Scientists identify fructose as a surprise driver of cancer spread
A new study has uncovered an unexpected link between fructose—a common dietary sugar—and the spread of an aggressive form of ovarian cancer. Published in Nature Aging, the study found that cancer cells not killed by chemotherapy send signals to neighboring tumor cells, helping them become more capable of spreading.
The researchers identified fructose as a key messenger in this process, revealing a previously unrecognized way that treatment-surviving cancer cells may promote the spread of cancer. Even more interesting, they found that without chemotherapy treatment, consuming the high levels of fructose found in sugary drinks can also signal cancer cells to spread. The fructose finding is especially compelling because it raises the possibility that simple dietary changes could help shape how cancer progresses.
Chemotherapy-surviving ovarian cancer cells secrete fructose, which signals neighbouring tumour cells to become more metastatic in preclinical models. Exogenous fructose at levels typical of sugary drink intake similarly promotes spread. Mechanistically, fructose suppresses cholesterol synthesis, weakening cell–cell adhesion; statins mimic this effect, suggesting potential interaction with chemotherapy responses.
The researchers next aimed to understand why fructose increases cancer cell spread. Through a variety of large-scale analytical techniques, including the use of a CRISPR screen, they discovered that fructose suppresses cholesterol within neighboring cells. Cholesterol is important for cells to stick to each other like a biological glue, so decreased cholesterol allows cells to more easily escape and spread.
The finding that fructose lowers cholesterol production has important clinical implications. Statins, which are taken by 39 million people in the United States, lower cholesterol production.
The team found that statins alone reduced the glue between cells, promoting escape. The research team is now examining whether these medications could be interfering with the effects of chemotherapy—though they stress this isn't a reason for patients to stop taking them.
The researchers are also looking into how this mechanism might extend beyond ovarian cancer.
The chemotherapy-induced senescence-associated secretome promotes cell detachment and metastatic dissemination through metabolic reprogramming, Nature Aging (2026). DOI: 10.1038/s43587-026-01172-5.
New technique pinpoints human DNA inherited from 'ghost' ancestors
Researchers have identified regions of DNA that humans inherited from two unknown ancestors as a result of long-ago interbreeding among modern humans and at least four other archaic human relatives.
While previous research found hints that modern humans had interbred with ancient hominins in addition to now-extinct Neanderthals and Denisovans, the current study pinpoints areas of the genome inherited from these unknown ancestors and establishes a timeline. This was possible using a new technique the researchers developed that leverages hundreds of genomes from modern-day humans to find ancient genealogical relationships. One of the unknown ancestors, which the researchers refer to as a ghost ancestor, interbred with modern humans in Africa prior to 50,000 years ago, before the most recent migration of Homo sapiens out of Africa into Europe and Asia. These genes comprise around 1% of the genomes of modern humans, comparable to the amount of Neanderthal DNA in the human genome. That unknown hominin lineage split from the modern human lineage around the same time that Neanderthals and Denisovans diverged, about 800,000 years ago, though it interbred with modern humans earlier.
A genealogical method (TRACE) applied to modern human genomes identifies ~2% archaic DNA from two unknown hominin lineages. A “ghost” lineage, diverging ~800,000 years ago, contributed ~0.5–1% of DNA to all humans via gene flow in Africa >50,000 years ago. A “super-archaic” lineage (~1.8 million years old) introgressed into Denisovans, then indirectly into modern humans.
Papers with open peer-review reports are less likely to be retracted, says a preprint study. Researchers analysed more than 116,000 papers in Public Library of Science (PLOS) journals and found that among the 40% that opted for publicly available peer-review reports, there were around 100 retractions. There were more than 300 in the closed-review group. It might be that researchers who are confident in their work and who broadly embrace open-science practices are more likely to choose open peer review. In that case, the choice itself could serve as an indicator of article quality.
Dr. Krishna Kumari Challa
Scientists identify fructose as a surprise driver of cancer spread
A new study has uncovered an unexpected link between fructose—a common dietary sugar—and the spread of an aggressive form of ovarian cancer. Published in Nature Aging, the study found that cancer cells not killed by chemotherapy send signals to neighboring tumor cells, helping them become more capable of spreading.
The researchers identified fructose as a key messenger in this process, revealing a previously unrecognized way that treatment-surviving cancer cells may promote the spread of cancer.
Even more interesting, they found that without chemotherapy treatment, consuming the high levels of fructose found in sugary drinks can also signal cancer cells to spread. The fructose finding is especially compelling because it raises the possibility that simple dietary changes could help shape how cancer progresses.
Chemotherapy-surviving ovarian cancer cells secrete fructose, which signals neighbouring tumour cells to become more metastatic in preclinical models. Exogenous fructose at levels typical of sugary drink intake similarly promotes spread. Mechanistically, fructose suppresses cholesterol synthesis, weakening cell–cell adhesion; statins mimic this effect, suggesting potential interaction with chemotherapy responses.
The researchers next aimed to understand why fructose increases cancer cell spread. Through a variety of large-scale analytical techniques, including the use of a CRISPR screen, they discovered that fructose suppresses cholesterol within neighboring cells. Cholesterol is important for cells to stick to each other like a biological glue, so decreased cholesterol allows cells to more easily escape and spread.
The finding that fructose lowers cholesterol production has important clinical implications. Statins, which are taken by 39 million people in the United States, lower cholesterol production.
The team found that statins alone reduced the glue between cells, promoting escape. The research team is now examining whether these medications could be interfering with the effects of chemotherapy—though they stress this isn't a reason for patients to stop taking them.
The researchers are also looking into how this mechanism might extend beyond ovarian cancer.
The chemotherapy-induced senescence-associated secretome promotes cell detachment and metastatic dissemination through metabolic reprogramming, Nature Aging (2026). DOI: 10.1038/s43587-026-01172-5.
yesterday
Dr. Krishna Kumari Challa
New technique pinpoints human DNA inherited from 'ghost' ancestors
Researchers have identified regions of DNA that humans inherited from two unknown ancestors as a result of long-ago interbreeding among modern humans and at least four other archaic human relatives.
While previous research found hints that modern humans had interbred with ancient hominins in addition to now-extinct Neanderthals and Denisovans, the current study pinpoints areas of the genome inherited from these unknown ancestors and establishes a timeline. This was possible using a new technique the researchers developed that leverages hundreds of genomes from modern-day humans to find ancient genealogical relationships.
One of the unknown ancestors, which the researchers refer to as a ghost ancestor, interbred with modern humans in Africa prior to 50,000 years ago, before the most recent migration of Homo sapiens out of Africa into Europe and Asia. These genes comprise around 1% of the genomes of modern humans, comparable to the amount of Neanderthal DNA in the human genome. That unknown hominin lineage split from the modern human lineage around the same time that Neanderthals and Denisovans diverged, about 800,000 years ago, though it interbred with modern humans earlier.
A genealogical method (TRACE) applied to modern human genomes identifies ~2% archaic DNA from two unknown hominin lineages. A “ghost” lineage, diverging ~800,000 years ago, contributed ~0.5–1% of DNA to all humans via gene flow in Africa >50,000 years ago. A “super-archaic” lineage (~1.8 million years old) introgressed into Denisovans, then indirectly into modern humans.
Yulin Zhang et al, Recovering signatures of archaic hominin introgression using ancestral recombination graphs, Science (2026). DOI: 10.1126/science.aef8874. www.science.org/doi/10.1126/science.aef8874
yesterday
Dr. Krishna Kumari Challa
Fewer retractions with open peer-review
Papers with open peer-review reports are less likely to be retracted, says a preprint study. Researchers analysed more than 116,000 papers in Public Library of Science (PLOS) journals and found that among the 40% that opted for publicly available peer-review reports, there were around 100 retractions. There were more than 300 in the closed-review group. It might be that researchers who are confident in their work and who broadly embrace open-science practices are more likely to choose open peer review. In that case, the choice itself could serve as an indicator of article quality.
https://osf.io/preprints/metaarxiv/2b7z5_v1
https://www.nature.com/articles/d41586-026-02282-1?utm_source=Live+...
yesterday