumor growth. Tumor growth remained significantly slower for the entire period of the study.

Not surprisingly, ATP-synthase, ATP levels, and the ATP/AMP ratio were all significantly lowered in the curcumin group. These results indicate that energy starvation was a mechanism of action by which curcumin slowed tumor growth.

Curcumin Prevents New Blood Vessel Growth

Cancers need to trigger new blood vessel development (called angiogenesis) to support their nutrient needs as they rapidly grow. Blocking this process is an important way to limit the growth and spread of a tumor.

After removing tumors from the mice in this study, the researchers found that the curcumin-supplemented animals’ tumors had fewer new blood vessels compared with control-fed mice.

This indicates that curcumin reduced the tumors nutrient energy access by limiting blood flow.2

Curcumin’s Known Tumor-Fighting Properties

This most recent study adds to an abundance of evidence pointing to curcumin’s potent cancer-fighting abilities. It focuses on curcumin’s unique ability to combat a variety of cancers by cutting off their energy supply.

Previous studies have shown curcumin’s tumor-fighting properties in multiple specific types of cancer. Here are some highlights from the most recent literature.

Colorectal Cancer

Cancers of the colon and rectum are among the most common malignancies in men and women. Curcumin has a long track record of achievements in preventing colorectal cancers.

A Phase IIa human clinical trial has shown that 4 grams/day of curcumin significantly reduces the number of aberrant crypt foci found during endoscopy. This is a critical finding because if aberrant crypt foci are left untreated, they can produce malignant tumors.3

Weight loss is common in cancer patients. A human study showed that colon cancer patients who were supplemented with curcumin gained more weight, had less inflammation, and had increased numbers of cancer cells dying by apoptosis.4 This effect has been traced to curcumin’s ability to activate a “programmed cell death” gene in tumor cells.

Finally, curcumin has been shown to selectively reduce the survival of cancer stem cells.5 These cells account for much of the metastatic spread and tumor recurrences seen in aggressive malignancies. Cutting their numbers is an appealing approach to preventing tumors from spreading.

While a high-dose (4,000 mg) of curcumin was used in this study, more bioavailable curcumin forms can enable one to achieve a similar dose with two capsules a day.

WHAT YOU NEED TO KNOW

Curcumin Starves Cancer Cells to Death

• Curcumin is a powerful, multi-functional polyphenol that is gaining increasing recognition for its cancer chemopreventive properties.
• A new study shows that curcumin sharply restricts cancer cells’ ability to extract energy from glucose in the blood.
• This mechanism is especially appealing for cancer chemoprevention because it would target the great majority of cancers.
• Previous studies also show that curcumin can reduce inflammation, prevent chemical stress, shut down cancer-promoting pathways, and interfere with malignant cells’ growth and development.
• These multiple mechanisms of action make it clear that curcumin should be a central element of any comprehensive cancer chemoprevention regimen.

Breast Cancer

Breast cancer is the most common cancer in women, and it’s the second leading cause of cancer deaths among women worldwide.6,7

Curcumin has shown promise in combatting breast cancer. This is especially true of estrogen receptor-negative tumors, which respond poorly to cancer chemotherapy.6

Studies show that giving curcumin to animals with implanted human breast cancers shrinks the tumors, deprives them of their blood supply, and triggers their self-destruction by apoptosis.6,8

More recently, research revealed that curcumin can also combat breast cancer by reversing the excessive methylation of certain genes that is associated with increased cancer development.9

Prostate Cancer

Prostate cancer strikes one in nine American men, yet is among the most preventable cancers because of its slow growth.10

Curcumin has multiple actions against prostate cancer. It defends prostate cells against the dysfunctional proteins produced during cancer progression. It also slows invasion of nearby healthy tissue by the cancer, which helps to keep the tumor at a lower grade (meaning it grows more slowly and has a better prognosis).11-13

One study showed that when human prostate cells were implanted into mice, they grew into sizable tumors. But when these animals were supplemented with curcumin, the tumors grew 27% more slowly. In addition, the time it took to double levels of prostate specific antigen (PSA) was extended or delayed by about two-fold.14 (Doubling time is an indicator of how aggressive the cancer is.)

Curcumin can also reduce tumor-derived testosterone production in prostate cancer cells.15 This is a hidden source of male hormones that often contributes to treatment-resistant disease.16 This development offers a welcome new approach to treating these challenging tumors.

Liver Cancer

Liver cancer is increasing in incidence worldwide, spurred by epidemic hepatitis C virus and rampant fatty liver disease.17 

In lab studies, curcumin was shown to help prevent liver cancer by reducing inflammatory signaling, inhibiting cell growth, and activating cell death by apoptosis.18-20 It has also been shown to reduce populations of liver cancer stem cells.19,21

In one study, curcumin inhibited the growth of liver cancer cells, while also promoting their death by apoptosis. And in a mouse model of liver cancer, treatment with curcumin caused the tumors to grow much more slowly.22

And, in an exciting development, a study published in 2018 showed that when curcumin is combined with the AMPK-activator drug metformin, the combination worked better than either alone in preventing growth, metastasis, and new blood vessel formation in hepatocellular carcinoma, the most common—and most deadly—type of liver cancer.23

Lung Cancer

A new study shows that
curcumin sharply restricts
cancer cells’ ability to
extract energy from
glucose in the blood.

Lung cancer continues to be the top cause of cancer-related deaths, making it a huge priority for prevention.24,25

An abundance of animal and basic lab studies show curcumin’s potential against lung cancer.

For example, curcumin has been shown to reduce the growth of implanted human lung cancers in mice.26  Lab studies on lung cancer show that curcumin alters proteins required for metastasis, boosting the function of immune cells that are inactivated by cancers, and targeting blood vessel growth.24,26,27

A unique way in which curcumin combats lung cancer is by modulating microRNA inside cancer cells.28-30 These short stretches of genetic material regulate how the main genes in tumor cells are translated into functional proteins.

Studies reveal that curcumin inhibits lung cancer cell growth by downregulating a gene that promotes tumor formation, while upregulating genes that suppress transformation.28 Other research shows similar favorable modulation of miRNAs involved in metastatic spread.30

Summary

Curcumin is the polyphenol that gives the yellow color to the spice turmeric. It has been front and center in the scientific press for years—mostly recognized for its ability to suppress inflammation.2,31,32

Curcumin has also been shown to prevent cancer progression through a variety of mechanisms. Most recently, a study found that curcumin starves cancer cells of much-needed energy.

This mechanism is especially appealing for cancer prevention because it would target the great majority of cancers.

This confirms previous studies showing that curcumin has specific effects against colorectal, breast, prostate, lung, and liver cancers.

Starving malignant cells of their energy supply is an ideal way of boosting our bodies’ natural cancer resistance, helping it quench cancer long before a tumor is detectable.

If you have any questions on the scientific content of this article, please call a Life Extension® Wellness Specialist at 1-866-864-3027.

References

1. Available at: https://www.ncbi.nlm.nih.gov/pubmed/?term=curcumin+and+cancer. Accessed September 21, 2018.
2. Bianchi G, Ravera S, Traverso C, et al. Curcumin induces a fatal energetic impairment in tumor cells in vitro and in vivo by inhibiting ATP-synthase activity. Carcinogenesis. 2018 Sep 21;39(9):1141-50.
3. Carroll RE, Benya RV, Turgeon DK, et al. Phase IIa clinical trial of curcumin for the prevention of colorectal neoplasia. Cancer Prev Res (Phila). 2011 Mar;4(3):354-64.
4. He ZY, Shi CB, Wen H, et al. Upregulation of p53 expression in patients with colorectal cancer by administration of curcumin. Cancer Invest. 2011 Mar;29(3):208-13.
5. James MI, Iwuji C, Irving G, et al. Curcumin inhibits cancer stem cell phenotypes in ex vivo models of colorectal liver metastases, and is clinically safe and tolerable in combination with FOLFOX chemotherapy. Cancer Lett. 2015 Aug 10;364(2):135-41.
6. Bimonte S, Barbieri A, Palma G, et al. Dissecting the role of curcumin in tumour growth and angiogenesis in mouse model of human breast cancer. Biomed Res Int. 2015;2015:878134.
7. Wang Y, Yu J, Cui R, et al. Curcumin in Treating Breast Cancer: A Review. J Lab Autom. 2016 Dec;21(6):723-31.
8. Ferreira LC, Arbab AS, Jardim-Perassi BV, et al. Effect of Curcumin on Pro-angiogenic Factors in the Xenograft Model of Breast Cancer. Anticancer Agents Med Chem. 2015;15(10):1285-96.
9. Kumar U, Sharma U, Rathi G. Reversal of hypermethylation and reactivation of glutathione S-transferase pi 1 gene by curcumin in breast cancer cell line. Tumour Biol. 2017 Feb;39(2):1010428317692258.
10. Available at: https://www.cancer.org/cancer/prostate-cancer/about/key-statistics.html. Accessed September 24, 2018.
11. Sundram V, Chauhan SC, Ebeling M, et al. Curcumin attenuates beta-catenin signaling in prostate cancer cells through activation of protein kinase D1. PLoS One. 2012;7(4):e35368.
12. Liu T, Chi H, Chen J, et al. Curcumin suppresses proliferation and in vitro invasion of human prostate cancer stem cells by ceRNA effect of miR-145 and lncRNA-ROR. Gene. 2017 Oct 5;631:29-38.
13. Yang J, Wang C, Zhang Z, et al. Curcumin inhibits the survival and metastasis of prostate cancer cells via the Notch-1 signaling pathway. APMIS. 2017 Feb;125(2):134-40.
14. Hong JH, Lee G, Choi HY. Effect of curcumin on the interaction between androgen receptor and Wnt/beta-catenin in LNCaP xenografts. Korean J Urol. 2015 Sep;56(9):656-65.
15. Ide H, Lu Y, Noguchi T, et al. Modulation of AKR1C2 by curcumin decreases testosterone production in prostate cancer. Cancer Sci. 2018 Apr;109(4):1230-8.
16. Armandari I, Hamid AR, Verhaegh G, et al. Intratumoral steroidogenesis in castration-resistant prostate cancer: a target for therapy. Prostate Int. 2014 Sep;2(3):105-13.
17. Global Burden of Disease Liver Cancer C, Akinyemiju T, Abera S, et al. The Burden of Primary Liver Cancer and Underlying Etiologies From 1990 to 2015 at the Global, Regional, and National Level: Results From the Global Burden of Disease Study 2015. JAMA Oncol. 2017 Dec 1;3(12):1683-91.
18. Dai XZ, Yin HT, Sun LF, et al. Potential therapeutic efficacy of curcumin in liver cancer. Asian Pac J Cancer Prev. 2013;14(6):3855-9.
19. Marquardt JU, Gomez-Quiroz L, Arreguin Camacho LO, et al. Curcumin effectively inhibits oncogenic NF-kappaB signaling and restrains stemness features in liver cancer. J Hepatol. 2015 Sep;63(3):661-9.
20. Elmansi AM, El-Karef AA, Shishtawy M, et al. Hepatoprotective Effect of Curcumin on Hepatocellular Carcinoma Through Autophagic and Apoptic Pathways. Ann Hepatol. 2017 Jul-Aug;16(4):607-18.
21. Tsai CF, Hsieh TH, Lee JN, et al. Curcumin Suppresses Phthalate-Induced Metastasis and the Proportion of Cancer Stem Cell (CSC)-like Cells via the Inhibition of AhR/ERK/SK1 Signaling in Hepatocellular Carcinoma. J Agric Food Chem. 2015 Dec 9;63(48):10388-98.
22. Pan Z, Zhuang J, Ji C, et al. Curcumin inhibits hepatocellular carcinoma growth by targeting VEGF expression. Oncol Lett. 2018 Apr;15(4):4821-6.
23. Zhang HH, Zhang Y, Cheng YN, et al. Metformin incombination with curcumin inhibits the growth, metastasis, and angiogenesis of hepatocellular carcinoma in vitro and in vivo. Mol Carcinog. 2018 Jan;57(1):44-56.
24. Liu D, You M, Xu Y, et al. Inhibition of curcumin on myeloid-derived suppressor cells is requisite for controlling lung cancer. Int Immunopharmacol. 2016 Oct;39:265-72.
25. Available at: https://www.cancer.org/latest-news/facts-and-figures-2018-rate-of-deaths-from-cancer-continues-decline.html. Accessed September 24, 2018.
26. Chen QY, Jiao DM, Yao QH, et al. Expression analysis of Cdc42 in lung cancer and modulation of its expression by curcumin in lung cancer cell lines. Int J Oncol. 2012 May;40(5):1561-8.
27. Xu X, Zhu Y. Curcumin inhibits human non-small cell lung cancer xenografts by targeting STAT3 pathway. Am J Transl Res. 2017;9(8):3633-41.
28. Lelli D, Pedone C, Majeed M, et al. Curcumin and Lung Cancer: the Role of microRNAs. Curr Pharm Des. 2017;23(23):3440-4.
29. Liu WL, Chang JM, Chong IW, et al. Curcumin Inhibits LIN-28A through the Activation of miRNA-98 in the Lung Cancer Cell Line A549. Molecules. 2017 Jun 3;22(6).
30. Zhan JW, Jiao DM, Wang Y, et al. Integrated microRNA and gene expression profiling reveals the crucial miRNAs in curcumin anti-lung cancer cell invasion. Thorac Cancer. 2017 Sep;8(5):461-70.
31. Chadalapaka G, Jutooru I, Chintharlapalli S, et al. Curcumin decreases specificity protein expression in bladder cancer cells. Cancer Res. 2008 Jul 1;68(13):5345-54.
32. Kelany ME, Hakami TM, Omar AH. Curcumin improves the metabolic syndrome in high-fructose-diet-fed rats: role of TNF-alpha, NF-kappaB, and oxidative stress. Can J Physiol Pharmacol. 2017 Feb;95(2):140-50.

Ketogenic diet could be the key to making a cancer treatment work

PI3K inhibiting drugs have shown little success. Now researchers may have figured out why.

4th July 2018

A ketogenic diet is low carbs and high in fat. This can help keep insulin levels low, which is believed to improve the effectiveness of certain cancer drugs. 

For their study, scientists tested the drugs in mice who’d been fed either a standard or ketogenic diet. While it was largely ineffective for the mice eating standard fare, the treatment shrunk the tumors of mice who’d eaten the ketogenic diet.

The drugs in question work by inhibiting the PI3K pathway, a cell-signaling network that’s overactive in many types of cancer. However, while there are lots of PI3K inhibitors in development, researchers and pharmaceutical companies have struggled to make them effective. “While more than 20 PI3K inhibitors have entered cancer clinical trials, only two have been approved,” said Benjamin Hopkins, a postdoctoral medical researcher at Cornell University who is one of the study’s authors.

The researchers posited that insulin may be the reason these drugs aren’t living up to their promise. The PI3K enzyme regulates glucose metabolism. 

When glucose levels are high, the body produces insulin. Insulin stimulates the PI3K pathway which then leads to cell proliferation and tumor growth. This means that rising insulin levels could counteract any drugs taken to inhibit the enzyme.

So the team started looking for ways to keep patients’ insulin low while they’re taking PI3K inhibiting drugs. 

They tested two approaches in mice: a diabetes medication and a ketogenic diet, which prevents glycogen from being stored in liver and muscle tissue. “Both interventions caused dramatic improvements in responses to multiple PI3K inhibitors in multiple cancer types,” said Hopkins.
The researchers stress that their study doesn’t suggest a ketogenic diet alone would help prevent or treat cancer. In a leukemia model, the ketogenic diet even seemed to make the cancer worse in mice who hadn’t received a PI3K inhibiting drug. 

“But the combination of a PI3K inhibitor and ketogenic diet was effective in a surprisingly wide spectrum of cancers,” said Hopkins. “Our study suggests that more patients would respond to these drugs if their serum insulin could be maintained at low levels during therapy by these interventions.”

To see if their approach will also work in humans, the study’s authors plan to conduct a clinical trial within a year. This could provide some of the answers researchers, drug developers, and patients are looking for. Hopkins explains: “Patients often ask whether they should change their eating habits when diagnosed with cancer, and physicians admit that there is little evidence that this can improve the outcome. Conducting a clinical trial to test this idea is critical.”

Featured image courtesy of jensteele via flickr

https://www.researchgate.net/blog/post/ketogenic-diet-could-be-the-key-to-making-a-cancer-treatment-work

London pensioner used turmeric to fight off blood cancer

Woman, 67, who battled blood cancer for five years 'recovers after treating it with TURMERIC' in the first recorded case of its kind

• Dieneke Ferguson, 67, had given up on gruelling treatments and chemotherapy
• With her myeloma spreading she began taking 8g of curcumin a day
• The cancer stabilised in what doctors say was the first case of its kind 

By BEN SPENCER, MEDICAL CORRESPONDENT FOR THE DAILY MAIL

PUBLISHED: 00:06 BST, 3 January 2018 | UPDATED: 15:23 BST, 3 January 2018

A woman who battled blood cancer for years without success finally halted the disease with turmeric, it has been reported.

Dieneke Ferguson is now leading a normal life after giving up on gruelling treatments that failed to stop it.

Doctors say her case is the first recorded instance in which a patient has recovered by using the spice after stopping conventional medical treatments.

With her myeloma spreading rapidly after three rounds of chemotherapy and four stem cell transplants, the 67-year-old began taking 8g of curcumin a day – one of the main compounds in turmeric. ( Myeloma, also known as multiple myeloma is a blood cancer related to lymphoma and leukemia.)

Dieneke Ferguson had been diagnosed with the blood cancer myeloma in 2007 and had undergone three rounds of chemotherapy as well as four stem cell transplants



Dieneke is still taking 8g of curcumin in tablet form daily — the equivalent of about two teaspoonfuls of pure powdered curcumin

The cancer, which has an average survival of just over five years, was causing increasing back pain and she had already had a second relapse.

But it stabilised after Mrs Ferguson, from north London, came across the remedy on the internet in 2011 and decided to try it as a last resort.

 The tablets are expensive – £50 for ten days – but as kitchen turmeric contains just 2 per cent curcumin it would be impossible to eat enough to get the same dose.

Mrs Ferguson, who was first diagnosed in 2007, continues to take curcumin without further treatment and her cancer cell count is negligible.

Her doctors, from Barts Health NHS Trust in London, wrote in the British Medical Journal Case Reports: ‘To the best of our knowledge, this is the first report in which curcumin has demonstrated an objective response in progressive disease in the absence of conventional treatment.’

The experts, led by Dr Abbas Zaidi, said some myeloma patients took dietary supplements alongside conventional treatment but ‘few, if any, use dietary supplementation as an alternative to standard antimyeloma therapy’. 

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Doctors say Dieneke Ferguson's case is the first recorded instance in which a patient has recovered by using turmeric (pictured) after stopping conventional medical treatments

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Since the turn of the century, more than 50 studies have tested curcumin – the pigment in turmeric that gives it its bright yellow colour

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Dieneke tried Curcumin, a component of turmeric, and five years on, her cancer cell count is negligible. Pictured: Dieneke Ferguson with the Olympics Torch in Brazil

Doctor explains how acute myeloid leukaemia effects patients

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But they added: ‘In the absence of further antimyeloma treatment the patient plateaued and has remained stable for the past five years with good quality of life.’

Since the turn of the century, more than 50 studies have tested curcumin – the pigment in turmeric that gives it that bright yellow colour.

A CENTURIES-OLD EASTERN REMEDY

• Turmeric is a yellow spice widely used as a flavouring in the Indian subcontinent and as a food colouring by industry
• It is ground from the dried root of an Asian plant called Curcuma longa and has been used in Eastern medicine for centuries
• Curcumin - turmeric’s active ingredient - has significant antioxidant, anti-inflammatory and antiseptic properties
• Studies have shown it is an effective painkiller and also reduces the risk of lung disease, Alzheimer’s, heart disease and depression

They suggest the spice can protect against several cancers, as well as Alzheimer’s, heart disease and depression.

It has also been shown to help speed recovery after surgery and effectively treat arthritis. 

But although it is widely used in Eastern medicine, and has been studied for its anti-inflammatory and antiseptic effects, curcumin is not widely prescribed because it has never been tested in large-scale trials.

The doctors wrote that the ‘biological activity of curcumin is indeed remarkable’, including its ‘anti-proliferative effects in a wide variety of tumour cells’. 

But Professor Jamie Cavenagh, one of the authors of the paper, stressed it may not work for all patients. He said: ‘A lot of my patients take curcumin at different stages of their treatment. I don’t object to it.

‘Dieneke’s is the best response I have observed and it is clear-cut because we had stopped all other treatment.’

Mrs Ferguson, who runs Hidden Art, a not-for-profit business helping artists market their work, is frustrated doctors cannot recommend the spice and wants more research carried out.

She said: ‘I hope my story will lead to more people finding out about the amazing health benefits of curcumin.’

Myeloma affects some 5,500 people in the UK every year, killing nearly 3,000. 

https://www.dailymail.co.uk/health/article-5230201/Pensioner-used-turmeric-fight-blood-cancer.html

ALSO:

How Dieneke beat her incurable cancer through curcumin

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