Thaidy

Postdoctoral scholar at @UCSF studying PCa evolution in response to targeted therapy | Molecular biologist & genomics | (she/her) | @[email protected]

[Arc Institute @arcinstitute]

mTOR inhibitors stop cancer cells from dividing, but they rarely kill them. New work in @MolecularCell from @LukeGilbertSF & lab reveals a mechanism connecting mTOR signaling, cholesterol biology, and ferroptosis that could turn growth arrest into cancer cell death.

[Itai Yanai @ItaiYanai]

How does a cell learn? In our new perspective in @Nature we propose a model where the properties of the AP-1 family of transcription factors – stress-induced feedback, regulatory combinatorics & cellular memory – encode a mechanism for cellular learning. https://t.co/Hzmq319EaD

[Ivano Amelio @ivanoamelio]

"A mechanism for adaptive genome regulation in cancer"
@Nature
by @ItaiYanai

https://t.co/6RXXR2EKYA

[Thomas Vierbuchen @TommyVierbuchen]

AP-1 is both day science and night science.

[Paul Brennan @Lyonpaul]

our review on how non-mutagenic factors promote cancer out now in @Nature. Thanks to PROMINENT @CancerGrand colleagues Allan, Eve, Abel and @nlbigas. @IARCWHO

[Cancer Grand Challenges @CancerGrand]

For over two decades, the Hallmarks of Cancer have shaped how we understand, study, and treat cancer and has consistently represented a unifying conceptual framework for cancer biology.

But cancer research doesn’t stand still. New discoveries are challenging long-held assumptions and reshaping the field.

A new review published today as part of the special issue to commemorate 25 years of the original “Hallmarks of Cancer” paper in @CellCellPress highlights how team eDyNAmiC is reframing our understanding of extrachromosomal DNA (ecDNA) and its central role in therapy resistance.

Led by @PaulMischel, team eDyNAmiC is proposing a more holistic perspective by integrating ecDNA into the broader Hallmarks of Cancer framework.

🔗https://t.co/lHO0ZZRb6O

[Hsieh Lab @HsiehLab]

Ever wonder how toggling protein synthesis impacts cellular identity? Dr. Rashmi Mishra @HsiehLab did and through a clever drug screen discovered that the cap-binding domain of eIF4E regulates lineage fate in prostate cancer. Story hit newsstands today: https://t.co/dwv6z2untc

[Niko McCarty. @NikoMcCarty]

Many people think of the genome as a string of "letters." The human genome, say, has 3.2 billion base pairs of DNA organized across 23 pairs of chromosomes.

But the genome is a 3D object. Genes located on entirely different chromosomes might be clustered together. Mutations in these "distant" genes can lead to disease in surprising ways.

For a new paper in @Nature, researchers released several "maps" of human genomes from two types of cells: embryonic stem cells and fibroblasts. They compared methods to see which ones are least biased, and found many long-range interactions between genes.

The article does a good job explaining how “the genome is organized at different scales”:
> On a single chromosome, histones control which parts of the DNA sequence are accessible and expressed.
> At the scale of hundreds of thousands of bases, “chromatin loops in a dynamic manner,” the authors write, bringing distant genes closer together. > Across chromosomes, sequences "cluster together in space to form subnuclear compartments."

Examples abound. Enhancers, for example, are short DNA sequences that regulate the expression of far away genes. They do this by *physically* touching the genes they control; a protein called cohesin grabs the DNA and tugs it into big loops.

Even promoters, which are thought of as being associated with one gene or operon, can cluster together across many genes! A protein, Ronin, grabs promoters and pulls them together. This is apparently done mostly for genes that tend to be "on," as it helps enzymes find genes faster/not have to diffuse far away to find targets. (This also happens with genes that tend to be "off;" so-called polycomb proteins grab onto promoters, cluster them up, and silence all of them at once. It's a way for the cell to conserve energy.)

One consequence of this spooky "action-at-a-distance" is that diseases might arise from mutations in unexpected locations. Editing these regulatory sequences, in other words, might in turn affect a gene located on an entirely different chromosome that *is* associated with that disease.

Genetic mutations linked to autism, for example, are known to disrupt the 3D organization of the genome. A single deletion at a gene, TAL1, also affects its ability to form long-range chromatin interactions with other genes, leading to leukemia. There are probably many other, as-yet-undiscovered, instances of this.

[bioRxiv Genomics @biorxiv_genomic]

Extending cis-regulatory networks using chromatin-RNA interactions https://t.co/e84DO8XqGz #biorxiv_genomic

[Nature Methods @naturemethods]

A Method to Watch: Understanding enhancer logic through synthetic design
https://t.co/2RlZlVbpgl

[Salma Kaochar @Kaochar2]

Congratulations to the @PCFnews 2025 PCF Young Investigators! 👏👏🙌
Over 50% are women this year — a long-awaited milestone. We finally broke the ceiling! #PCFRetreat25

[Prostate Cancer Foundation @PCFnews]

Honoring the legacy of Dr. Felix Feng, a visionary leader whose work transformed how we understand and treat #prostatecancer. Dr. Daniel Spratt reflects on his groundbreaking research in genomics and prostate cancer biology.

[antisense. @razoralign]

SEAM: Uncovering the Mechanistic Landscape of Regulatory DNA with Deep Learning https://t.co/BiN3nlH2I2

[Shyam Prabhakar Lab @shyam_lab]

Years ago we tried to model cancer-associated fibroblast (CAF) subtypes in vitro, but gave up because only the proliferative subtype survived culture (duh!). This study could change all that: Perturb-seq with CRISPRa of 1,836 TFs induces diverse fibroblast states in vitro(!). 👏

[Nature Biotechnology @NatureBiotech]

Programmable promoter editing for precise control of transgene expression https://t.co/6jC9QnVgzn

[Oded Rechavi @OdedRechavi]

Fwd: Fwd: “I hope this email finds you well”

[Molecular Cell @MolecularCell]

Single-stranded DNA-binding proteins are essential components of the architectural LDB1 protein complex https://t.co/epgjSsGX9Z

[Science Magazine @ScienceMagazine]

Researchers have developed a #DeepLearning system called BioEmu that rapidly generates diverse protein conformations, enabling fast, accurate insights into protein flexibility and function.

Learn more this week in Science: https://t.co/Pe15hm9F52

[Filip K. Knop @Filip_Knop]

Today, @HannahVigh et al. unleash a freely available and searchable database of the human intestinal transcriptome - an atlas of the expression of 19,739 genes from 16 sites along the intestinal tract. Check out the landscape of your favourite gene here: https://t.co/ydcWR4pbCX

[Prof. Nikolai Slavov @slavov_n]

The heterogeneity of HeLa cell-lines undermines reproducibility.

HeLa cells were obtained without informed consent.

==> Researchers should avoid using HeLa cells unless required by a special justification.