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Noticias de la lucha contra el cáncer

Hablemos de salud, consejos médicos, buena Alimentación, la sexualidad y mucho mas.
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New class of drug could treat leukemia with fewer side effects
Michael Irving, August 25, 2022

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Researchers have identified a new class of drugs that could prove useful in fighting leukemia with less side effects than existing chemotherapy drugs

Scientists have identified two molecules that could help treat leukemia, in a way that’s far less damaging to healthy cells than existing chemotherapy. The compounds work using a different mechanism that’s more selective for cancerous cells, and importantly, they’re already in use for other purposes.

Abnormal activity in an enzyme called DNMT3A has previously been linked to acute myeloid leukemia, by promoting the formation of abnormal blood cells. Many current chemotherapy drugs work by disabling the DNMT3A enzyme – but unfortunately, they also interfere with the activity of DNMT1, a similar enzyme with vital roles in healthy cells. This causes many of the toxic side effects experienced by patients undergoing chemotherapy.

For the new study, the researchers investigated ways to home in on DNMT3A alone. The enzyme is known to form complexes with partner proteins while it gets to work, so the team scoured a chemical library of existing drugs until they found two that interfere with this partnering-up process.

Imagen
The two compounds target a non-active site on the DMT3A enzyme

The two compounds, pyrazolone and pyridazine, target a non-active site on DNMT3A, which works to prevent it from forming complexes and ultimately stops the cascading effects that can lead to leukemia. Importantly, this mechanism means it doesn’t affect DNMT1.

The team says this breakthrough could lay the foundation for a new class of drugs, which could eventually help treat leukemia and other forms of cancer with much less toxicity than existing chemotherapy drugs. However, there’s still plenty of work left to do to uncover how it works in the long-term, and how it could be made even more potent.

Thankfully there is one less roadblock in the way – because the drugs are already in use for other diseases, it should be a more straightforward process to get them approved for use against leukemia.

The research was published in the Journal of Medicinal Chemistry.

Source: UCSB

https://newatlas.com/medical/leukemia-n ... ug-cancer/
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Experimental drug combo halts growth of deadly lung cancer in mice
Michael Irving, September 05, 2022

Small cell lung cancer (SCLC) is one of the deadliest forms of the disease, but now scientists may have a promising new avenue for treatment. By combining a new drug with an outdated one, the team found that they could halt growth of tumors in mice.

Most commonly occurring in smokers, small cell lung cancer is an aggressive form of the disease with a low survival rate. While chemotherapy is effective initially, the cancer can quickly develop a resistance to the drugs, leading to recurrence and progression of the disease.

For the new study, researchers at Washington University in St. Louis, Grenoble Alpes University and the University of Texas investigated how SCLC cells resist the damage caused by chemotherapy, and how that could be countered.

In previous work, the scientists found that a protein called RNF113A was implicated in cancer cells’ ability to repair alkylation damage, which is the mode of attack for common chemotherapy drugs. On closer inspection, the team discovered that RNF113A is regulated by another protein, SMYD3, which is expressed in higher amounts in SCLC cells and other cancers. In particular, higher levels of SMYD3 are linked to more aggressive cancer and stronger drug resistance.

With this new target in their sights, the scientists examined whether blocking SMYD3 could improve the effects of chemotherapy drugs. The team grafted human SCLC cells into mice, and waited until they grew tumors in their lungs. Then, they treated some mice with a drug called cyclophosphamide, some with an SMYD3 inhibitor, some with both, and some with none.

In mice given the chemotherapy alone, the tumors stopped growing for about two weeks before starting up again, indicating drug resistance had built up. But in the mice given both cyclophosphamide and the SMYD3 inhibitor, the tumors stopped growing for the entire several-month duration of the experiment. Intriguingly, the treatment worked just as well on tumors grown from a human patient whose cancer had already developed resistance to chemotherapy drugs.

Cyclophosphamide has somewhat fallen out of favor in recent decades, thanks to its stronger side effects compared to platinum-based chemotherapy agents, but the new study might mean it's worth dusting off. The team hopes that the research could lead to new treatments for an aggressive form of cancer for which there are currently few options.

“We’re talking to a number of other groups about starting a phase 1 clinical trial as soon as possible,” said Nima Mosammaparast, co-senior author of the study. “People with small cell lung cancer are in desperate need of better treatments, and I’m very excited about the possibilities here.”

The research was published in the journal Cancer Discovery.
Source: Washington University in St. Louis

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Self-assembling molecules suffocate cancer cells within hours
Nick Lavars, September 08, 2022

https://assets.newatlas.com/dims4/defau ... 6%20pm.png
Artist's impression of a new anti-cancer drug at work, using tiny hairs to block the oxygen supply of cells

By deploying a newly-developed drug against a key energy source of cancer cells, scientists at the Max Planck Institute for Polymer Research have developed a new way of eliminating them in mere hours. The technique relies on self-assembling molecules that take on a potent form in the cellular environment, and in doing so effectively starve the cancerous cells of the oxygen they need to thrive.

The technology at the heart of this research takes aim at one of the key metabolic functions of cells in all living things called ATP, or adenosine triphosphate. This molecule is the primary energy carrier in cells, capturing chemical energy from the breakdown of food molecules and distributing it to power other cellular processes.

Among those cellular processes is the proliferation of cancerous cells, and because of this we have seen ATP implicated in previous anti-cancer breakthroughs. The authors of the new study sought to cut off the supply of ATP, which is generated as mitochondria soak up oxygen and convert it into the molecule.

The team was able to achieve this through a newly-developed drug described as a platinum(II)-containing tripeptide. When this enters the cellular environment it responds to endogenous hydrogen peroxide by banding its molecules together to form tiny hairs, thousands of times thinner than a human hair.

“These hairs are fluorescent, so you can look at them directly with a microscope as they form,” said study author Zhixuan Zhou.

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For the first time, scientists can switch cancer-fighting cells on and off
CAR-T therapy is effective — but dangerous. An on/off switch could make it safer, faster, and cheaper.
By B. David Zarley, September 27, 2022

Presenting at the CAR-TCR Summit in Boston, researchers from La Jolla’s Scripps Research described an off/on switch for CAR-T therapy, a potentially groundbreaking safety improvement for this powerful but risky therapy.

As reported by STAT, the team from Calibr, Scripps’ drug development and discovery division, announced that the majority of patients in the nine person study responded to their experimental treatment.

Most of those had a “complete response” — meaning no signs of cancer could be detected.

But perhaps even more importantly for the future of the therapy, the researchers were also able to halt the potentially lethal side effects of the body’s immune cells. Using their new switch, they were able to turn off the souped up, cancer-killing cells and stop the side effects in days, rather than weeks.

Their technique may not only make immunotherapy safer, but also allow CAR-T cells to be tweaked to whatever cancer needs hunted — meaning off-the-shelf CAR-T cells may be possible, rather than every patient needing a custom-engineered treatment.

“It’s a very smart strategy,” Yubin Zhou, a bioengineer at Texas A&M who has kept tabs on the work, told STAT. “You can reduce the cost. I think this will win the market in the long run.”

Harnessing the immune system: At its core, cancer immunotherapy means using the body’s immune system to fight cancerous tumor cells, just like it would a bacteria, virus, or parasite.

In CAR-T therapy, researchers pull out a specific type of immune system cell, called a T cell, from the patient. These recruits are then kitted out with a “chimeric antigen receptor,” or CAR, which helps the T cells spot and kill cancerous cells. Thus armed, the CAR-T cells are put back in the patient with their new marching orders: kill the cancer!

But the immune system can have a negative impact on us, as well. CAR-T and other immunotherapies run the risk of triggering a scorched-earth attack that leads to dangerous inflammation.

This can result in a “cytokine storm,” where the overactive immune system releases too much of a protein called cytokine. The results can range from flu-like symptoms to life-threatening complications. Neurotoxicity (specifically “immune effector cell-associated neurotoxicity syndrome, or ICANS) can hurt a patient’s brain.

Unfortunately, both of these complications are common. The risk is often worth it to try to stop the cancer, but it makes mitigating the side effects crucial to better treatment. Scientists are developing numerous approaches to make immunotherapy safer, including drafting different immune cells, like the awesomely-named natural killer cells.

Another option is Calibr’s off switch.

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https://www.freethink.com/health/switchable-car-t
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Descubren cómo superar un mecanismo de resistencia al tratamiento en uno de los cánceres de mama más agresivo
SINC 5/10/2022 09:44 CEST

Una investigación liderada por un equipo del Instituto Hospital del Mar de Barcelona ha determinado el papel de las células que contribuyen a la formación de los tejidos, los fibroblastos, en la capacidad de los tumores de generar resistencia al tratamiento biológico más habitual dirigido contra la proteína HER2.

El microambiente que rodea los tumores en el cáncer de mama HER2 + los protege y facilita la generación de resistencia al tratamiento más utilizado contra él, el fármaco trastuzumab, un anticuerpo monoclonal. Y en este proceso, un tipo concreto de células de este microambiente, los fibroblastos, tiene un papel determinante. Estas células tienen la capacidad de bloquear al sistema inmunitario y así el tumor queda protegido. Encontrar una vía para superarlo potencia la capacidad del tratamiento para eliminar las células tumorales.

En concreto, la presencia de fibroblastos activados por TGF-beta, que expresan una molécula llamada FAP, es lo que protege de la acción de las células inmunitarias al tumor. El trastuzumab tiene la capacidad de atacar las células cancerosas que muestran niveles altos de la proteína HER2, y cuando se une al cáncer, activa una fuerte respuesta inmunitaria, que contribuye de manera muy importante a su eficacia contra el tumor.

A pesar de ello, en muchos tumores, el sistema inmunitario no es capaz de travesar el microambiente que rodea al tumor y eliminarlo. De esta manera, se genera resistencia al tratamiento y se incrementa la capacidad de este tipo de cáncer de eludir al fármaco y volver a proliferar. Un mecanismo que han podido descubrir el equipo de investigadores del IMIM-Hospital del Mar y del CIBER del Cáncer (CIBERONC), en un estudio que ha publicado la revista Nature Communications.

El trabajo también ha identificado una vía para superar esta capacidad del tumor de protegerse y de abrir la puerta al sistema inmunitario para actuar sobre las células tumorales. Mediante un modelo ex vivo, es decir, un modelo que permite trabajar con células vivas de los pacientes con cáncer de mama, los autores del estudio han comprobado como marcando con inmunoterapia la molécula FAP que expresan los fibroblastos, se puede revertir su capacidad para evitar el acceso de las células inmunitarias.

Modelo aplicable a otro tipo de tumores
“Cuando a un tumor recreado ex vivo que contiene este microambiente resistente al tratamiento, en contacto con células inmunitarias, se le añade esta molécula, FAP-IL2v, se devuelve la efectividad al trastuzumab” ha explicado Alexandre Calon, autor principal de la investigación y responsable del Laboratorio de Investigación Traslacional en Microambiente Tumoral del IMIM-Hospital del Mar. Hay que destacar que el modelo que se ha generado utiliza células humanas y también es aplicable a otros tipos de tumores.

El estudio ha validado los resultados con tres cohortes de pacientes, con más de 120 muestras. En todas ellas se ha podido comprobar cómo los niveles de activación de los fibroblastos tienen una relación directa con la capacidad del sistema inmunitario de actuar sobre el tumor. A niveles más altos, más dificultad para acceder y eliminar las células tumorales a pesar de la acción del trastuzumab.

Calon ha destacado que esto permite seleccionar mejor a los pacientes que se beneficiarán del tratamiento con FAP-IL2v dirigido a desactivar la acción del microambiente tumoral. “Si filtramos a los pacientes basándonos en estas características, podemos aislar una población de pacientes resistentes al tratamiento que se pueden tratar con esta molécula y restablecer la efectividad del tratamiento contra el cáncer de mama”, ha apuntado.

En estos momentos ya existen fármacos que se pueden utilizar para conseguir este efecto, "a pesar de que todavía habrá que llevar a cabo más estudios para evaluar su aplicación en pacientes, como indica Joan Albanell, jefe del Servicio de Oncología del Hospital del Mar, director del Programa de Investigación en Cáncer del IMIM-Hospital del Mar y coautor del estudio.

Según Albanell, “el estudio identifica los tumores en los cuales la resistencia a la terapia anti-HER2 es causada principalmente por un tipo de fibroblastos y no por otras causas. Este importante descubrimiento tendría que servir para diseñar ensayos clínicos con medicamentos que superen esta resistencia solo para aquellos pacientes en que esta resistencia está operativa. Es hacia donde tenemos que ir en la oncología de precisión”.

El trabajo ha contado con la colaboración de investigadores del Instituto de Investigación Biomédica de Barcelona (IRB) y del Instituto de Bioengeniería de Cataluña (IBEC), así como del Instituto de Investigación Sanitaria INCLIVA de Valencia y con el apoyo de la Fundación Privada Cellex, del Instituto de Salud Carlos III y la Asociación Española contra el Cáncer.

Referencia:
Rivas, E.I., Linares, J., et al. “Targeted immunotherapy against distinct cancer-associated fibroblasts overcomes treatment resistance in refractory HER2+ breast tumors”. Nat Commun (2022).
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A modified herpes virus completely wiped out a terminal cancer
The dramatic result was part of a small study testing modified viruses against difficult cancers.

B. David Zarley, October 7, 2022

A patient in a trial testing a herpesvirus-based cancer treatment saw his cancer completely disappear, and has remained cancer free in the 15 months since his treatment began, the Institute of Cancer Research (ICR) in London announced.

The outcome for West London builder Krzysztof Wojkowski was the most dramatic result seen in the small phase 1 trial of the experimental cancer therapy, called RP2. Thirty-nine patients who had exhausted all other treatment options received the treatment. Nine received the virus therapy on its own, while 30 got it in combination with immunotherapy.

“I was told there was no options left for me and I was receiving end-of-life care,” Wojkowski said in the statement. “It was devastating, so it was incredible to be given the chance to join the trial.”

Although it’s early doors, the results, which were presented at the 2022 European Society for Medical Oncology Congress in Paris, offers more evidence that cancer-killing viruses may be up to the job of snuffing out cancer where other methods have failed, and “can provide potent systemic anti-tumor effects,” the authors wrote in their poster.

The virus: RP2 isn’t just any old herpesvirus: it’s a genetically modified version of herpes simplex virus (HSV-1), the culprit behind cold sores (and an incredibly common pathogen, present in over 50% of adults in the US).

Herpesviruses, which also include the viruses behind chickenpox and genital herpes, have evolved a number of remarkable abilities, including the trick of infecting and hiding in nerve cells, from which they periodically sally forth to cause flare ups of sores or rashes, like shingles.

They also prefer to infect cancer cells. The HSV-1 in the UK trial was further modified to specifically target tumor cells, and made “oncolytic” — meaning they infect, and kill, cancer cells.

Injected directly into tumors, the virus hijacks the tumor cells, replicates, and explodes them from within — while also blocking the production of a protein called CTLA-4, which the tumor uses to hold back your immune system.

With the virus running interference, the immune system can then do what it does best: killing rogue cells.

This isn’t the first time we’ve drafted a modified herpesvirus to fight cancer — modified versions of HSV-1 have previously shown success against melanoma and brain cancer.

In fact, IRC researchers previously developed T-Vec, a virus approved by the NHS for treating skin cancer. Lead researcher Kevin Harrington told the BBC that RP2 is like T-Vec with even more teeth.

“It’s had other modifications to the virus so that when it gets into cancer cells it effectively signs their death warrant,” Harrintgon said.

The trial: The ongoing phase 1 trial, run with the The Royal Marsden NHS Foundation Trust and sponsored by RP2’s manufacturer Replimune, was designed to test the safety and best dosage for the drug, as well as its ability to shrink several different kinds of tumors.

It has enrolled thirty-nine patients whose cancers have not responded to other treatments.

Of the nine patients who only received RP2, three saw results. Two of them, one with oesophageal cancer and the other with a rare eye cancer called uveal melanoma that had spread to the liver, had their tumors shrink, with the cancer’s progression still halted 15 and 18 months, respectively, after treatment.

The other patient, West London builder Wojkowski, had his salivary gland cancer completely wiped out.

Of the 30 patients who received RP2 along with an immunotherapy called nivolumab, seven of them responded to the combined drugs. Melanoma, uveal melanoma, and head and neck cancer patients all had their cancer’s growth stop or shrink. After 14 months, there had still been no progression in six of the seven cancers.

When patient’s tumors were biopsied before and after injection, they found evidence that herpes was working to activate the immune system, with more immune cells present around the tumor. The drug caused mild side effects, including fever, chills, and fatigue.

Although a small and still ongoing trial, these early results are promising, Jonathan Zager of Tampa’s Moffitt Cancer Center told Insider.

“We’ll see some more studies done in the very near future, and I’m excited — certainly not disheartened or skeptical,” Zager said.

Next steps: “Our study shows that a genetically engineered, cancer-killing virus can deliver a one-two punch against tumours – directly destroying cancer cells from within while also calling in the immune system against them,” Harrington said in a statement.

The next step is to continue testing RP2 in more patients, to see if its efficacy holds up, especially against cancers that resist current treatments.

“Viruses are one of humanity’s oldest enemies, as we have all seen over the pandemic,” Kristian Helin, the chief executive of IRC, said.

“But our new research suggests we can exploit some of the features that make them challenging adversaries to infect and kill cancer cells.”

https://www.freethink.com/health/herpes-vs-cancer
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Homing missile molecule eradicates even advanced cancers in mice
Michael Irving, October 19, 2022

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A new cancer treatment pairs an acidity-seeking molecule with an immunotherapy drug Depositphotos

Researchers at Yale and the University of Rhode Island (URI) have demonstrated a new technique to fight cancer by attaching immunotherapy drugs to a molecule that seeks out the acidic environment of cancer cells. In tests in mice, a single dose was enough to eradicate even advanced tumors.

Our greatest weapon against cancer – and indeed all disease – is our immune system, but even it needs a helping hand sometimes. Immunotherapy provides that helping hand, with one method being what are called immune checkpoint inhibitors. These drugs effectively take the natural brakes off the immune response, allowing it to battle against cancer for longer.

As promising as these drugs seem so far, they don’t work on “cold” tumors that have little immune activity to start with. So another type of drug known as STING agonists are designed to fire up these cold tumors into hot ones that are more receptive to immunotherapy. But these also have their drawbacks – namely, it’s hard to target them to cancer cells.

And that’s where the new study comes in. The researchers from Yale and URI used a molecule called pH-low insertion peptide (pHLIP) to guide the drug to where it needs to go. pHLIP is drawn to acidic environments, conveniently like the kind that cancer makes around itself.

“When pHLIP encounters a cell membrane with a neutral pH, it will sit on the surface briefly and then pull away,” said Donald Engelman, co-author of the study. “But if it’s in an acidic environment, then the peptide folds into a helix, crosses the cell membrane and stays there.”

Imagen
An untreated tumor (top left) is highly acidic, as seen with its fluorescence profile (top right). Within days of the new treatment however, the tumor (bottom right) starts to shrink and its acidity goes down (bottom right)University of Rhode Island

The team coupled pHLIP to STING agonists, so that the former carries the latter to cancer cells and helps them inside to get to work. And tests in mice proved promising – the researchers administered pHLIP-STING to 20 mice with small colorectal tumors and found that after a single injection, the tumors disappeared entirely in 18 mice within a few days. In another group with larger tumors, seven out of 10 mice saw their tumors disappear completely.

By comparison, another group of 10 mice received just STING without the guidance of pHLIP. Tumor growth slowed slightly in all 10, but tumors remained.

The treatment even seemed to have a long-lasting effect. The team injected new cancer cells into treated mice that had been tumor-free for 60 days – and no new tumors developed, indicating an immune memory had formed.

While the technique sounds promising, the usual caveats apply – the results of animal tests don’t always carry across to humans. Far more work needs to be done before any potential treatment based on pHLIP-STING could find use.

The research was published in the journal Frontiers of Oncology.
Source: URI

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Experimental breast cancer vaccine passes first human trials
Rich Haridy, November 06, 2022

A therapeutic vaccine being trialed is designed to help the immune system better target breast cancer by homing in on a certain protein over-expressed by tumors

A new paper in the journal JAMA Oncology has reported the results of a decade-long Phase 1 human trial testing an experimental breast cancer vaccine. The novel treatment was found to be "very safe" and a larger Phase 2 trial is now underway testing efficacy.

Up to 30% of breast cancers involve the overproduction of a protein called human epidermal growth factor receptor 2 (HER2). These HER2-positive cancers are often more aggressive than other types of breast cancer, growing faster and being more likely to reoccur.

For the last couple of decades one of the more effective clinical treatments for this type of breast cancer has been a monoclonal antibody therapy designed to block the activity of HER2 on tumor cells. However, researchers have long been working on vaccines that can train the immune system to target these HER2-positive tumor cells.

These kinds of cancer vaccines are not designed to be preventative vaccines that stop cancers from appearing in the first place. Instead, these are known as therapeutic vaccines, given to patients after they are diagnosed with a cancer in the hopes they help the immune system better seek and destroy certain tumors.

In this instance researchers are working with what is called a DNA vaccine. These vaccines deliver DNA blueprints for the production of certain proteins into the nucleus of a cell. That protein is then produced by the cell, triggering an immune response. The vaccine being tested prompts cells to produce a specific fragment of the HER2 protein.

This Phase 1 trial began 20 years ago, slowly enrolling 66 patients with advanced HER2-positive breast cancer. Three different dose levels were tested, with the primary goal of the trial to evaluate the long-term safety of the vaccine. Because HER2 proteins can be found on other cell types in the body, the researchers planned a 10-year follow-up for each participant to make sure there were no lingering problems of immune activity against healthy tissue.

“The results showed that the vaccine was very safe,” said lead author on the new study Mary Disis. “In fact, the most common side effects that we saw in about half the patients were very similar to what you see with COVID vaccines: redness and swelling at the injection site and maybe some fever, chills and flu-like symptoms.”

The trial was not geared to evaluate how effective the experimental vaccine is at treating breast cancer. But Disis did point out promising early signs of efficacy, with 80% of the treated trial participants surviving the full 10-year follow-up. Disis said only around 50% of patients with advanced HER2 breast cancer would generally be expected to survive more than five years, so it's likely the vaccine is working.

A Phase 2 trial is currently underway, testing the vaccine's efficacy in a larger cohort of HER2-positive patients. That trial kicked off a few years ago and only has a two-year follow-up period. So preliminary results could start coming within the next couple of years.

“If the results of the new randomized-controlled Phase 2 trial of the vaccine are positive, it will be a strong signal for us to rapidly move forward to a definitive phase III trial,” Disis added. “I have high hopes that we’re close to having a vaccine that can effectively treat patients with breast cancer.”

The new study was published in JAMA Oncology.

Source: UW Medicine

https://newatlas.com/health-wellbeing/h ... an-trials/
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Diseñado por una científica checa, un revolucionario fármaco contra el cáncer de próstata es aprobado por la Comisión Europea
Radio Praga, 13/01/2023

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Diseñado por una científica checa, un revolucionario fármaco contra el cáncer de próstata es aprobado por la Comisión Europea

La Comisión Europea aprobó un nuevo medicamento contra el cáncer de próstata codesarrollado por una química checa. El revolucionario tratamiento se administra en Chequia como parte de un ensayo clínico en el Hospital Universitario de Olomouc.

Luego de cosechar exitosos resultados, un revolucionario fármaco contra el cáncer de próstata acaba de ser aprobado por la Comisión Europea. El medicamento fue desarrollado por la química checa Martina Benešová en el Centro Alemán de Investigación Oncológica de Heidelberg.

Según explicó la científica en su momento durante una entrevista con Radio Praga Internacional, este nuevo método se diferencia sustancialmente de los ya existentes.

“El fármaco es definido como lo que se conoce como teranóstico, lo que significa que se puede usar tanto para el diagnóstico como para el tratamiento. También es nuevo en la forma en que funciona para los pacientes que ya recibieron todas las terapias disponibles para el cáncer de próstata y, a pesar de que eran resistentes a todas estas terapias aprobadas, aceptadas y en uso, la aplicación de la endorradioterapia con PSMA- 617 funciona en estos pacientes que prácticamente no tienen otras opciones de tratamiento”.

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This device can easily, cheaply detect cancer cells in a blood sample
Bronwyn Thompson, February 27, 2023

Imagen
The Static Droplet Microfluidic device Majid Warkiani

It’s one of the most exciting areas of cancer research, but identifying the tumors through blood tests remains difficult, particularly for early-stage detection.

Despite breakthrough blood-test research for many types of cancers and specific sources such as lung and breast cancers, and the flourishing field of development of multi-cancer early detection (MCED) tests, screening generally still involves invasive biopsies of cells.

Researchers at the University of Technology (UTS) in Sydney, Australia, are hoping to change that, with the development of their new biotech, the Static Droplet Microfluidic (SDM) device. It can quickly detect circulating tumor cells (CTC) that have split from the cancer source to enter the bloodstream. It paves the way for very early detection, monitoring and treatment.

“A single tumor cell can exist among billions of blood cells in just one milliliter of blood, making it very difficult to find," said Majid Warkiana, professor from the UTS School of Biomedical Engineering. "The new detection technology has 38,400 chambers capable of isolating and classifying the number of metabolically active tumor cells."

The SDM can pick out tumor cells through a unique metabolic signature involving waste product lactate.

“In the 1920s, Otto Warburg discovered that cancer cells consume a lot of glucose and so produce more lactate,” said Warkiani. “Our device monitors single cells for increased lactate using pH-sensitive fluorescent dyes that detect acidification around cells.”

Once the SDM has sounded the alarm on the problem cells, they can undergo further genetic and molecular analysis to determine the source and inform treatment.

CTCs are the precursors of metastasis, in which the cancer migrates to other organs and is the responsible for 90% of the roughly 600,000 deaths from the disease each year in the US, according to the Centers for Disease Control and Prevention. The ability of the device to detect a very small number of CTCs could lead to lifesaving intervention.

The device is also designed to be operated by medical staff, meaning easy and inexpensive integration into clinics and a much less involved, invasive and risky experience for the patient.

“Managing cancer through the assessment of tumor cells in blood samples is far less invasive than taking tissue biopsies," said Warkiani. "It allows doctors to do repeat tests and monitor a patient’s response to treatment."

The development team is so confident in the SDM that it’s filed for a provisional patent and plans on a commercial release of the device.

The study was published in the journal Biosensors and Bioelectronics (NB! Para suscriptores).

Source: University of Technology Sydney

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Experimental vaccine reprograms cancer to launch immunotherapy attack
Michael Irving, March 05, 2023

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Cancer cells can be converted into cells that help the immune system launch an attack on the disease, according to a new study Depositphotos

Scientists have developed a new type of cancer vaccine that shows promise in clearing out leukemia in mice. The technique involves reprogramming cancer cells into immune cells so that they can teach the immune system how to fight off the disease.

In a fair fight, our immune system would defeat cancer every time. But this dastardly disease doesn’t fight fair, instead using a range of underhanded tricks to evade detection. Immunotherapy is an emerging treatment that involves supercharging the immune system to better fight off cancer, with some very promising early results.

One of the most common forms of immunotherapy works by removing T cells from a patient, programming them to recognize specific cancer antigens, and setting them loose in the body to hunt down cancers with those antigens. The problem is, this requires a degree of guesswork in figuring out which antigens would be most useful for each patient.

So for the new study, scientists at Stanford Medicine developed a way to teach T cells to recognize a broader swathe of antigens, increasing the chances that a patient’s immune system would successfully attack their cancer. The trick is to convert cancer cells into macrophages, which are a type of antigen-presenting cell (APC) that teaches T cells what to look for.

“We hypothesized that maybe cancer cells reprogrammed into macrophage cells could stimulate T cells because those APCs carry all the antigens of the cancer cells they came from,” said Ravi Majeti, senior author of the study.

To test the idea, the researchers induced leukemia cells in mice to transform into APCs. And sure enough, the mice in the control group successfully cleared out their cancer. Better yet, the vaccine strategy seemed to work longer term to prevent the disease recurring.

“When we first saw the data showing clearance of the leukemia in the mice with working immune systems, we were blown away,” said Majeti. “We couldn’t believe it worked as well as it did. What’s more, we showed that the immune system remembered what these cells taught them. When we reintroduced cancer to these mice over 100 days after the initial tumor inoculation, they still had a strong immunological response that protected them.”

Next, the team tested the technique on mice with three different types of solid tumors – fibrosarcoma, breast cancer and bone cancer. The results weren’t quite as effective as in leukemia, but still showed positive effects.

And finally, the researchers experimented with cells taken from human patients. Sure enough, APCs derived from human leukemia cells seemed to be successful in teaching T cells from the same patient what to look for. That suggests that the method could eventually be applied to humans, but far more work still needs to be done.

“We showed that reprogrammed tumor cells could lead to a durable and systemic attack on the cancer in mice and a similar response with human patient immune cells,” said Majeti. “In the future we might be able to take out tumor cells, transform them into APCs and give them back to patients as a therapeutic cancer vaccine. Ultimately, we might be able to inject RNA into patients and transform enough cells to activate the immune system against cancer without having to take cells out first. That’s science fiction at this point, but that’s the direction we are interested in going.”

The research was published in the journal Cancer Discovery. (NB! Por subscripción)
Source: Stanford Medicine

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New drug could extend lives of people with deadly bone cancer
Mice treated with the med lived 50% longer.
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an x-ray of a human pelvis Credit: Stockdevil / Adobe Stock

Kristin Houser, Free Think, March 11, 2023

One in three people with primary bone cancer will die within five years of diagnosis — but a new drug has the potential to help patients live longer without subjecting them to painful or unpleasant treatments.

The challenge: Cancer that starts in the bones is rare, with fewer than 4,000 new diagnoses every year in the US. However, 25% of those cases are people under the age of 20, and because bone cancer spreads rapidly, treatments are often drastic.

“Currently children have to undergo very toxic treatment, which has very unpleasant and sometimes life-long side effects, and sometimes life-changing amputation,” said co-author Alison Gartland from the University of Sheffield.

What’s new? Now, Garland and colleagues from the University of East Anglia (UEA) are developing a new bone cancer treatment that they hope will not only be more effective, but also more tolerable for patients.

For their latest study, the team used sequencing technology to analyze bone and tumor samples donated by 19 patients. This led to the discovery that a gene called RUNX2 is activated in bone cancer.

According to the researchers, the protein this gene expresses is not usually required by normal cells, but it does help bone cancer spread, so they developed a drug, called “CADD522,” that blocks its effect.

“We want to save lives and reduce the amount of disability caused by surgery.”

In preclinical trials of mice implanted with human bone cancer, CADD522 increased metastasis-free survival rates by 50%. That means treated animals lived 50% longer than untreated animals before they had to be put down due to effects of their cancer spreading.

“The new drug that we have developed is effective in all of the main bone cancer subtypes and, so far, our experiments show that it is not toxic to the rest of the body,” lead researcher Darrell Green from the UEA told BBC News.

“This means that it would be a much kinder treatment for children with bone cancer, compared to the grueling chemotherapy and life-changing limb amputation that patients receive today,” he continued.



Looking ahead: The drug is now undergoing more testing so that the researchers will have the data needed to seek approval for a clinical trial.

Many treatments that work in mice don’t translate to people, but Green — who lost a childhood friend to bone cancer — is optimistic about this one.

“Ultimately, we want to save lives and reduce the amount of disability caused by surgery,” he said, “and now we have developed a new drug that potentially promises to do just that.”

https://www.freethink.com/health/bone-cancer
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Dual-action hydrogel prevents brain cancer returning in 100% of test mice
Michael Irving, April 25, 2023

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An injectable hydrogel, loaded with chemotherapy and immunotherapy drugs, could help prevent deadly brain cancer from returning after being surgically removed Depositphotos

Scientists at Johns Hopkins University have developed a treatment that could provide new hope for aggressive brain cancers. Injecting a drug-laden hydrogel into the brain after tumors have been surgically removed was found to launch a combined chemo- and immunotherapy attack that prevented the cancer from returning in 100% of treated mice.

Glioblastoma is one of the most common and, unfortunately, deadly brain cancers in humans. Surgery to remove it is usually the best treatment option, but frustratingly the cancer tends to return with a vengeance in most cases, leading to very low survival rates.

But the new study may offer renewed hope. The Johns Hopkins team developed a hydrogel that can be applied to the cavity in the brain left behind after the tumor is removed, slowly releasing medication over a few weeks to kill any cancer cells left behind and prevent their resurgence.

The hydrogel is made up of nano-filaments containing an FDA-approved chemotherapy drug called paclitaxel, as well as an antibody called aCD47 that helps the immune system better recognize the disease and fight back.

“This hydrogel combines both chemotherapy and immunotherapy intracranially,” said Betty Tyler, co-author of the study. “The gel is implanted at the time of tumor resection, which makes it work really well.”

The team tested the technique in five groups of mice, each containing eight individuals. A control group had their tumors removed but no hydrogel implanted afterwards, and unsurprisingly 100% of them had died within about five weeks. A second group, which received hydrogel with no drugs in it, lasted about the same time.

The third group received hydrogel loaded with paclitaxel but no antibodies, which saw a 50% survival rate. A group that received hydrogel with antibodies but no paclitaxel, meanwhile, saw a survival rate of just 25%. The fifth and final group received hydrogel with both paclitaxel and the aCD47 antibodies, and they had an astonishing 100% survival rate.

“We don't usually see 100% survival in mouse models of this disease," said Tyler. “Thinking that there is potential for this new hydrogel combination to change that survival curve for glioblastoma patients is very exciting.”

Even more encouraging results followed when the scientists later injected the mice with new glioblastoma cells, and found that the animals’ immune systems were still able to fight off the cancer, indicating a kind of vaccine effect at play.

Of course, as promising as these results look there’s still plenty of work to do before this treatment could find its way to humans. It does, however, add to a growing body of work that finds that hydrogels that slowly release drugs could be an important new therapy for various cancers.

The research was published in the journal Proceedings of the National Academy of Sciences (NB! Por subscripción).

Source: Johns Hopkins University

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Nano-robotic scalpel swarm shreds brain cancer cells from the inside
Michael Franco, April 27, 2023

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The new technique allows a very precise level of surgery that doesn't damage surrounding tissue / Created by The Hospital for Sick Children (SickKids) research team using Midjourney

When it comes to fighting the deadly brain cancer known as glioblastoma, options are very much limited. This led a Canadian research team to take a novel approach. They tricked cancer cells into taking up carbon nanotubes, and they then shredded those cells by spinning the tubes using magnetic force. The treatment in mice shrunk tumor size and extended the rodents' lives, a finding that has the researchers hopeful for a similar result in humans.

Glioblastoma tumors grow quickly, invade local brain tissue, and develop resistance to chemotherapy and radiation treatments, making them very difficult to fight. Also, any left-behind cancer cells tend to return with a vengeance, although efforts are underway to keep that from happening.

Building on previous work, researchers at the University of Toronto Robotics Institute and The Hospital for Sick Children (SickKids), filled carbon nanotubes with iron oxide particles to make them magnetic. Then they coated them with an antibody that allowed the tubes to bind with a protein on the outside of glioblastoma cells. After binding, the tubes were ingested by the cancer cells.

Next, by activating a magnetic field near the cancer cells, the tubes were made to spin, wreaking havoc to the internal structure of the cells – particularly to their mitochondria, which fundamentally provides cellular energy. In effect, the tubes acted like thousands of mini scalpels that sliced up the cancer cells from the inside.

In tests using mice, the researchers saw significant reductions in tumor size. They also were able to extend the rodents' median life spans from roughly 22 days to about 27 days.

"Through the use of nanotechnology deep inside cancer cells, mechanical nanosurgery is a 'Trojan Horse' approach that could allow us to destroy tumor cells from within," said study co-author Xi Huang, a Senior Scientist in the Developmental & Stem Cell Biology program at SickKids.

The process now needs more fine-tuning before it can be tested out on humans, but any new development in the field of glioblastoma treatment, such causing the cancerous cells to self-destruct based on diet, is a welcome one for anyone who's ever been touched by the disease.

While developed specifically to help fight glioblastoma, Huang also says that the new nano-bot technique could also be adjusted to work on other types of tumors. "Theoretically, by changing the antibody coating and redirecting nanotubes to the desired tumor site, we could potentially have a means to precisely destroy tumor cells in other cancers," he said.

The work has been published in the journal, Science Advances. You can learn more about it in the following video.


Mechanical Nanosurgery explained

Sources: SickKids, University of Toronto

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Giving exhausted T cells a second wind boosts cancer treatment
Paul McClure, May 04, 2023

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Researchers have discovered a novel way of reviving T cells that become exhausted from fighting cancer / Depositphotos

Constantly fighting cancer or other diseases can exhaust our immune system’s T cells, impeding their ability to kill invaders. A new study has identified a way of reviving exhausted T cells so they’re ready to fight again, improving the effectiveness of cancer immunotherapy.

A type of white blood cell, T cells play an important role in protecting the body from foreign invaders such as cancer. But they can only fight for so long before they become exhausted. When this happens, T cells don’t produce as many immune-response-stimulating proteins and are less effective at killing cancer tumor cells.

Immunotherapy is the umbrella term for a range of biologically based cancer treatments that uses T cells to fight cancer by boosting the immune system’s ability to stop or slow cancer cell growth or help it recognize and destroy cancer cells. For immunotherapy to be effective requires T cells to be in peak – non-exhausted – condition.

Researchers at Sanford Burnham Prebys in California studied T cell exhaustion in the setting of melanoma and discovered that a protein called P-selectin glycoprotein ligand-1 (PSGL-1), found on the surface of T cells, is key to T cell exhaustion.

“Slowing or reversing T cell exhaustion is a huge focus in cancer research, and many researchers are working on different ways to accomplish this,” said Jennifer Hope, lead author of the study. “This new approach could be a viable treatment on its own, but it also has tremendous potential to work synergistically with existing therapies.”

The approach is unique because it tackles the problem of T cell exhaustion from multiple angles.

After studying mice with a genetic deficiency in PSGL-1, the researchers found that the protein causes T cell exhaustion and that T cell exhaustion was slowed by an antibody that blocked PSGL-1 activity in mice with immunotherapy-resistant melanoma. They also noticed that exhausted T cells regained their function.

“One of the things that makes this approach unique compared to existing immunotherapies is that it directly alters the way T cells become exhausted and helps them regain their function,” Hope said.

After seeing success using their antibody-based approach on mice with melanoma, the researchers tested it on mice with mesothelioma, an aggressive and deadly form of cancer that usually affects the lung tissues and is linked to asbestos exposure. They found that their approach worked with that type of cancer, too.

The next step for the researchers is to adapt their approach so that it’s suitable for use in humans with the potential that it can be used to treat a wide range of treatment-resistant cancers.

“Once we’ve done all the necessary science, this could be really valuable, or even lifesaving, for a lot of people with cancers that are resistant to current treatments,” said Linda Bradley, corresponding author of the study. “We still have a long way to go, but I’m optimistic that we’re onto something game-changing here.”

The study was published in the journal Cell Reports.
Source: Sanford Burnham Prebys

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Completely new mechanism behind some cancers discovered
Michael Irving, May 09, 2023

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Scientists have discovered a new cause of cancer – a mutation in a specific gene that interferes with a cellular cleanup process / Depositphotos

Cancer can be the end result of a wide range of things that go wrong, and understanding how is key to prevention and treatment. Now, scientists have discovered a cancer-causing mechanism that has never been seen before – a kind of clog in a cellular garbage disposal system.

The breakthrough began when Harvard Medical School researcher Megan Insco identified a tumor-suppressing gene called CDK13 while studying zebrafish. Mutations in this gene were found to speed up the development of melanoma. When checked against human melanoma, CDK13 was found to be mutated in many cases.

On closer inspection into CDK13’s function, Insco found that the protein is involved in a cellular cleanup system. It regulates a series of other proteins that ensures defective RNAs made in the cell are removed in a timely manner, but mutations interfere with that vital cleanup.

“There are hundreds of steps in making RNAs, and sometimes it doesn’t go right,” said Insco. “They’re mistakes that are usually discarded. In this case, we found that the cell was not cleaning them up. The vacuum cleaner was broken, so the RNAs were building up.”

Sure enough, when Insco tested the effect of these leftover RNA molecules on melanoma, she found that they drastically accelerated the progression of the cancer. The team checked a series of human cancers for mutations in CDK13 or the proteins it regulates, and found that 21% of the melanoma tumors they checked had such mutations. Similar mutations were also found in cancers of the lung, uterus, colon, and non-melanoma skin cancers.

Identifying the problem is an important step, but it’s just the first. Now begins the research into how to target this mechanism to uncover new potential treatments. The team’s next step is to investigate whether the cancer-promotion is caused by the damaged RNA molecules themselves or if they’re producing abnormal proteins.

The research was published in the journal Science (NB! Por subscripción).
Source: Harvard Medical School

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AI tool can predict pancreatic cancer up to three years in advance, says study
Anugraha Sundaravelu, Tuesday 9 May 2023 3:53 pm

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The research team trained the AI algorithm on two data sets of nine million patient records from Denmark and the United States (Picture: Getty Images/Science Photo Libra)

Researchers have created an AI tool that can identify individuals at high risk for pancreatic cancer up to three years before a diagnosis.

According to the research published in the journal Nature Medicine, the diagnosis is based solely on the patient's medical records.

Pancreatic cancer is one of the most lethal forms of cancer, and this discovery offers hope of earlier diagnosis, and therefore, better chances of survival.

Currently, pancreatic cancer is difficult to diagnose early on, leading to a low survival rate, and a need for better screening tools.

Without any population-based tools to screen for pancreatic cancer, only individuals with a family history of the disease or certain genetic mutations are screened. This approach leaves out cases that fall outside these categories.

Chris Sander, faculty member in the Department of Systems Biology at Harvard Medical School and co-senior investigator of the study, noted that determining who is at high risk for a disease is one of the most important decisions clinicians face.

Sander stated that an AI tool that can identify those at high risk of pancreatic cancer and would benefit most from further tests, could improve clinical decision-making, leading to earlier diagnosis, treatment, and better outcomes.

The research team trained the AI algorithm on two data sets of nine million patient records from Denmark and the United States.

The model used disease codes and the timing of their occurrence to predict which patients were likely to develop pancreatic cancer in the future. Notably, many of the symptoms and disease codes were not directly related to or stemming from the pancreas.

The AI model was tested on different versions for its ability to detect people at elevated risk of disease development within different timescales, ranging from six months to three years.

Scientinst on microscope
Currently, pancreatic cancer is difficult to diagnose early on, leading to a low survival rate, and a need for better screening tools (Picture: Unsplash)
The researchers found that each version of the AI algorithm was substantially more accurate at predicting who would develop pancreatic cancer than current population-wide estimates of disease incidence.

They found the model to be at least as accurate as current genetic sequencing tests available for only a small subset of patients in data sets.

One significant advantage of the AI tool is that it can be used on all patients with available health records and medical history, not just those with a known family history or genetic predisposition for the disease.

This is particularly important because many patients at high risk may not be aware of their genetic predisposition or family history. Without clear indications that someone is at high risk of pancreatic cancer, clinicians may be cautious to recommend expensive testing.

An AI tool that identifies those at high risk of pancreatic cancer would ensure that clinicians test the right population, while sparing others unnecessary testing and additional procedures, the researchers said.

Pancreatic cancer has a low survival rate, and early diagnosis is essential for better outcomes.

Only 12% of pancreatic cancer cases are diagnosed early, which has led to a call for better screening tools. The AI tool developed by the researchers offers hope for earlier diagnosis and treatment, as well as improved survival rates.

According to Sander, there is a clear need for better screening, more targeted testing, and earlier diagnosis, and this is where the AI-based approach comes in.

https://metro.co.uk/2023/05/09/ai-tool- ... -18754460/
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