Nano-based cancer therapies may be less effective in younger patients, finds study

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Researchers at The University of Texas MD Anderson cancer Center have discovered that certain nano-based cancer therapies may be less effective in younger patients, highlighting the need for further investigation into the impact of aging on the body’s ability to respond to treatment.

oncology.pencis.com/” target=”_blank”>The researchers found age-related differences are due to how effectively the liver filters the bloodstream. Younger livers are more efficient at this process, which helps limit toxins in the Blood but also filters out beneficial treatments, potentially rendering them ineffective.

oncology.pencis.com/” target=”_blank”>The study, published today in Nature Nanotechnology, was led by Wen Jiang, M.D., Ph.D., associate professor of Radiation oncology, and Betty Kim, M.D., Ph.D., professor of Neurosurgery.

oncology.pencis.com/” target=”_blank”>Put simply, our liver is designed to protect us, but for young people it might also be protecting them in a way that limits the effectiveness of nanotherapies. There’s so much interest right now in nano-scale delivery systems and designs, but nobody has really considered how age plays a role in the effectiveness of these systems. In preclinical models, younger livers actually work so well that they filter out a significant amount of the nanomedicine. That means, in some cases, these drugs may be less effective in younger patients than in older ones.”

oncology.pencis.com/” target=”_blank”>Wen Jiang, M.D., Ph.D., Associate Professor of Radiation oncology, Professor of Neurosurgery, University of Texas M. D. Anderson cancer Center

oncology.pencis.com/” target=”_blank”>Unlike traditional cancer therapies, in which medicine is directly introduced to the body, nanomedicines use nano-scale carriers to deliver treatments. Some of the advantages of nanomedicine formulations can include reduced toxicity, increased target specificity and increased dosage, depending on the goal of the treatment.

oncology.pencis.com/” target=”_blank”>To date, more than 50 nano-based therapies have been approved by the Food and Drug Administration, including 19 currently listed by the National cancer Institute for use in cancer. The study treatment was Nanoparticle-albumin-bound paclitaxel, which has been used since 2005 for certain refractory or relapsed cancers.

oncology.pencis.com/” target=”_blank”>Scientists do not fully understand all the mechanisms for how, exactly, the liver filters the bloodstream, but previous studies have indicated a correlation between the rate of clearance and the expression of the scavenger receptor MARCO. This protein is expressed more in younger Kupfer cells, the immune cells that reside in the liver.

oncology.pencis.com/” target=”_blank”>After confirming the disparity in results between young and old models, the team investigated therapeutic blockade of MARCO as a possible strategy to avoid drug clearance. Blocking MARCO reduced the uptake of the nanomedicine and improved the drug’s antitumor effects from the cancer therapeutics, but only in the younger models.

oncology.pencis.com/” target=”_blank”>”This is just one example, but these results show that there may not always be a one-size-fits-all Conference-terms-conditions/”>Drug Delivery strategy that is effective across diverse patient populations, and that personalized design is warranted in future nanomedicines,” Jiang said. “Hopefully, this study also opens the door for more thorough investigation of the clearance process and how to overcome it.”

oncology.pencis.com/” target=”_blank”>Jiang emphasized that while this study focuses on cancer, it examines a potential hurdle for any nanodrug delivery system. There are different proteins, antibodies and viruses with unique clearance mechanisms, but it all comes down to the liver, he explained.

oncology.pencis.com/” target=”_blank”>Source:

oncology.pencis.com/” target=”_blank”>University of Texas M. D. Anderson cancer Center

oncology.pencis.com/” target=”_blank”>Journal reference:

oncology.pencis.com/” target=”_blank”>Wang, Y., et al. (2023) Age-associated disparity in phagocytic clearance affects the efficacy of cancer nanotherapeutics. Nature Nanotechnologydoi.org/10.1038/s41565-023-01502-3.

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DPP4 inhibitors for target therapy resistance in renal cell carcinoma

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Credit: CC0 Public Domain

A new editorial paper titled “Potential repurposing of DPP4 inhibitors for target therapy resistance in renal cell carcinoma” has been published in Oncotarget.

In their new editorial, researchers Kuniko Horie and Satoshi Inoue from Saitama Medical University and Tokyo Metropolitan Institute for Geriatrics and Gerontology discuss renal cell carcinoma (RCC)—a major adult kidney cancer, which is often incidentally discovered as an asymptomatic disease on imaging in the developed countries.

RCC has the most fatal disease among urological cancers, as a recent 5-year relative survival rate in the U.S. (2009–2015) is less than 80%. While RCC is known as a cancer resistant to chemo- and radiotherapies, the prognosis of RCC has been remarkably improved after the clinical application of tyrosine kinase inhibitors (TKIs) and immunotherapy.

The rationale for the efficacy of TKIs in RCC is mainly based on the angiogenetic status, particularly in clear cell RCC (ccRCC) that is the most common type of RCC (70–75% of RCC), in which the loss of function mutation of Von Hippel-Lindau (VHL) tumor suppressor gene activates hypoxia inducible factor (HIF) and vascular endothelial growth factor (VEGF) pathways.






The first-line TKIs that predominantly target VEGF receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR) (e.g., sunitinib and sorafenib) have been clinically used since late 2000s, and the second-line TKIs such as cabozantinib, which targets more receptor tyrosine kinases including MET and TAM kinases as well as VEGFR, have been further applied to the treatment of advanced RCC since early 2010s in which the first-line TKIs are ineffective.

“In our recent study, we established a panel of patient-derived ccRCC spheroid cultures with the enhancement of cancer stemness gene signature including DPP4. Focusing on TKI sunitinib sensitivity, we demonstrated that DPP4 inhibition increased sunitinib efficacy in DPP4-high RCC spheroids and DPP4 was upregulated in sunitinib-resistant RCC cells,” the researchers explain.

More information:
Kuniko Horie et al, Potential repurposing of DPP4 inhibitors for target therapy resistance in renal cell carcinoma, Oncotarget (2023). DOI: 10.18632/oncotarget.28463

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Citation:
DPP4 inhibitors for target therapy resistance in renal cell carcinoma (2023, September 20)
retrieved 21 September 2023
from https://medicalxpress.com/news/2023-09-dpp4-inhibitors-therapy-resistance-renal.html

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Bone Cancer: Understanding the Basics



Bone Cancer: Understanding the Basics More information – https://oncologyandcancerresearch.blogspot.com/

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The UK’s Looming Cancer Catastrophe

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There are now many more days, where I feel like giving up on fighting the cancer culture in this country. SimPal is incredibly busy and I can feel the change we are making daily. In my early days I could see some wins for people affected by cancer. But not now! Politicians, totally disinterested. NHS England fighting with it’s own people. Individuals, inside or out of the service, with next to no chance of making a difference on their own now. I’m totally bored with most large charities, bringing up the same issues, I’ve seen more than 10 years ago, and still begging for more money. Even though they are continuing on the circle of failure.

cancer casts a long, dark shadow over the UK today. As incidence rates continue to rise, our overburdened health system struggles to keep pace. Years of neglect have left cancer care fragmented, underfunded and woefully unprepared. Unless we urgently prioritize reform, this burgeoning crisis threatens to eclipse all other concerns.

Already, outcomes lag far behind other nations. The UK has the lowest cancer survival rates among comparable Western countries. And the gap is only widening, with progress stalled for a decade as European neighbours surge ahead. Despite pouring billions into cutting-edge research, we fail where it matters most – aiding those currently battling the disease.

Behind the statistics lie real people betrayed. Patients denied swift access to ground breaking innovations. Families shattered when timely treatment could have made all the difference. And an exhausted, demoralized workforce battling valiantly against the odds. Without recognition of these urgent human costs, cancer will continue its insidious spread through society.

Why has it come to this? Firstly, while research breakthroughs provide hope, many now languish unused. Rigid barriers prevent rapid translation into clinical practice. Patients most in need are last to benefit, as proven treatments gather dust awaiting formal approval. We must find faster pathways to get innovations where they matter most – into hospitals and clinics across the nation.

Secondly, early diagnosis remains a key stumbling block. GPs face ever-growing demands, leaving little time to suspect cancer amidst a 10-minute appointment. Public awareness campaigns can encourage vigilance for warning signs. But we also need systematic changes – better diagnostic equipment in local practices, prompt specialist referral processes, and strategies to identify those at highest risk. The difference between Stage one and Stage three cancer, is the difference between life and death.

Workforce shortages also hamper efforts, with chronic understaffing now the status quo. Vital posts sit vacant for months, patient loads grow untenable, and staff burnout fuels an exodus from the cancer field. Without Valuing those providing care, we cannot hope to retain them.

Finally, and most critically, years of austerity have left services emaciated. Budgets tighten, equipment ages, and rising need outpaces capacity. Patients now wait months where weeks once sufficed. The system creaks under unsustainable strain – a superficial bandage on a gaping wound.

What will continued disregard for these realities entail? Projections forecast a 63% rise in cancer cases over the next two decades. Our cancer infrastructure is already bursting at the seams. Without urgent investment in staff, equipment and facilities, this influx of new cases will trigger total collapse.

Rising demand will extend delays even further as exhausted resources are stretched beyond breaking point. Patients will have outcomes decided the day they receive their cancer diagnosis – not by tumour biology but by postcode and luck in timing.

Ultimately, the real victims are not statistics but human beings. Sons and daughters, partners and parents, valued members of every community. Behind every percentage are shattered lives and devastated families. If outcomes worsen, hundreds of thousands more will lose loved ones each year.

We stand at a crossroads today. Further neglect and underfunding set society on a path toward tragedy on an unprecedented scale. Only through collective action can we alter course – championing reform, embracing innovation, investing in clinical care, and making cancer the priority it deserves to be. The time has come to step out of the shadow.

With comprehensive modernization, improved prevention and early diagnosis, the UK can still deliver world-leading cancer care to meet this growing threat. But the hour is late, and the storm is nearing. We must come together, stand up and say enough – no more lip service, no more half measures. The time for change is now.

I haven’t come this far to turn back now! The odds for me to survive were dreadful, but here I am. I will continue to fight, for future generations who deserve better. Not being stuck on life limiting waiting lists, dying whilst waiting for care. As always, these are my opinions, based on personal experiences. Please feel free to share your own, below.

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RefleXion Highlights Clinical Study Results for Future Prostate Cancer Treatment

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oncology.pencis.com/” target=”_blank”>July 3, 2023 — RefleXion Medical, Inc., a therapeutic oncology company, today announced that results of a prospective investigator-initiated clinical imaging study conducted on its X1 platform by City of Hope using positron emission tomography (PET) were presented on June 24 during an oral session at the Society of Nuclear Medicine and Medical Imaging (SNMMI) annual meeting in Chicago. The study results serve as the foundation for evaluating the use of RefleXion’s SCINTIX biology-guided radiotherapy with a prostate-specific PET radiotracer for controlling external-beam radiotherapy delivery to prostate cancer tumor targets. City of Hope, one of the largest cancer Research and treatment organizations in the U.S., is among the first in the nation to adopt this new radiotherapy technology that has the potential to change the way metastatic cancer patients are treated. 

oncology.pencis.com/” target=”_blank”>Recently cleared by the U.S. Food and Drug Administration (FDA), SCINTIX technology is the first and only cancer therapy that uses each cancer’s unique biology to autonomously determine where to deliver radiotherapy, second-by-second, during the actual cancer treatment to indicated solid tumors of any stage. SCINTIX therapy uses signals produced by a PET radiotracer interacting with cancer cells to control delivery of external-beam radiotherapy to tumor targets. 

oncology.pencis.com/” target=”_blank”>The prostate-specific PET radiotracer used in the presented study – 18F-DCFPyL (PyL) – binds to prostate-specific membrane antigen (PSMA), a protein that is expressed in significantly elevated amounts by prostate cancer cells. Also recently approved by the FDA for diagnosing and staging prostate cancer, PyL can accurately and precisely pinpoint tumors in both the prostate and in other body areas where the cancer may have spread or metastasized. 

oncology.pencis.com/” target=”_blank”>“It is well established that PyL exquisitely detects tumors present in patients with prostate cancer, but targeting and treating those tumors can be challenging using existing radiotherapy approaches,” said Jeffrey Wong, M.D., professor of the Department of Radiation oncology and the Department of Immunology and Theranostics at City of Hope, and principal investigator of the RefleXion-supported PyL imaging study. “SCINTIX therapy could overcome these barriers, and our study results support continued exploration of leveraging PyL’s precision to expand SCINTIX therapy to patients with prostate cancer.” 

oncology.pencis.com/” target=”_blank”>The prospective PyL imaging study established that tumors arising from prostate cancer could be visualized on the RefleXion X1 platform using signals from PyL consistent with PyL diagnostic imaging studies, and that SCINTIX treatment plans could be generated using these data. PSMA-directed SCINTIX treatment plans also met conventional radiotherapy organ dose constraints, suggesting the ability to spare nearby organs and other healthy tissue from potentially damaging radiation. SCINTIX therapy is currently cleared for use with 18F fludeoxyglucose (FDG), a common PET radiotracer, to treat primary and metastatic tumors in the lung and bone. 

oncology.pencis.com/” target=”_blank”>“We look forward to offering FDG-directed SCINTIX therapy to our patients in the next several weeks,” said Terence Williams, M.D., Ph.D., professor and chair of City of Hope’s Department of Radiation oncology. “As early collaborators in evaluating SCINTIX technology, it is gratifying to see Research and clinical development efforts already advancing it toward another patient population in great need of improved radiotherapy approaches using the well-characterized benefits of PyL.” 

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¿Comer alimentos a la parrilla o asados puede provocar cáncer?

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Para muchas personas, las hamburguesas asadas o las verduras crujientes son los platos favoritos. Pero, ¿comer alimentos a la parrilla o asados o alimentos cocinados a altas temperaturas puede afectar al riesgo de desarrollar cáncer?

Se encuentran varios tipos de sustancias químicas en carnes a la parrilla, asadas y bien cocidas, así como en algunos alimentos a base de plantas horneados, tostados o fritos cuando se cocinan a altas temperaturas. Aquí encontrará información sobre cuáles son estas sustancias químicas, cómo pueden afectar al riesgo de desarrollar cáncer y qué puede hacer para reducir su exposición a sustancias químicas al cocinar.

¿Cuáles son las sustancias químicas que se encuentran en los alimentos a la parrilla o en los alimentos cocinados a altas temperaturas?

Dos sustancias químicas, los hidrocarburos aromáticos policíclicos (HAP) y las aminas heterocíclicas (AHC), se desarrollan de forma natural al cocinar carne. Cuando cocina carne, la grasa y el jugo gotean en la bandeja de goteo de la parrilla, lo que provoca llamas y humo que contienen HAP. Esto, a su vez, recubre la carne con HAP. Los HAP también se encuentran en los alimentos ahumados, el humo del tabaco y el escape del auto. Mientras tanto, las AHC se producen de forma natural cuando se calienta carne, como carne de res, pollo, cerdo o pescado, a altas temperaturas.

Otra sustancia química llamada acrilamida se desarrolla de forma natural al cocinar, tostar o freír papas u otros alimentos a base de plantas a altas temperaturas. La acrilamida es una sustancia química que se forma cuando los azúcares reaccionan con aminoácidos en los alimentos que se hornean, fritan o tuestan. Puede encontrar acrilamida en papas fritas u horneadas, galletas y otros productos horneados, y café. El agua potable y el humo del tabaco también contienen acrilamida, y las personas que fuman tienen niveles más altos de biomarcadores de acrilamida en la sangre que los no fumadores, según un estudio de 2010 sobre Perspectivas de salud medioambiental (en inglés).

Si desea obtener más información sobre qué alimentos contienen acrilamida, la Food and Drug Administration (FDA, Administración de Alimentos y Medicamentos) de los EE. UU. publica en línea el contenido de acrilamida en miles de alimentos (en inglés).

¿Pueden los HAP y las ACH causar cáncer?

En estudios con animales, los roedores que siguieron una dieta con dosis elevadas de HAP y AHC desarrollaron varios tipos diferentes de cáncer. Por ejemplo, en un estudio publicado en la revista Carcinogenesis (en inglés), los roedores alimentados con AHC en su dieta tenían más probabilidades de desarrollar cáncer de mama y cáncer de colon. Sin embargo, los estudios en seres humanos no han demostrado que los HAP o las AHC causen cáncer, y esta sigue siendo un área de investigación en curso.

El estudio de estas sustancias químicas en humanos es especialmente difícil porque es difícil identificar la cantidad exacta de HAP o AHC que una persona consume basándose en cuestionarios sobre su ingesta diaria de alimentos. Además, los niveles de HAP y de AHC pueden variar según el tipo de carne, la duración de la cocción y la temperatura de cocción. Por último, la forma en que su cuerpo metaboliza estas sustancias químicas o su exposición a estas sustancias químicas en su entorno pueden diferir de la de otra persona. Para algunas personas, esto podría afectar probablemente a su riesgo de desarrollar cáncer.

“No hay una recomendación clara sobre lo que es una cantidad segura (para consumir),” dice Julie Lanford, MPH, RD, CSO, LDN, una dietista registrada y la autora y creadora de CancerDietitian.com. Pero Lanford no recomienda evitar por completo las carnes a la parrilla. En su lugar, aconseja a las personas que cocinan a la parrilla con más frecuencia, como una o dos veces a la semana, que seleccionen diversos alimentos, como verduras, pescado cocido en papel de aluminio o carnes bajas en grasa, para reducir su exposición a HAP y AHC.

Otras formas de reducir posiblemente la exposición a estas sustancias químicas incluyen:

  • Intentar evitar las llamaradas que pueden carbonizar la carne
  • Precocer parcialmente las carnes para reducir el tiempo en la parrilla
  • Marinar la carne previamente para proporcionar una capa protectora contra estas sustancias químicas
cancer.net/sites/cancer.net/files/julie-lanford-circle.png” alt=”” width=”100″ height=”100″/>

Coma muchas frutas, verduras, cereales integrales, fríjoles, frutos secos y semillas. Si puede equilibrar los alimentos que podrían tener un mayor riesgo de carcinógenos con grandes cantidades de alimentos buenos, saludables y nutritivos, obtendrá el equilibrio adecuado”.–Julie Lanford, MPH, RD, CSO, LDN, una nutricionista registrada y la autora y creadora de CancerDietitian.com

¿Puede la acrilamida causar cáncer?

La acrilamida se identificó por primera vez en alimentos en 2002 (en inglés) y, aunque probablemente no sea una sustancia química nueva, desde entonces han ido aumentando los estudios de sus efectos sobre la salud.

En estudios con animales, se ha descubierto que los niveles altos de acrilamida causan varios tipos de cáncer, según la FDA (en inglés). Sin embargo, los estudios en personas no son concluyentes. Esto podría deberse a la dificultad para calcular el nivel de ingesta de acrilamida en la dieta de una persona. Además, los niveles de acrilamida en los alimentos pueden variar en función de la temperatura de cocción, la duración de la cocción, el almacenamiento de los alimentos y otros factores.

El panel de la Autoridad Europea de Seguridad Alimentaria (en inglés) y la Organización Conjunta de Agricultura y Alimentos de las Naciones Unidas/el Comité Experto de la Organización Mundial de la Salud sobre Aditivos Alimentarios (en inglés) categorizan la acrilamida como una inquietud y recomiendan seguir estudiando el posible riesgo de cáncer en las personas. Mientras tanto, la Agencia Internacional para la Investigación del Cáncer (en inglés) considera que la acrilamida es un probable carcinógeno humano, y el Programa Nacional de Toxicología de los EE. UU. (en inglés) clasifica la acrilamida como “previsto razonablemente como carcinógeno humano”.

La FDA no publica qué niveles de acrilamida son aceptables en una dieta y no aconseja dejar de comer alimentos con acrilamida. En su lugar, se recomienda seguir una dieta equilibrada y saludable que contenga una variedad de verduras, frutas, cereales, productos lácteos sin grasa o bajos en grasa y proteínas.

Sin embargo, si desea reducir la acrilamida en su dieta, la FDA le ofrece estos consejos:

  • Tueste el pan hasta que esté de un marrón dorado en lugar de uno oscuro.
  • Siga las instrucciones de la etiqueta de los alimentos para freír o cocinar alimentos congelados, como las papas fritas, y evite sobrecocinarlos.
  • Almacene las papas en una zona fresca y seca, pero no en el refrigerador; esto puede aumentar la acrilamida durante la cocción.

La información de esta publicación se basa en la investigación actual y en las opiniones de expertos disponibles hoy en día. Estos hallazgos pueden cambiar a medida que surjan más investigaciones sobre este tema.

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Tumor vs Cancer



Tumor vs. Cancer  

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 #shorts #shortsvideo  #breastcancer #prostatecancer #lungcancer #coloncancer #ovariancancer #pancreaticcancer #leukemia #lymphoma     #OncologyConference #CancerResearch #OncologyAwards #CancerTreatment #OncologyCommunity #CancerCare #OncologyEducation #CancerSurvivorship #OncologyInnovation #CancerAwareness #OncologyLeadership #CancerPrevention #OncologyExcellence #CancerBreakthroughs #OncologyCollaboration #CancerAdvancements #OncologyImpact #CancerPatientsFirst #OncologyFuture #OncologyInspiration #CancerFighters #OncologyHeroes #CancerAwarenessMonth  #OncologyProgress #CancerSolutions #OncologyExperts #CancerSurvivors  #shorts #shortsvideo #cancerConference #OncologyConference #pencis #oncologyconference  #CardioOnc  #radonc #medonc #caxtx #GeriOnc #psyonc #oncorn #hsronc #camets #cancer #fuckcancer #cancersucks #breastcancerawareness #breastcancer #cancermemes #cancerousmemes #cancersurvivor #cancerawareness #cancerdemama #breastcancerawarenessmonth #cancerresearch #fightcancer #childhoodcancerawareness #beatcancer #childhoodcancer #cancerseason #breastcancersurvivor #cancerfree #cancerfighter #cancerous #fcancer #cancerwarrior #teamcancer #ovariancancer #americancancersociety #standuptocancer #cancerresearchuk #cancersupport #skincancer #cancermeme #cancer #feminismiscancer #curecancer #anticancer #cancerzodiac #prostatecancer #cancers #fucancer #pediatriccancer  #cancerawareness #beatcancer #cancersucks #cancerresearch #cancerfighter #cancerwarrior #cancertreatment #cancersurvivor #cancerprevention #cancerawarenessmonth #cancerpatientsupport #breastcancer #prostatecancer #lungcancer #coloncancer #ovariancancer #pancreaticcancer #leukemia #lymphoma #melanoma #braincancer #childhoodcancer #cancerfree #oncology #cancercare #cancerdiagnosis #cancerribbon #cancerjourney

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Tumour growth can be prevented by removing excess chromosomes from cancer cells: Study

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Tumour growth can be prevented by removing excess chromosomes from cancer cells: Study(Shutterstock)

According to a recent Yale study, cancer cells with additional chromosomes rely on those chromosomes for tumour formation, and removing them stops the cells from growing tumours. The results, according to the researchers, point to the possibility of a novel cancer treatment strategy that specifically targets additional chromosomes. The study was published in the journal Science.

Human cells typically have 23 pairs of chromosomes; extra chromosomes are an anomaly known as aneuploidy.

“If you look at normal skin or normal lung tissue, for example, 99.9% of the cells will have the right number of chromosomes,” said Jason Sheltzer, assistant professor of surgery at Yale School of Medicine and senior author of the study, adding, “But we’ve known for over 100 years that nearly all cancers are aneuploid.”

ALSO READ: cancer can occur at any time or age; symptoms and warning signs to look out for

However, it was unclear what role extra chromosomes played in cancer for instance, whether they cause cancer or are caused by it.

“For a long time, we could observe aneuploidy but not manipulate it. We just didn’t have the right tools,” said Sheltzer, who is also a researcher at Yale cancer Center, adding, “But in this study, we used the gene-engineering technique CRISPR to develop a new approach to eliminate entire chromosomes from cancer cells, which is an important technical advance. Being able to manipulate aneuploid chromosomes in this way will lead to a greater understanding of how they function.”

The study was co-led by former lab members Vishruth Girish, now an M.D.-Ph.D. student at Johns Hopkins School of Medicine, and Asad Lakhani, now a postdoctoral researcher at Cold Spring Harbor Laboratory.

Using their newly developed approach which they dubbed Restoring Disomy in Aneuploid cells using CRISPR Targeting, or ReDACT the researchers targeted aneuploidy in melanoma, gastric cancer, and ovarian cell lines. Specifically, they removed an aberrant third copy of the long portion also known as the “q arm” of chromosome 1, which is found in several types of cancer, is linked to disease progression, and occurs early in cancer development.

“When we eliminated aneuploidy from the genomes of these cancer cells, it compromised the malignant potential of those cells and they lost their ability to form tumors,” said Sheltzer

Based on this finding, the researchers proposed cancer cells may have an “aneuploidy addiction” — a name referencing earlier Research that discovered that eliminating oncogenes, which can turn a cell into a cancer cell, disrupts cancers’ tumor-forming abilities. This finding led to a model of cancer growth called “oncogene addiction.”

When investigating how an extra copy of chromosome 1q might promote cancer, the researchers found that multiple genes stimulated cancer cell growth when they were overrepresented — because they were encoded on three chromosomes instead of the typical two.

This overexpression of certain genes also pointed the researchers to a vulnerability that might be exploited to target cancers with aneuploidy.

Previous Research has shown that a gene encoded on chromosome 1, known as UCK2, is required to activate certain drugs. In the new study, Sheltzer and his colleagues found that cells with an extra copy of chromosome 1 were more sensitive to those drugs than were cells with just two copies, because of the overexpression of UCK2.

Further, they observed that this sensitivity meant that the drugs could redirect cellular evolution away from aneuploidy, allowing for a cell population with normal chromosome numbers and, therefore, less potential to become cancerous. When researchers created a mixture with 20 per cent aneuploid cells and 80% normal cells, aneuploid cells took over: after nine days, they made up 75 per cent of the mixture. But when the researchers exposed the 20 per cent aneuploid mixture to one of the UCK2-dependent drugs, the aneuploid cells comprised just 4% of the mix nine days later.

“This told us that aneuploidy can potentially function as a therapeutic target for cancer,” said Sheltzer, adding, “Almost all cancers are aneuploid, so if you have some way of selectively targeting those aneuploid cells, that could, theoretically, be a good way to target cancer while having minimal effect on normal, non-cancerous tissue.”

More Research needs to be done before this approach can be tested in a clinical trial. But Sheltzer aims to move this work into animal models, evaluate additional drugs and other aneuploidies, and team up with pharmaceutical companies to advance toward clinical trials.

“We’re very interested in clinical translation,” said Sheltzer, adding, “So we’re thinking about how to expand our discoveries in a therapeutic direction.”

This story has been published from a wire agency feed without modifications to the text. Only the headline has been changed.

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Reps 4 Ryan

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Each year, cancerCare hosts “Do Something for cancerCare,” an annual DIY event where people create their own fundraising activities to raise money and give back to the organization which impacted their cancer journey, or helped a loved one during their experience.

As we launch this year’s Do Something campaign, we wanted to share a story about a group of young men who are doing something in memory of their friend:

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In Fairfield, Connecticut, a group of childhood friends shared an unbreakable bond with Ryan Van Zandt, who was “anything but boring and knew how to entertain those around him,” shared Ryan’s friend, Conor. From childhood to his early twenties, His contagious smile, humor and kindness endeared him to everyone who met him.

It was Ryan’s love of sports and his second diagnosis of a rare form of cancer that led his friends to start “Reps 4 Ryan” in 2015. Combining golf and fitness, the group organized a local golf tournament at the Fairchild Wheeler Golf Course, along with a viral social media challenge.

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“Each and every day had more and more people posting pictures and videos of them throwing reps up in the gym in their Reps 4 Ryan gear,” said Conor. This online presence became so large that it eventually caught the attention of a few Miami Dolphins football players, Ryan’s favorite NFL football team.

At only 25 years old, “to see Ryan receive his second diagnosis was not just devastating, but aggravating at the same time. That’s two times too many and two times more than most people have to go through such an experience.”

“All of those horrible feelings were quickly channeled into motivation to act for Ryan and his tremendous family.” Conor added that “as sad of a time as it was for us with Ryan’s health, it was an incredibly special thing to see so many people band together. Short on energy and strength due to his ailing health at the time, Ryan rallied and joined everyone at the course for that first tournament in 2015.”

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When Ryan passed away in 2016, his friends channeled their feelings of grief and loss into Reps 4 Ryan, now an annual tradition that continues to make an impact. Drawing over 100+ participants each fall, the funds raised at the tournament go towards cancerCare‘s support services and cancer research. Reps 4 Ryan is no longer just an event – it’s a reunion, a celebration and a way to remember the warmth of their family member and friend. It brings Ryan’s community back each year, honoring his memory and the enduring bonds they share.

Ryan’s mother, Lorette, added that he “inspired more than just the Reps 4 Ryan team.” Two books were actually written about him. “Everyone has grieved in different ways,” she said. “But largely, those around him have found the outlets of continuing to help others and connect more with their community as the most positive and helpful way to confront our devastating loss.”

In honoring Ryan’s spirit, Reps 4 Ryan exemplifies the impact a close-knit community can wield as a force for good. “There’s a tremendous buzz around this tournament for so many people and that buzz is something each of us are proud to be a part of and we’re confident that Ryan would love knowing how much he is still loved and missed by all.”



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Prof Dr. Mario Diaz-Fluorescent tamoxifen derivatives as biophotonic probes for the study of human



This speech was delivered by Prof Dr. Mario Diaz, Universidad de La Laguna, Spain during the International Conference on Oncology and Cancer Research that was Organized by Pencis on16th Edition of Oncology Summit | 21-23 August 2023 | Berlin, Germany

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