The Guardian
Email YouTube Facebook Instagram Twitter WhatsApp

Natural ‘cures’ for pancreatic cancer

Related


*Tumours disappeared in 70% of mice treated with cannabis compound, Harvard University study reveals
*Black seed, soursop, turmeric, Moringa, intravenous vitamin C, aspirin, others stop disease in clinical trials
Pancreatic cancer is becoming more common. In recent times, more Nigerians have lost their lives to one of the hardest-to-treat, most lethal malignancy and the fourth cause of cancer-related deaths worldwide, which has a median five-year survival rate of only eight per cent.

Several researches have shown that as people age, the risk of developing pancreatic cancer goes up. Most patients are older than 45, and nearly 90 per cent are older than 55. The average age at diagnosis is 71.Men have a slightly higher likelihood of developing pancreatic cancer than women, which may partly result from increased tobacco use in men. In the past, when men more commonly smoked than women, the gender gap was wider. Currently, the lifetime risk of developing it is about one in 63 for men and one in 65 for women.

There is also a noted association with race: Black Africans are more likely to develop pancreatic cancer than whites. Doctors do not know why but speculate that higher rates of men smoking and having diabetes, and women being overweight, may contribute to that association.Pancreatic cancer is aggressive with few symptoms until the cancer is advanced. Symptoms may include abdominal pain, weight loss, diarrhoea, and jaundice.

Unfortunately, conventional medicine has not been able to find a cure for the deadly disease and the available surgery, chemotherapy, radiotherapy come at a very high cost with undesirable and deadly side effects. But natural medicine has shown great promise.

Recent studies have demonstrated that Cannabis sativa (marijuana), Nigella sativa (black seed), Annona muricata (soursop), Curcuma longa (turmeric), Moringa oleifera, Piper nigrum (black pepper), dual thermal ablation technique among others could provide cure for pancreatic cancer.Commonly called weed, marijuana, hemp, igbo, gbana, kaya, wee-wee, or abana, Cannabis sativa has become a novel adjunct treatment for cancer, pain, poor appetite, nausea, epilepsy to mention but a few.

Scientists at the Harvard University, United States (U.S.) tested the effects of marijuana-derived compounds called flavonoids on pancreatic cancer cells in petri dishes and on animals with the disease. According to the research published in journal Frontiers of Oncology last month, flavonoids treatment killed all the tumor cells in 70 percent of mice with pancreatic cancer that the researchers tested for the study. The treatment also supercharged more traditional radiation therapy, giving the researchers hope that by 2020, the promising treatment could be ready for testing in humans.

Notably, the compound that the Harvard team is studying comes from cannabis, but is neither a cannabinoid, like CBD, nor a psychoactive component of the plant, like THC. Cannabidiol (CBD) is an active ingredient in cannabis derived from the hemp plant. It may help treat conditions like pain, insomnia, and anxiety.Tetrahydrocannabinol is one of at least 113 cannabinoids identified in cannabis. THC is the principal psychoactive constituent of cannabis.

Instead, flavonoids are the compounds present in virtually all plants (including fruits and vegetables) that give them their vibrant colours. There are more than 6,000 variations of flavonoids but the Harvard scientists see great potential in one found in cannabis and used to make a compound dubbed FBL-03G.

Interestingly, a US company Flavocure Biotech has expanded their research into FBL-O3G for pancreatic cancer, in collaboration with Harvard Medical School. The results of the FBL-03G molecule have shown statistically significant results against pancreatic cancer, in vivo (inside a living organism). The company plans to continue their collaboration with Harvard Medical School in order to advance FBL-03G towards an improved treatment and cure for pancreatic cancer.

Meanwhile, cannabinoids are already used and studied for treating the unpleasant side effects of standard cancer therapies like chemo and radiation.
In more recent years, a slew of studies have explored the plant’s potential for treating cancer itself. Research has pointed to the possibility that cannabis may block tumour growth in a variety of ways – but it’s been spotty, and how the plant has these effects remains unclear. Co-author of the new Harvard study, Dr. Wilfred Ngwa, told DailyMail.com: “People have done studies before showing that sometimes cannabis works against cancer, and sometimes, it does not.”

He attributed a lot of these discrepancies to the wide variation in the composition of any given cannabis strain or plant and lack of consistency in this sense from study to study.

Scientific studies have shown the drug can alleviate depression, anxiety and stress, but heavy use may worsen depression in the long term by reducing the brain’s ability to let go of bad memories.According to research, it can also contribute to mental health problems among people who already have them, or increase users’ risk of psychosis or schizophrenia.

Marijuana can be prescribed for medical uses in more than half of US states, where it is used to combat anxiety, aggression and sleeping problems. Researchers are also looking into whether it could help people with autism, eczema or psoriasis.Ngwa and his team first separated out many parts of the cannabis plant and ran preliminary tests to see which parts showed the most ‘activity’ against tumours.

That is how they landed on the flavonoid FBL-03G. So they put FBL-03G in a petri dish with pancreatic cancer cells – a type of tumor they happened to already have been studying in their lab – and watched it work. They also used a type of smart radiation therapy to shoot the compound directly into metastasized tumors in mice with pancreatic cancer. Ngwa said: “We were very surprised with the results we got. We expected it to show some inhibition of tumor growth, but we were quite surprised that it also inhibited tumor progression in other parts of the body. We actually had to run some (additional) measurements to see if this was really true.”

It was. Not only did the treatment stop the tumours from growing, but also in about 70 percent of the animals, the radiation therapy and FBL-03G combination shrank the tumours out of existence. It is unclear if the cancer might return, but for the time being, the majority of the mice were cancer free.

Ngwa and his team are not exactly sure how the flavonoid treatment works, but they have a couple of theories. “We believe that cannabinoids have immune modulation properties,” Ngwa said. One of their theories is that the cannabis flavonoid “can create these antigen cells that train the T-cells, like a vaccine – to recognize the disease,” he explained.

Their other hypothesis involves a process call “apoptosis.” “It kills cancer cells, but it does it in such a way that it exposes the camouflage of the cancer cells that hides them from T-cells.” It is possible that these processes mean that the immune system would “remember” the cancer if it came back, too. But do these promising results mean that cancer patients should be turning to cannabis, its oils and extracts? “We get a lot of patients who are asking that question,” said Ngwa. “We need more studies,” to know that, he said.

“People are just using formulations of cannabis oil and you do not really know what are the active components in those.” He is fairly confident that there are active, anti-cancer components in cannabis, but that “each cannabis plant produces completely different levels of active components.”

It is possible, too, that the plants various elements work “sytnergistically,” Ngwa said, and even deriving a single component, as he and his team did is much cheaper than making most drugs. But for the time being patients “need some patience,” he said.
Black seed oil kills pancreatic cancer cells

Also, an herb used in traditional medicine by many Middle Eastern countries may help in the fight against pancreatic cancer, one of the most difficult cancers to treat. Researchers at the Kimmel Cancer at Jefferson in Philadelphia, US, have found that thymoquinone, an extract of Nigella sativa (Black seed) seed oil, blocked pancreatic cancer cell growth and killed the cells by enhancing the process of programmed cell death.

Commonly called black seed, Nigella sativa belongs to the plant family Ranunculaceae. It is a widely used medicinal plant throughout the world. It is very popular in various traditional systems of medicine like Unani and Tibb, Ayurveda and Siddha. Seeds and oil have a long history of folklore usage in various systems of medicines and food. The seeds of N. sativa have been widely used in the treatment of different diseases and ailments. In Islamic literature, it is considered as one of the greatest forms of healing medicine. It has been recommended for using on regular basis in Tibb-e-Nabwi (Prophetic Medicine).

According to a study published in Asian Pacific Journal of Tropical Biomedicine titled “A review on therapeutic potential of Nigella sativa: A miracle herb”, the plant has been widely used as antihypertensive, liver tonics, diuretics, digestive, anti-diarrheal, appetite stimulant, analgesics, anti-bacterial and in skin disorders.

Meanwhile, while the new studies are in the early stages, the findings suggest that thymoquinone could eventually have some use as a preventative strategy in patients who have gone through surgery and chemotherapy or in individuals who are at a high risk of developing cancer.

According to Hwyda Arafat, associate professor of Surgery at Jefferson Medical College of Thomas Jefferson University, Nigella sativa helps treat a broad array of diseases, including some immune and inflammatory disorders. Previous studies also have shown anticancer activity in prostate and colon cancers, as well as antioxidant and anti-inflammatory effects.

Using a human pancreatic cancer cell line, she and her team found that adding thymoquinone killed approximately 80 percent of the cancer cells. They demonstrated that thymoquinone triggered programmed cell death in the cells, and that a number of important genes, including p53, Bax, bcl-2 and p21, were affected. The researchers found that expression of p53, a tumor suppressor gene, and Bax, a gene that promotes programmed cell death, was increased, while bcl-2, which blocks such cell death, was decreased. The p21 gene, which is involved in the regulation of different phases of the cell cycle, was substantially increased. She presented her findings at the Digestive Disease Week in San Diego.

Arafat and her co-workers also found that thymoquinone caused “epigenetic” changes in pancreatic cancer cells, modifying the cells’ Deoxy ribonucleic Acid (DNA)/genetic material. She explained that these changes involve adding acetyl groups to the DNA structure, specifically to blocks of proteins called histones. This “acetylation” process can be important for genes to be read and translated into proteins. In this case, it could involve the genes that are key to initiating programmed cell death.“We looked at the status of the histones and found surprisingly that thymoquinone increased the acetylation process,” Arafat said. “We never anticipated that.”

At the same time, adding thymoquinone to pancreatic cancer cells reduced the production and activity of enzymes called histone deacetylases (HDACs), which remove the acetyl groups from the histone proteins, halting the gene transcription process. Arafat noted that HDAC inhibitors are a “hot” new class of drugs that interfere with the function of histone deacetylases, and is being studied as a treatment for cancer and neurodegenerative diseases. Finding that thymoquinone functions as an HDAC inhibitor, she said, “was very remarkable and really exciting.”
Soursop for pancreatic cancer

Scientists have demonstrated how extracts of soursop stops pancreatic cancer (PC) in clinical trials.The study titled “Emerging therapeutic potential of graviola and its constituents in cancers” was published in the journal Carcinogenesis. Annona muricata is also known as soursop, graviola or guanabana. Extracts from the fruit, bark, seeds, roots and leaves of graviola, along with several other Annonaceous species, have been extensively investigated for anticancer, anti-inflammatory and antioxidant properties.

Phytochemical studies have identified the acetogenins; a class of bioactive polyketide-derived constituents, from the extracts of Annonaceous species, and dozens of these compounds are present in different parts of graviola. The researchers wrote: “Although many natural products have been explored for PC therapeutics, unfortunately, none have translated clinically. Our lab reported the antiproliferative and antitumor effects of graviola (capsules containing leaf and stem powder) in PC cells and subcutaneous xenografts; these actions involved induction of cell cycle arrest accompanied by apoptosis. Similar antiproliferative effects of the hexane fraction of A. muricata leaves, rich in flavonoids, were reported.”

Combination of natural products with gemcitabine
A study published in BioMed Research International and titled “Natural Products as Adjunctive Treatment for Pancreatic Cancer: Recent Trends and Advancements has identified several natural products that could be effectively used to treat pancreatic cancer.

Irofulven (MGI 114, HMAF, 6-hydroxymethylacylfulvene), a novel cytotoxic agent synthesized from the sesquiterpene mushroom metabolite of the natural product illudin S, has a unique mechanism of action involving the formation of macromolecule adduct, cell cycle arrest of S-phase, and induction of apoptosis [49]. Phase I clinical combination trial study of irofulven and gemcitabine in the patients with advanced solid tumor was underway. Van Laar et al. showed similar marked activity of irofulven against pancreatic xenografts, which was observed at lower total doses of an intermittent dosing regimen, compared to consecutive daily dosing. Further, enhanced antitumor activity was observed when irofulven and gemcitabine were combined against the MiaPaCa pancreatic xenograft model, which indicated at least an additive interaction compared to single-agent activity.

Psorospermin, a natural product isolated from the stembark and roots of the African plant Psorospermum febrifugum, had the activity against drug-resistant leukemia lines and Human Immuno-deficiency Virus (HIV)/Acquired Immune Deficiency Syndrome (AIDS)-related lymphoma. Fellows et al. showed that psorospermin had the same effect as gemcitabine in inhibiting the growth of tumor in vivo in the MiaPaCa pancreatic xenograft model. Moreover, psorospermin combined with gemcitabine was found to have an at least additive effect in slowing the growth of MiaPaCa pancreatic cancer cells.

3,3-Diindolylmethane (DIM) is a natural compound, which can be easily obtained by consuming the cruciferous vegetables. Banerjee et al. present in vitro and in vivo preclinical evidence supporting chemosensitization of pancreatic cancer cells by DIM. DIM potentiates chemosensitization and killing of pancreatic cancer cells by downregulation of constitutive as well as drug-induced activation of NF-kappaB and its downstream genes (XIAP, Bcl-xL, survivin, and cIAP). Compared with monotherapy, DIM pretreatment of pancreatic cancer cells resulted in a significantly increased apoptosis with suboptimal concentrations of chemotherapeutic agents such as gemcitabine, cisplatin, and oxaliplatin.

Thymoquinone is a bioactive compound extracted from the oil of folklore medicine black seed (Nigella sativa). Banerjee et al. reported the chemosensitizing effect of thymoquinone to conventional chemotherapeutic agents (gemcitabine and oxaliplatin) both in vitro and in vivo using an orthotopic model of pancreatic cancer. By downregulation of nuclear factor-kappaB (NF-kappaB/NF-κB), Bcl-2 family, and NF-kappaB-dependent antiapoptotic genes (survivin, X-linked inhibitors of apoptosis, and cyclooxygenase-2), thymoquinone could potentiate the killing of pancreatic cancer cells induced by chemotherapeutic agents (gemcitabine and oxaliplatin).

Cucurbitacin B, a member of the cucurbitacins, is derived from Cucurbitaceae family “Trichosanthes kirilowii Maximowicz,” a plant that has long been used in oriental medicine for its abortifacient, antidiabetic, and anti-inflammatory effects. Thoennissen et al. for the first time showed that cucurbitacin B has profound antiproliferative effects against human pancreatic cancer cells in vitro and in vivo and cucurbitacin B may potentate the antiproliferative activity of nucleoside analogue gemcitabine, associated with inhibition of activated JAK2/STAT3 and decrease of expression of Bcl-XL with subsequent upregulation of caspase-3 and caspase-9.

Isothiocyanate sulforaphane (SF) is a natural compound present in broccoli and other cruciferous vegetables with high concentration. Kallifatidis et al. showed that SF increased the effectiveness of cytotoxic drugs (gemcitabine, cisplatin, 5-fluorouracil, and doxorubicin) against pancreatic cancer stem cells (CSCs) without inducing additional toxicity in mice. Combination of SF with cytotoxic drugs intensified inhibition of spheroid formation, clonogenicity, and aldehyde dehydrogenase 1 activity along with the expression of c-Rel and Notch-1, which indicated that the characteristics of CSCs were targeted. Dimethylamino parthenolide (DMAPT) is a sesquiterpene lactone extracted from the medicinal herb feverfew (Tanacetum parthenium). In association with the suppression of NF-κB, Holcomb et al. indicated that DMAPT enhanced the antiproliferative effects of gemcitabine in pancreatic cancer cells in vitro and in vivo, which supported the evaluation of NF-κB-targeted agents to complement gemcitabine-based therapies.

Dimethylaminoparthenolide (DMAPT) is a novel orally bioavailable analog of parthenolide, a sesquiterpene lactone extracted from the medicinal herb feverfew (Tanacetum parthenium). Yip-Schneider et al. showed that the combination of DMAPT and gemcitabine significantly decreased the multiplicity and incidence of pancreatic adenocarcinomas by reducing the levels of eotaxin, tumor necrosis factor-alpha (TNF-α), macrophage inflammatory protein-1 beta (MIP-1β), inflammatory cytokines IL-12p40, and monocyte chemotactic protein-1 (MCP-1), all of which are NF-κB target genes. Yip-Schneider et al. also indicated DMAPT and sulindac (nonselective COX inhibitor) in combination with gemcitabine may prevent or delay the progression of premalignant pancreatic lesions in the LSL-Kras (G12D), Pdx-1-Cre mouse model of pancreatic cancer.

The phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), is a major active ingredient extracted from the seed oil of Croton tiglium L., a leafy shrub of the Euphorbiaceae family, which is native to Southeastern Asia. Our laboratory indicated that the combination of TPA with gemcitabine synergistically inhibited growth and induced apoptosis in human pancreatic cancer PANC-1 cells cultured in vitro or PANC-1 cells grown in NCr immune-deficient nude mice. 0.16 nM TPA in combination with 0.5 μM gemcitabine induced a remarkable increase in the expression of phosphorylated c-Jun NH2-terminal kinase (JNK) in PANC-1 cells. Guggulsterone-pregnadiene-3,16-dione is a dietary plant sterone obtained from the gum resin of the Indian Ayurvedic medicinal plant, Commiphora mukul, which has been used as traditional medicine since 600 BC. It has been known to show hypolipidemic activity, cardiovascular protecting activity, anti-inflammatory activity, and the activity of antagonist to bile acid receptor (farnesoid X receptor).

Thymoquinone is a bioactive constituent isolated from the volatile oil of the black seed (Nigella sativa). Mu et al. showed thymoquinone pretreatment following gemcitabine treatment synergistically caused an increase of apoptosis and tumour growth inhibition in pancreatic cancer cells both in vitro and in vivo, through abrogation of Notch1, PI3K/Akt/mTOR regulated signaling pathways. Namba et al. indicated zidovudine, developed from spongothymidine extracted from Cryptotethya crypta, resensitized gemcitabine-resistant pancreatic cancer cells to gemcitabine by inhibiting the Akt-GSK3β-Snail pathway. Piperlongumine is a natural alkaloid/amide component extracted from the fruit of the pepper Piper longum. Wang et al. indicated that Piperlongumine enhanced the antitumour properties of gemcitabine in human pancreatic cancer cells in vitro and in vivo by modulating the NF-kappaB pathway.

Zyflamend is a polyherbal formulation comprised of ten standardized and concentrated herbal extracts (ginger, holy basil, rosemary, huzhang, oregano, turmeric, Chinese goldthread, baikal skullcap, barberry, and green tea). Kunnumakkara et al. showed Zyflamend in combination with gemcitabine synergically inhibited the growth of human pancreatic cells in vitro and in vivo by inhibiting NF-κB signaling pathways. MK615, called Ume in Japanese, is a sticky extract from Japanese apricot, which has been used to treat intestinal disorders for many years as an antipyretic and an anti-inflammatory agent. Hattori et al. indicated MK615, in both the presence and absence of gemcitabine, significantly inhibited the growth of human pancreatic cancer cells in vitro and in vivo without apparent adverse effects through a reactive oxygen species-dependent mechanism.

Moringa oleifera Lam. (Moringaceae) is a tree that grows widely in the tropics and subtropics of Asia and Africa. Leaves of Moringa oleifera consist of flavonoid pigments, such as kaempferitrin, kaempferol, isoquercitrin, and rhamnetin. Berkovich et al. indicated that Moringa oleifera leaf extract synergistically inhibited tumor growth and enhanced the cytotoxic effect of cisplatin in human pancreas cancer PANC-1 cells in vitro, by elevating the sub-G1 cell population of cell cycle and reducing the expression of p65, p-IkBα, and IkBα proteins. Reis et al. indicated that the combination of lathyranes, the chemical compound isolated from Euphorbia piscatoria, and doxorubicin synergistically enhanced the antiproliferative activity on human pancreatic cells in vitro.

Mohammad et al. showed that the combination of (−)-gossypol (a natural polyphenolic compound extracted from cotton seeds) with genistein (a prominent soy isoflavone) more significantly inhibited the growth of BxPC-3 pancreatic cancer cells, compared with either agent alone. Genistein, which inactivated NF-kB and caused transcriptional inactivation of Bcl-XL and Bcl-2, could be combined with (−)-gossypol to inactivate the function of Bcl-XL and Bcl-2 and then enhanced the death of pancreatic cancer cells.

Srivastava et al. indicated that sulforaphane, an active compound in cruciferous vegetables, synergistically inhibits self-renewal capacity of pancreatic cancer stem cells with quercetin, a major polyphenol and flavonoid commonly detected in many fruits and vegetables, by inhibiting the expression of Nanog, phosphorylation of FKHR, Bcl-2, XIAP, activating caspase-3, and proteins involved in the epithelial-mesenchymal transition (beta-catenin, twist-1, ZEB1, and vimentin).

Ding et al. showed the combination of that wogonin, a naturally occurring flavone, with the structurally related natural flavones apigenin and chrysin could enhance TRAIL-mediated apoptosis in pancreatic carcinoma CaPan-1 cells, by upregulation of TRAIL receptor 2 (TRAIL-R2) and transcriptional downregulation of c-FLIP (a key inhibitor of death receptor signaling).

Yue et al. indicated that metformin combined with aspirin synergistically inhibited tumor growth, migration, and colony formation in human pancreas cancer PANC-1 and BxPC-3 cells cultured in vitro and pancreas tumor xenografts in nude mice, by remarkably inhibiting the phosphorylation of STAT3 and mTOR, significantly downregulating the antiapoptotic proteins Bcl-2 and Mcl-1 and significantly upregulating the proapoptotic proteins Puma and Bim.

Hauns et al. indicated that Ginkgo biloba extract GBE 761 ONC combined with 5-fluorouracil (5-FU) was shown favourable effect to treat the patients with pancreatic cancer in the clinical trial phase II study, compared to the clinical trial of 5-FU monotherapy.

Curcumin, which is called diferuloyl methane, is a hydrophobic polyphenol isolated from rhizome (turmeric) of the herb Curcuma longa. Curcumin has shown various activities, such as a mediator of chemoresistance and radio-resistance, antioxidant, anti-inflammatory, and immunomodulatory activities, enhancing of the apoptotic process, cytokines release, and antiangiogenic properties.

The anticancer effect has been seen in a few clinical trials, mainly as a native chemoprevention agent in colon and pancreatic cancer, cervical neoplasia, and Barrett’s metaplasia . Although curcumin may potentiate the antitumor effect of gemcitabine by intervening with several intracellular signal transduction pathways in pancreatic cancer cells in vitro and in vivo, Epelbaum et al. showed that a combination of gemcitabine and oral curcumin at a dose of 8,000 mg/day to treat the patients with advanced pancreatic cancer is not feasible and 29 per cent patients had to stop oral curcumin due to gastrointestinal toxicity. The preliminary results suggest that a combination of curcumin and gemcitabine for the patients with advanced pancreatic cancer is feasible.

Mistletoe extracts from the medicinal herb Viscum album L. are widely used to treat cancer patients in Europe. Matthes et al. indicated that mistletoe extract (Iscador®, Weleda, Arlesheim, Switzerland) could be supportive care in an adjuvant chemotherapy setting with gemcitabine or 5-fluorouracil (5-FU) in the patients undergoing curative intent resection of pancreatic cancer. Löhr et al. reported the phase Ib study of 16 chemotherapy-native patients with inoperable pancreatic carcinoma treated with gemcitabine and AXP107-11, the sodium salt dihydrate form of genistein (genistein-SSDH, a novel multicomponent crystalline form of genistein). The results demonstrated that treatment of pancreatic cancer patients with AXP107-11 in combination with gemcitabine led to a favorable pharmacokinetics with high serum levels without toxicity.
Paricalcitol, hydroxychloroquine, intravenous vitamin C, statins, metformin, curcumin, and aspirin as adjunct therapies

A study published in the journal Cancer Management and Research have reviewed evidence-based complementary treatment of pancreatic cancer and adjunct therapies including paricalcitol, hydroxychloroquine, intravenous vitamin C, statins, metformin, curcumin, and aspirin.

According to the researchers from the Department of Allergy, Asthma and Immunology, Rutgers New Jersey Medical School, Newark, NJ, US, a variety of relatively safe and inexpensive treatment options that have shown success in preclinical models and/or retrospective studies are currently available. Patients require their physicians to provide therapeutic guidance and assistance in obtaining and administrating these various therapies.

Paricalcitol, an analog of vitamin D, has been shown by researchers at the Salk Institute for Biological Studies to break through the protective stroma surrounding tumor cells. Hydroxychloroquine has been shown to inhibit autophagy, a process by which dying cells recycle injured organelles and internal toxins to generate needed energy for survival and reproduction. Intravenous vitamin C creates a toxic accumulation of hydrogen peroxide within cancer cells, hastening their death. Metformin inhibits mitochondrial oxidative metabolism utilized by cancer stem cells. Statins inhibit not only cholesterol but also other factors in the same pathway that affect cancer cell growth, protein synthesis, and cell cycle progression. A novel formulation of curcumin may prevent resistance to chemotherapy and inhibit pancreatic cancer cell proliferation. Aspirin therapy has been shown to prevent pancreatic cancer and may be useful to prevent recurrence.

Dual thermal ablation technique may offer novel treatment approach for pancreatic cancer
Researchers at Binghamton University and CPSI Biotech have developed a novel technique that uses cryotherapy and hyperthermia therapy to attack pancreatic cancer cells.The technique, called dual thermal ablation (DTA), involves a five-minute heat exposure to cancer cells, followed by a five-minute freezing of the cells.

“Pancreatic cancer is one of the leading causes of cancer-related deaths in the world today. It is estimated that 95 per cent of patients diagnosed with pancreatic cancer will die because of limited treatment options,” John M. Baust, PhD, president and founder of CPSI Biotech, and colleagues wrote in a study published in Liver and Pancreatic Sciences. “As standard treatments have not yielded an improvement in patient outcome, alternative approaches, such as thermal ablation, may offer a new treatment path.”

The United States Food and Drug Administration (FDA) has announced a study of breakthrough device to treat aggressive pancreatic cancer
New York-based oncology and vascular technologies company AngioDynamics recently said it received FDA approval to begin a clinical study of its NanoKnife technology in Stage 3 pancreatic cancer patients under an investigational device exemption.

The NanoKnife system received a breakthrough device designation from FDA in January 2018, giving the company an expedited pathway to develop treatment for the aggressive cancer. Use of the technology, which gained 510(k) clearance in 2008 for the surgical ablation of soft tissue, has been documented in the treatment of more than 800 patients with Stage 3 pancreatic cancer from 2012 to 2019, the company said.

The NanoKnife uses low energy electrical pulses to permanently open pores in target cell membranes, resulting in cell death. The body’s natural processes then remove the treated tissue within weeks.AngioDynamics said its DIRECT clinical study of the NanoKnife would support a proposed expanded indication for the device to treat Stage 3 pancreatic cancer and facilitate reimbursement for hospitals and physicians.

The DIRECT study will have a randomized controlled trial at up to 15 sites and a real-world evidence registry at up to 30 sites. Each site will have a NanoKnife treatment arm and a control arm. The company expects to enroll about 250 patients in each arm. The primary endpoint of the study is overall survival.

Robert Martin, co-principal investigator of the DIRECT study and surgical oncologist at the University of Louisville, said evidence that has accumulated over the past 10 years has shown that the device’s irreversible electroporation technology is an effective adjunctive treatment for patients with locally advanced pancreatic cancer.


Receive News Alerts on Whatsapp: +2348136370421

No comments yet