Recommendable! Cancer is history (soon)!
Showing posts with label cancer is history. Show all posts
Showing posts with label cancer is history. Show all posts
Saturday, October 17, 2026
Stanford researchers create molecule to ‘shut off’ cancer-causing protein
Reprogrammed NK immune cells target cancer and autoimmune disorders
Good news! Impressive! Cancer is history (soon)!
"... have developed a new way to program natural killer (NK) immune cells to target cancerous T cells or T cells that have become autoreactive, leading to diseases such as lymphoma and autoimmune hepatitis.
Using their new technique, the researchers can reprogram NK cells to target diseased T cells without ever removing the NK cells from the patient’s body. Instead, they use lipid nanoparticles to deliver messenger RNA directly to NK cells. These mRNA molecules encode proteins that allow the NK cells to seek and destroy the dysfunctional T cells.
Known as CAR NK cells, these cells could be deployed against a variety of diseases. ...
To generate these cells, the ... team designed lipid nanoparticles (LNPs) that can deliver an mRNA payload. These strands of mRNA encode a CAR that can be targeted to specific cell types. For example, they could deliver a CAR that targets CD19, a protein found on B cells, or CD3, a protein found on autoreactive T cells.
The particles are coated with antibody fragments that bind to receptors found on the surface of NK cells, to ensure they reach the correct targets. ...
In a mouse model of an aggressive form of melanoma, three of the five mice that received LNPs that reprogrammed their NK cells to target the cancer cells went into complete remission. ...
The researchers also saw significant tumor destruction when they used the LNPs to treat T cell lymphoma in a humanized mouse model, created when mice receive transfusions of human blood cells, allowing them to transiently generate a human-like immune system.
In these mice, tumors were eradicated after five injections of the reprogramming LNPs. ..."
From the abstract:
"Targeted lipid nanoparticles (LNPs) offer a nonviral approach for in vivo cell engineering but efficient programming of natural killer (NK) cells remains underexplored.
Here we develop NK cell-targeted LNPs (NtLNPs) using engineered biparatopic NK cell ligands to drive receptor-specific uptake and mRNA delivery.
Lead NtLNPs achieve up to ~80% NK cell transfection with minimal off-target effects in mice.
Systemic delivery of chimeric antigen receptor (CAR) mRNA using NtLNPs generates CAR NK cells in vivo.
CD19-targeted CAR NKs completely deplete circulating B cells in healthy mice and CD3-targeted CAR NKs eliminate nearly all autoreactive T cells in an autoimmune hepatitis model, highlighting a potential advantage over CAR T therapies for T cell-driven disease.
CD19-targeted CAR NKs completely deplete circulating B cells in healthy mice and CD3-targeted CAR NKs eliminate nearly all autoreactive T cells in an autoimmune hepatitis model, highlighting a potential advantage over CAR T therapies for T cell-driven disease.
In solid tumors, NtLNPs targeting the inhibitory checkpoint NKG2A enhance antitumor efficacy by relieving Qa-1b-mediated immunosuppression.
Lastly, we optimized NtLNPs for in vivo engineering of human CAR NK cells, enabling regression of two humanized hematologic malignancy models and establishing NtLNPs as a modular immunotherapy system."
In vivo engineering of CAR natural killer cells for immunotherapy using ligand-directed lipid nanoparticles (no public access)
Preprint paper not found for this article!
Friday, October 16, 2026
Tumours passed between two identical twins before birth, both died shortly after birth
What a tragic story!
"A genetic analysis has revealed a rare case of a tumour passing from one identical twin to another in utero. The twins died shortly after birth and the
family gave consent for researchers to study their cancers.
The team found that the mutations in the tumour cells taken from each twin were too genetically similar for them to have arisen independently, meaning that the cancer must have passed from one twin to the other."
From the abstract:
"Studying monozygotic twins who present with identical cancers informs on the developmental origins of childhood tumours.
Here, we perform whole genome sequencing on multiple tumour, normal, and placental samples to reconstruct the phylogeny of a soft tissue cancer that spread in utero between monozygotic twins.
We demonstrate the origin of the tumour from one twin and time its diversification and transplacental spread to the other twin, showing that the spread occurred only once.
This generalisable and scalable approach additionally allows us to dissect the earliest stages of twinning, revealing unexpected asymmetrical contributions of embryonic lineages to the placenta and each twin and challenging the classical model of twinning."
Embryonic origin of cancer in newborn twins (open access)
Sunday, October 11, 2026
The five-year relative survival rate for US cancer patients rose from 49% for patients diagnosed in 1975–1979 to 71% for those diagnosed in 2016–2022
Good news! Impressive! Cancer is history (soon)!
Keep in mind: With every extra year, a cancer patient has the chance to receive the latest new cancer treatments as they become available possibly extending the life even further. Every extra year matters a lot.
"The five-year relative survival rate for US cancer patients rose from 49 percent for patients diagnosed in 1975–1979 to 71 percent for those diagnosed in 2016–2022, according to a recent report from the American Association for Cancer Research. Relative survival adjusts for deaths from causes other than cancer by comparing patients with the general population."
Wednesday, September 30, 2026
1 in 8 cancer cases worldwide are caused by viral and bacterial infections
Serious stuff! Cancer is history (soon)!
"... These viruses, bacteria and other microbes are the focus of a new paper published Monday in The Lancet Oncology that linked an estimated 2.3 million new cancer cases in 2024 — 12 per cent of all new cases — to these infectious agents.
A team of researchers at The International Agency for Research on Cancer (IARC), an arm of the World Health Organization, conducted the study. They found the largest number of cancer cases attributed to infections globally were caused by the bacterium Helicobacter pylori, which can increase the risk of stomach cancer and accounted for 760,000 cases, predominantly in eastern Asia. ...
For the first time, researchers linked even more cancers to infections, expanding their list to include 16 additional ones. ..."
From the abstract:
"Background
Infectious agents are an important preventable cause of cancer globally. To inform prevention efforts, we provide a comprehensive picture of cancer burden attributable to infections, including newly established, carcinogenic infectious agents and latest global cancer incidence estimates.
Methods
In this worldwide incidence analysis, we used data from the Global Cancer Observatory's Cancer Today (GLOBOCAN) database of cancer incidence in 2024 to estimate population-attributable fractions (PAFs), absolute numbers, and age-standardised incidence rates (ASIRs) of new cancer cases attributable to 12 infectious agents classified as Group 1 carcinogens by the IARC Monographs Programme:
Helicobacter pylori, human papillomavirus (HPV), hepatitis B (HBV) and hepatitis C viruses (HCV), Epstein–Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus, Schistosoma haematobium, human T-cell lymphotropic virus, Opisthorchis viverrini, Clonorchis sinensis, Merkel cell polyomavirus, and HIV. Estimates stratified by sex, country, and age group were aggregated by UN geographical subregion and World Bank income group.
Findings
An estimated 2·3 million new cancer cases were attributable to infections globally in 2024, which is equivalent to 12% of all cancer cases.
The largest number of cases was attributable to
H pylori (n=760 000, PAF 4%), followed by
HPV (n=750 000, 4%), HBV (n=360 000, 2%),
EBV (n=260 000, 1%), and
HCV (n=160 000, <1%).
The largest burden of infection-attributable cancer was in eastern Asia, with 990 000 cases (42% of the global total, ASIR 31·9 per 100 000 cases). ASIRs were also higher than the global average (22·7) in sub-Saharan Africa (28·5), central and eastern Europe (24·3), and southeastern Asia (23·1).
Focused analysis of EBV-attributable cancers revealed regional variation in the distribution of cancer types."
1 in 8 cancer cases worldwide is caused by infections, study suggests "Researchers estimate infections caused 2.3 million new cancer cases worldwide in 2024"
Figure 1 ASIR of infection-attributable cancers per 100 000 person-years in 2024 for the six infectious agents with the most attributable cases
Scientists Identify Connection Between Nervous System and Aggressive Prostate Cancer
Good news! Cancer is history (soon)!
You wonder whether other cancers also manipulate the nervous system!
"A new study ... has found a link between the nervous system and the rapid development of neuroendocrine prostate cancer (NEPC), an aggressive form of the disease. ... the study found high levels of neuromedin U (NMU), a kind of neurotransmitter, present in prostate cells at the very early phase of NEPC formation, which support tumor progression by blocking the immune response. These findings could present a target for therapy for what is now a virtually untreatable disease. ..."
From the abstract:
"Neuroendocrine prostate cancer (NEPC) is an increasingly recognized, highly aggressive disease variant with no actionable therapeutic targets and a life expectancy of 7 months or less.
Using a transgenic mouse model, we now show that early stages of NEPC are associated with increased intraprostatic recruitment of Ly6G+ polymorphonuclear neutrophils (PMN) and reduced infiltration of CD8+ T cells. This coincided with expansive transcriptional changes of increased cell viability and cell migration, as well as upregulation of multiple neuronal mediators with the neuropeptide, Neuromedin U (NMU) as the top hit (Z score = 4.34; FDR < 5%; p = 3.62 × 10−9). Analysis of a large cohort of human patient samples revealed that NMU was highly expressed in early and late stage prostate cancer, preferentially segregating with AR-/NE+ metastases. Exposure of PMN to recombinant NMU was sufficient to stimulate cell migration, inflammatory gene expression with increased levels of the cytokine-like alarmin, S100A9 and suppression of T cell proliferation.
Genetic or pharmacological targeting of NMU/S100A9 signaling inhibited NEPC growth, reinvigorated an intratumoral immune microenvironment via recruitment of tumor antigen-specific CD8+ T cells with ‘stem-like’ (TCF1+/PD1+) and cytotoxic (GrzB+/KLRG1+) properties and enhanced the activity of therapeutic immune checkpoint inhibition, in vivo.
Therefore, NMU ‘innervation’ drives myeloid immunosuppression in NEPC and provides a therapeutic target to restore sensitivity to immunotherapy in this highly refractory malignancy."
Monday, September 28, 2026
Thursday, September 24, 2026
About 30% of adults would conceal loved ones' cancer. Really!
I am not sure how realistic this scenario is. Why would the patient not learn of his/her condition directly from the doctor?
This study seems to be odd if not contrived. Junk science?
What is here is the effect of cultural or religious factors? E.g. Buddhism?
Notice the difference is less than 10 percentage points. What is e.g. the margin of error in this case?
"Around 30% of adults in Thailand reported that if they were informed that a loved one had been diagnosed with cancer, they wouldn’t tell that person. The main reason for withholding the diagnosis was that they believed that receiving such bad news could worsen symptoms and cause fear of pain or death. The study surveyed more than 600 people, of whom around 80% were female. Previous studies have revealed similar trends in China, India and Saudi Arabia."
From the abstract:
"This study aimed to examine intentions to know one’s own cancer diagnosis and prognosis and intentions to allow family members to know the information.
A cross-sectional survey was conducted among adults without a history of cancer diagnosis. Data were collected using a questionnaire capturing participant characteristics, intentions to know cancer diagnosis and prognosis, and intentions to allow loved ones to know cancer diagnosis and prognosis. The proportion reporting each intention was estimated. Factors related to not allow loved ones to know cancer diagnosis and prognosis were examined using univariate and multivariate regression analyses.
Of 607, most participants were female (80.2%), with a mean age of 43.1 ± 14.7 years.
Intentions to know one’s own cancer-related information were consistently higher than intentions to allow loved ones to know the information: cancer diagnosis (79.9% vs. 70.5%), prognosis regarding cancer stage and chance of cure (80.7% vs. 72.0%), and end-of-life prognosis (77.1% vs. 67.1%).
Participants who did not wish to know their own cancer prognosis had significantly higher odds of intending to not allow their loved ones to know cancer diagnosis and prognostic information.
Future research should focus on developing and evaluating approaches to assess preferences for cancer-related information disclosure."
Thursday, September 17, 2026
Foreigners are travelling to China for low cost CAR T cancer therapy
Good news! Competition is good, more competition is better!
"China is becoming a destination-of-choice for foreign nationals with cancer looking for cheaper, faster CAR-T-cell therapy. Michael Walters, a 25-year-old from New Zealand with blood cancer, travelled to SinoUnited Hospital in Shanghai to receive CAR-T-cell therapy at less than half the cost of what he would have paid in Australia or the United States. He is now in remission. “China has basically done to CAR-T-cell therapy the same thing that it’s done to other industries, which is, they’ve industrialized it,” ..."
Patients Are Flying to China for the Latest Cancer Treatment (behind paywall) "Shanghai is a favored destination, with lower costs than the West and innovation in biotechnology"
Wednesday, September 16, 2026
Virtual cell model predicts best cancer drug
Good news! Cancer is history (soon)!
Again Nature journal uses the horrible ideological term "people" instead of women!!!
triple-negative breast cancer (TNBC)
"A new ‘virtual cell model’ could help to choose more personalized treatments for women people with hard-to-treat triple-negative breast cancer. Researchers trained the prototype artificial-intelligence-based model, called ProteinTalks, on millions of protein measurements collected over time from breast cancer cell lines that were treated with dozens of antitumour drugs. The model did a good job of predicting how cells would respond to drugs it hadn’t seen before and also real-world clinical outcomes. “This is the first time that a virtual cell model goes out of the laboratory and is tested in a clinical scenario,” ...
In experiments using biopsies taken from individuals with TNBC, the virtual cell model showed promising results in identifying the same drugs that would prove to be effective when given to women people. The authors say this raises the possibility of more personalized care for TNBC, which accounts for 15–20% of breast cancer cases. ...
In their study, Guo and his colleagues aimed to develop a virtual cell model of breast cancer cells using proteomics data. They trained an AI model on more than 38 million protein measurements collected from 18 breast cancer cell lines, 16 of which were TNBC cells. The researchers treated the cells with 63 antitumour drugs that have been approved by the US Food and Drug Administration, and 59 drug combinations. ..."
From the abstract:
"Artificial intelligence-empowered virtual cell models represent an emerging approach for in silico drug discovery, yet most existing approaches lack large-scale, time-resolved perturbation proteomics data and interpretable frameworks for predicting therapeutic responses.
Here we generated more than 38 million temporal protein-abundance measurements from systematically perturbed breast cancer cell lines, and developed ProteinTalks, a virtual cell model.
Central to ProteinTalks is the synergy of this large-scale dynamic proteomic resource and the model architecture, enabling a new pretraining framework that learns transferable dynamical latent representations from temporal proteome trajectories. By modelling how proteins respond conditionally to different perturbations, this approach enables the model to function as an operational tool for diverse drug discovery tasks: predicting drug efficacy and synergy, discovering new drug combinations, probing proteins associated with drug resistance, stratifying patient responses and prioritizing drug candidates for patient organoids.
It also shows robust transferability, extending beyond cell lines to patient-derived organoids and clinical biopsies, generally achieving higher performance than the selected benchmark implementations under the evaluated protocols.
Together, ProteinTalks shows how scalable pretraining of transferable dynamic representations enables operational, dynamics-aware, proteomics-based virtual cell models to advance in silico drug discovery."
AI model predicts which breast-cancer drugs work best (behind paywall) "Model trained on millions of protein measurements can gauge drug effectiveness in tissue samples taken from people with triple-negative breast cancer."
An operational perturbation proteomics-based virtual cell model (no public access, but article above contains link to PDF)
A perturbation proteomics-based foundation model for virtual cell construction (preprint, open access)
Fig. 1 Overview of this perturbation proteomics study.
Fig. 3 Development and performance of the ProteinTalks model.
Scientists engineer ready-to-use cancer-fighting T cells for solid tumors
Good news! Cancer is history (soon)!
"Key takeaways
- ... researchers have developed a way to mass-produce cancer-fighting T cells from blood stem cells found in cord blood, engineered to target a protein found in many solid tumors — creating uniform batches instead of custom treatments for each patient.
- This way, scientists ensure that all the T cells they produce carry the same single tumor-targeting receptor, avoiding the random receptors that can attack healthy tissue and cause a dangerous condition called graft-versus-host disease.
- In mouse models of ovarian cancer and melanoma, a single dose kept tumors in check and extended survival, outperforming conventional donor T cells, which caused toxic side effects in the same tests.
...
Rather than starting with mature, donor-derived T cells, the researchers began a step earlier — with blood stem cells found in cord blood, which naturally give rise to every type of blood and immune cell. They then added a gene for a receptor that targets NY-ESO-1, a protein found in many solid tumors. Fragments of NY-ESO-1 get pushed to the outer surface and displayed there, name-tag style. The researchers then grew these engineered stem cells into T cells in the lab. ...
“From a small number of cord blood stem cells, we can generate trillions of therapeutic cells — enough for thousands of doses — within about six weeks,” ... “At an estimated $5,000 per dose, this approach would be far more accessible than today’s therapies.” ..."
From the highlights and abstract:
"Highlights
• HSPC-derived AlloESO-T cells enable scalable, feeder-free T cell manufacturing
• AlloESO-T cells overcome autologous complexity, HLA restriction, and donor variability
• AlloESO-T cells display tumor homing, durable persistence, and TCR/NKR dual targeting
• AlloESO-T cells show minimal GvHD/CRS risk and stable hypoimmunogenicity
Summary
Adoptive T cell therapy for solid tumors is limited by autologous manufacturing complexity and, in allogeneic settings, risks including graft-versus-host disease (GvHD), HLA restriction, and donor variability.
We develop a scalable, feeder-free platform to differentiate gene-engineered hematopoietic stem and progenitor cells (HSPCs) into allogeneic, NY-ESO-1-specific cytotoxic T (AlloESO-T) cells.
Product phenotype, function, tumor homing, and safety are assessed against solid tumor models and benchmarked to peripheral blood mononuclear cell (PBMC)-derived TCR-engineered T cells. AlloESO-T cells display a uniform cytotoxic phenotype, with dual tumor targeting through a transgenic TCR and natural killer receptors.
Relative to PBMC-derived counterparts, AlloESO-T cells show superior cytotoxicity, selective solid-tumor homing, durable killing persistence, and resilience to immune evasion.
They also maintain low GvHD and cytokine release syndrome risk, while retaining stable hypoimmunogenic features. These findings establish HSPC-derived AlloESO-T cells as an off-the-shelf, mono-specific cytotoxic T cell therapy with scalable manufacturing, enhanced efficacy, and improved safety, which support broad applicability of AlloESO-T cells across solid tumors."
Scalable generation of hematopoietic stem cell-engineered off-the-shelf mono-specific cytotoxic T cells targeting solid tumors (open access)
Graphical abstract
Figure 1 Generation and characterization of Allo/15ESO-T cells
Friday, September 11, 2026
Chronic interferon exposure prompts a switch from anti-tumor activity to immunosuppression
Good news! Cancer is history (soon)!
"Type II interferon (IFN-II) normally activates the immune system to fight cancer. However, prolonged IFN-II exposure can promote an immunosuppressive tumor environment that supports cancer growth, a confounding factor in cancer therapies. Johnson et al. explored why IFN-driven inflammation can be tumor suppressive in certain contexts but tumor promoting in others.
Chronic IFN-II stimulation unveiled secondary protumorigenic type I IFN (IFN-I) signaling that increased production of prostaglandins, bioactive lipids that inhibit anticancer immune responses.
Suppressing prostaglandin synthesis restored the ability of the immune system to attack tumors and reversed resistance to immunotherapy in melanoma cells.
The IFN-II–mediated IFN-I response was instigated by the release of mitochondrial RNA that activated innate immune signaling.
Timely inhibition of IFN-I signaling or blocking mitochondrial RNA release may therefore provide a means to promote antitumor immunity."
"Highlights
- ... researchers identify what flips a molecular “switch” that causes anti-cancer interferon activity to transition into pro-cancer activity, a longstanding mystery in cancer biology
- Chronic interferon activates a mitochondrial signaling pathway that, when turned off, effectively reverses tumor growth and immunotherapy resistance in a mouse model of melanoma
- The study could reveal new therapeutic targets to sustain anti-tumor immune responses
..."
From the abstract:
"Interferons (IFNs) are proinflammatory cytokines that promote immune cell engagement to eliminate malignant cells.
Paradoxically, chronic interferon signaling can also activate anti-inflammatory mechanisms that allow cancer cells to evade the immune system.
In this study, we sought to determine the cellular mechanisms underlying this switch from antitumorigenic to protumorigenic interferon activity.
We show that chronic type II interferon (IFN-II) exposure distinctively induced tumor growth by activating a type I interferon (IFN-I) response mediated by release of double-stranded mitochondrial RNA (ds-mtRNA) into the cytoplasm. This IFN-I signal synergized with IFN-II to enhance tumor growth by increasing immunosuppressive prostaglandin E2 (PGE2) synthesis through increased cyclooxygenase 2 expression.
Elimination of PGE2 synthesis in immunotherapy-resistant melanoma cells restored their responsiveness to anti-PD1 treatment, indicating that this covert mtRNA-IFN-prostaglandin pathway could be a therapeutic target to combat immunotherapy resistance."
Why does the immune system sometimes help tumors grow? (original news release) "Salk Institute researchers define how chronic interferon exposure prompts a switch from anti-tumor activity to immunosuppression in mice, revealing a key target to sustain anti-tumor immune responses and combat immunotherapy-resistant cancer"
Representative images showing mitochondrial RNA (mtRNA) transcripts (red) present outside of the confines of mitochondria (cyan) in a melanoma cell following chronic interferon II exposure. Arrows point to specific examples of mtRNA outside the mitochondria.
Friday, September 04, 2026
Cancer cells release antioxidants to prevent immune cells from destroying them
Good news! Cancer is history (soon)! Are we finally cracking the secretes how cancer survives/counteracts immune responses and immunotherapy?
"Now, scientists have discovered that certain immune cells depend on these very molecules to activate and destroy cancer cells, and that tumours exploit this dependency by releasing natural antioxidants to shut down the immune attack. ...
A team ... analysed the fluid surrounding cells within tumours grown in mice and found that cancers chemically ‘smother’ T cells, stopping their activation and preventing them from destroying cancer cells.
Tumours do this by releasing large amounts of a protein that is a natural antioxidant, Peroxiredoxin 1 (PRDX1), which mops up reactive oxygen species and deprives T cells of the activating signals they need to perform cancer killing.
Next, the team used CRISPR gene-editing technology to create mouse cancer cells that could no longer make the antioxidant protein. They found that removing the capacity for the cancer cells to produce the antioxidant promoted immune-cell activity and limited tumour growth.
Finally, the team looked for the same mechanism in people. They analysed published data on the proteins released by human cancer cell lines, examined gene activity across thousands of human tumours, and isolated the fluid surrounding tumours removed from patients. All three approaches pointed the same way: human cancers also release PRDX1 into their surroundings, where it can strip away the reactive oxygen species that T cells depend on. ...
The findings also carry broader implications. Several large randomised clinical trials have found that antioxidant supplements fail to reduce cancer risk ..."
"New research reveals a promising new target for treating cancer by harnessing a type of molecule previously thought to do more harm than good.
For decades, reactive oxygen species, or ROS, often called free radicals, have been viewed primarily as harmful molecules linked to aging, DNA damage and cancer. A new study ... finds that cancer-fighting T cells need small amounts of ROS to attack tumors.
The investigators discovered that cancers exploit the T cell need for ROS by releasing an antioxidant protein that removes ROS from the tumor environment, effectively shutting down the attack by the immune system upon the cancer. ..."
From the editor's summary and abstract:
"Editor’s summary
Reactive oxygen species (ROS) have a paradoxical role in cancer.
Low to moderate ROS levels can stimulate tumor growth, whereas excessive ROS accumulation triggers oxidative stress and DNA damage.
Antioxidant therapies aim to neutralize free radicals and reduce oxidative stress, but clinical trials have not (yet) demonstrated improved cancer survival. Wesolowski et al. report that tumors can turn ROS dependency against the immune system, suppressing T cells and escaping antitumor immunity.
Cancer cells secrete antioxidant enzymes, including peroxiredoxin 1 (PRDX1), into the extracellular space, depriving T cells of ROS needed for T cells to attack tumors effectively.
Removing PRDX1 from cancer cells restored antitumor immunity and made otherwise resistant tumors sensitive to checkpoint blockade immunotherapy.
These results suggest that targeting extracellular redox mechanisms could enhance the efficacy of immunotherapy.
Abstract
Reactive oxygen species (ROS) promote genomic instability and fuel oncogenic signaling in cancer, but antioxidant therapies have so far failed to improve, or worsen, cancer outcomes.
Emerging data suggest that T cells depend on ROS for signal transduction.
In this study, we show that tumors exploit this dependency, releasing antioxidant enzymes into the tumor environment to suppress T cell–mediated antitumor immunity.
The interstitial fluid of tumors possesses potent antioxidant activity, associated with enrichment of the antioxidant enzyme peroxiredoxin 1 (PRDX1). Extracellular PRDX1 deprives T cells of ROS, preventing oxidative inactivation of phosphatases required for T cell receptor–driven kinase signaling and effector function.
Prdx1 is up-regulated upon cancer immunoediting, and loss of PRDX1 within tumors enhances antitumor immunity and immunotherapy responses.
These findings define a redox-dependent mechanism of tumor immunosuppression that is potentially amenable to therapeutic intervention."
Cancer cells use antioxidant protein to suppress T cells, resist immunotherapy, study finds (original news release 2) "OHSU co-author helps identify potential therapeutic target in tumors that evade the immune system"
Killer T cells surrounding a cancer cell
Tuesday, September 01, 2026
New mRNA immunotherapy eliminates pancreatic tumors in mice
Good news! Cancer is history (soon)!
"... have developed an immunotherapy using a cocktail of messenger RNAs (mRNA) that could potentially transform pancreatic cancer treatment.
The study ... combines immune cytokine and tumor-associated antigen mRNAs into a single injection to treat pancreatic ductal adenocarcinoma.
Approximately 50% of mice with pancreatic cancer treated with the mRNA immunotherapeutic cocktail had complete tumor responses and, more impressively, remained disease-free for a year, even after treatment had stopped.
"It's unheard of to get a response like this in these models of pancreatic cancer," ..."
From the abstract:
"Immunotherapy has limited success in pancreatic ductal adenocarcinoma (PDAC) due to an immune exclusive tumor microenvironment (TME) that lacks many cytokines necessary for Natural Killer (NK) and T cell responses.
Here, we design multiplexed mRNAs encoding interleukins, chemokines, and interferons as a safe and effective cytokine therapy for PDAC.
Intratumoral injection of IL-12, IL-18, CCL5, CXCL10, and IFNβ mRNAs achieves robust yet transient cytokine expression, leading to NK and CD8+ T cell activation and reduced tumor growth and fibrosis in PDAC transplant mouse models.
Combining cytokine with tumor antigen mRNAs enhances dendritic cell antigen presentation and CD8+ T cell priming locally and systemically that prolongs animal survival after a single dose.
Remarkably, nanoparticle encapsulation of the cytokine/antigen mRNA cocktail allows systemic administration and local delivery to autochthonous PDAC tumors in mice, culminating in curative responses in 50% of animals and antigen-reactive T cell persistence.
These results suggest that multiplexed mRNA approaches to deliver cytokines and antigens generally absent in the TME could pave the way for effective immunotherapy in PDAC."
mRNA immunotherapy developed by UMass Chan scientists eliminates pancreatic tumors in mice (original news release)
Multiplexed cytokine and antigen mRNA administration generates durable anti-tumor immunity against pancreatic cancer (open access)
Fig. 2: A multiplexed cytokine mRNA cocktail mobilizes innate and adaptive immunity and reduces tumor growth and desmoplasia in “cold” PDAC-bearing mice.
Fig. 3: Combinatorial cytokine mRNA therapy can achieve robust cytotoxic T cell immunity in a “hot” PDAC model after a single dose.
Monday, August 31, 2026
Scientists Identify Fructose as a Surprise Driver of ovarian Cancer Spread
Will this be the end of fructose in soda drinks? Don't bet on it! 😊
Sunday, August 30, 2026
Mouth Microbes transmitted to gut Could Help Diagnose gastrointestinal Cancers
Amazing stuff! Cancer is history (soon)!
Is this maybe another good reason to do daily tongue scraping?
"... In a new study, researchers have shown that mouth bacteria migrate through the gastrointestinal tract in certain types of cancer.1 The findings raise hope that the breakdown of these carefully sectioned-off compartments in the body could be an indicator of disease, leading to easier and quicker diagnostic tests for gastrointestinal cancers. ..."
"... In a study ... researchers report that by analyzing the make-up of oral microbes, they may be able to detect signals associated with gastric (stomach) and colorectal cancer. These findings could lead to the development of new, less-invasive screening tests for gastrointestinal cancers. ...
To conduct the study, the researchers recruited 507 volunteers to donate both oral and fecal samples, using a highly standardized collection process. The cohort included 129 healthy individuals; 215 people with metabolic disorders such as metabolic syndrome, hypertension, hyperlipidemia, and type 2 diabetes; 77 people with gastric cancer; and 86 people with colorectal cancer. For the volunteers with cancer, samples were collected before the start of any treatment. ...
The findings were more nuanced than a simple cancer-versus-healthy comparison. The MF index was significantly elevated in patients with gastric or colorectal cancer but not in people with metabolic disorders. After accounting for alcohol consumption, regular exercise, and BMI, the association remained robust for both gastric and colorectal cancers. ..."
From the highlights and abstract:
"Highlights
• Mouth and gut microbial compartmentalization is disrupted in gastrointestinal cancers
• Mouth-to-gut transmitted bacteria correlate with metabolic and inflammatory markers
• Oral-fecal transmission signatures enable cancer classification by oral microbiome alone
• Transmission-based classifier surpasses microbiota models and fecal occult blood testing
Summary
The human microbiome is spatially compartmentalized, yet oral bacteria can ectopically colonize distal sites such as the gut, potentially influencing disease.
By analyzing paired oral and fecal microbiomes from 507 participants across healthy controls and patients with metabolic disorders or gastrointestinal cancers, we established a quantitative mouth-to-feces (MF) index to measure MF microbial transmission.
The MF index revealed elevated mouth-to-gut transmission in cancer and a strong association with host metabolic and inflammatory indicators.
Using transmitted taxa, we developed a random forest classifier that accurately distinguished gastric/colorectal cancer from healthy controls across seven independent cohorts, even when trained solely on oral microbiome data.
When benchmarked against the conventional screening test, the MF-based model achieved markedly higher sensitivity than the fecal occult blood test.
These findings uncover disease-specific transmission signatures and highlight MF microbial profiling as a generalizable, non-invasive framework for gastrointestinal cancer diagnosis and risk stratification."
Graphical abstract
Figure 2. MF transmission index as an assessment of the mouth-gut microbiome axis
Saturday, August 29, 2026
New biobank of patient-derived tumour organoid 3D models reveals cancers’ weak spots of five different cancer types
Good news! Cancer is history (soon)! This could be a major advance!
"... The biobank is expected to have wide utility, enabling scientists to identify the genes that specific cancers depend on for growth, revealing potential weak points that could be targeted with future treatments.
The study is published alongside two complementary papers from international collaborators, reflecting a wider multi-year effort to refine organoid models and make them more accessible to the research community.
For decades, cancer researchers have relied on two-dimensional (2D) cell lines to study cancer. These workhorse models, in which cells are grown in a flat layer on laboratory plates, have provided important insights into cancer biology and remain widely used.
However, 2D models have limitations: they do not fully capture the diversity and complexity of tumours seen in patients and they have adapted to laboratory conditions over time. Researchers are therefore increasingly looking to develop next-generation models that better reflect tumours found in patients, such as organoids, to complement 2D cell lines and help address some of these gaps. ...
In a first of its kind study in organoids, the researchers went on to use CRISPR screening, a method they used to systematically switch off genes one by one to see if the cells survived, in order to map the genes that are critical to cancer cell survival across 162 of the organoid models. They identified thousands of genetic dependencies, including both common genes required by many cancers to survive, and more specific vulnerabilities linked to particular tumour types. ..."
From the abstract:
"Cancer cell lines remain foundational for research and drug discovery, yet they incompletely capture tumour diversity, lack linked patient context, and have undergone adaptation to culture.
Tumour organoids are three-dimensional cultures derived from patient tissue that offer a powerful complement to cell lines.
Here we derived and characterized 256 clinically annotated tumour organoids directly from colorectal, oesophageal, ovarian, pancreatic and gastric cancers as renewable, genetically stable models.
Extensive characterization of each model and matched patient tumour samples included whole-genome and transcriptome sequencing, and genome-wide CRISPR–Cas9 screens across 162 organoids mapped gene dependencies. Integrative analyses revealed genomic and clinical markers of dependency across common and rare subtypes, identified organoid-specific essential genes, and revealed targetable vulnerabilities following tumour evolution in paired pre- and post-treatment samples.
In colorectal cancer, functional and pharmacological interrogation of the EGFR–RAS–MAPK axis uncovered differential effects of KRAS variant alleles.
This open, publicly available resource provides a systematic map of gene dependencies in patient-derived organoids, expanding the model diversity and mechanistic insight needed to advance precision oncology."
Fig. 1: Establishment of organoid biobank and patient-linked clinical data.
Fig. 2: Genomic features are conserved between organoid and patient-matched tumour.
Hidden drivers of aggressive childhood cancer revealed
Good news! Cancer is history (soon)!
"New insights into why some children with rhabdomyosarcoma (RMS) develop aggressive disease despite being classified as non-high-risk have been uncovered. ...
RMS is broadly split into two different types, depending on whether the tumour contains a genetic risk marker. This marker is a fusion of two genes that are not normally connected. In patients with this marker, survival is substantially lower than in those who do not carry it, despite intense treatment.2
However, some children whose tumours do not carry the high-risk marker still develop aggressive disease, and it is unclear why this happens.
In a new study, researchers ... sought to understand why this group of non-high-risk patients go on to experience such an aggressive cancer. ...
In particular, they used single-cell RNA sequencing, which is a technique that allowed the team to examine gene activity in individual cancer cells. This revealed the true aggressive face of cancer cells that had ordinarily been classified as non-high-risk.
The team also used a method called spatial transcriptomics, which enabled the scientists to map where the cancer cells were located within the tumour, revealing how aggressive cell populations are organised within the cancer tissue.
The study revealed that aggressive tumours of children who had been classified as non-high-risk have gene expression patterns that closely resemble those of high-risk tumours, despite lacking the genetic risk marker.
They also found that children with non-high-risk tumours which behaved aggressively carry rare genetic changes that affect the same cellular pathway as high-risk tumours. This suggests that there are multiple genetic routes leading to the same aggressive tumours. ..."
From the abstract:
"Somatic mutations often predict survival in childhood cancers, as exemplified in rhabdomyosarcoma (RMS), in which FOXO1 gene fusion status is a key prognostic feature.
In this study, we examined single-cell transcriptomes and discovered that cancer cells of lethal disease converge on a common cell state with a shared transcriptional landscape, irrespective of fusion status.
Nuclear transcriptomics, chromatin accessibility, spatial transcriptomics, perturbation studies, and previously published datasets validated the overarching high-risk cell state.
The convergent cell state only partially overlapped with transcriptional effects of the FOXO1 fusion and unexpectedly exhibited neural features.
Overall, these findings delineate a cell state of high-risk RMS cells that transcends conventional molecular and histologic boundaries, suggesting an overarching disease phenotype that could transform target discovery and inform clinical practice."
Thursday, August 27, 2026
Cancer-killing cells in those humans live to 110 or longer
Amazing stuff! Good news! Cancer is history (soon)!
"People who live to 110 years and older have large populations of a rare type of immune cell that can kill cancer.
These killer T cells might help people to live to extraordinarily long ages by fighting off cancer — although this has yet to be proved.
“Most of immune ageing research has focused on decline,” [what a mistake!] ... “Our study suggests that even at extreme old age, the immune system may still selectively adapt.”"
"The current study builds on a 2019 finding by Hashimoto and his colleagues that supercentenarians have relatively large numbers of rare CD4 cytotoxic T lymphocytes (CD4 CTLs).
Cytotoxic cells kill other cells. CD4 CTLs typically make up less than 5% of the total population of T cells in the body. They’re not as well studied as other kinds of T cell, but they are commonly detected during viral infections, and there’s increasing evidence that they can kill cancer cells, including lung cancer and melanoma cells. Hashimoto says that his team wanted to find out at what age CD4 CTLs proliferate.
Supercentenarians are challenging to study because not many people live that long, says Hashimoto. In Japan, where his team did the study, there are only about 150 people aged 110 or older, he says. The study enrolled 28 participants, including some relatively young people: eight individuals aged 70–90, ten centenarians (people 100–109 years old) and ten supercentenarians.
As the researchers had previously found, CD4 CTLs were abundant in supercentenarians. But they were also found in large numbers in people aged 100 and older, suggesting that this immune adaptation begins around that age. The younger people had normal abundance of these cells, with CD4 CTLs making up 4% of their total T cells. The proportion was around 10% in centenarians and around 18% in supercentenarians.
And they found that these cells seem to be responding to specific immune threats. ... In the study’s centenarians and supercentenarians, the researchers found that single clonal lines made up a large percentage of the total CD4 CTLs. In the sample of one centenarian, for example, 53.8% of the cells were identical to each other. This suggests that their immune systems were leaping into action in response to a particular persistent trigger. ...
To get some clues, they examined the receptors found on the most common CD4 killer cell lines. They compared the amino-acid sequences of these cell lines with those in a database of CD4 cell receptors. Around 30 sequences from the study matched those from people with cancer in the database. Matches to people with lung cancer were most frequent, even though none of the people in the study had experienced any kind of cancer during their lives. ..."
From the highlights and abstract:
"Highlights
• CD4 CTLs expand around age 100 without signs of exhaustion
• A CD27−CD28+ state marks the intermediate helper-to-killer transition
• Large private CD4 CTL clones suggest repeated antigen exposure
• Single clones diversify cytokine profiles after ex vivo stimulation
Summary
Our previous study identified CD4 cytotoxic T lymphocytes (CD4 CTLs) as a hallmark of supercentenarians.
CD4 CTLs have primarily been studied in disease contexts; however, their role in healthy aging remains unclear.
Using single-cell immune profiling, we analyzed T cells from supercentenarians and found that CD4 CTLs begin to expand around the age of 100, characterized by sequential CD27/CD28 loss without exhaustion.
CD4 CTLs were dominated by large clones, with top clones averaging 33.3%, indicating repeated stimulation by persistent antigens.
Furthermore, CDR3β sequences of the top clones matched those of T cells expanded in tumors, particularly lung cancer.
Ex vivo stimulation experiments revealed that CD4 CTLs consist of subgroups defined by interleukin expression patterns, suggesting their plasticity within the same clone.
These findings suggest that CD4 CTLs expand and diversify as an adaptation to persistent antigens, potentially contributing to longevity through cancer suppression."
How do people live beyond 110? Abundance of cancer-killing cells might be key "Research on people 110 years and older reveals an immune system that continues to adapt."
Misao Okawa celebrated her 117th birthday in 2015. Is she still alive?
Graphical abstract
Figure 1 Overview of single-cell immune profiling
Figure 6 Characteristics of activated CD4 CTLs
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