Two Observatories, One Cosmic Eye: Hubble and Euclid View Cat’s Eye Nebula - UNIVERSE

ESA/Hubble & NASA, ESA Euclid/Euclid Consortium/NASA/Q1-2025, J.-C. Cuillandre & E. Bertin (CEA Paris-Saclay), Z. Tsvetanov

This new NASA/ESA Hubble Space Telescope image features one of the most visually intricate remnants of a dying star: the Cat’s Eye Nebula, also known as NGC 6543. This extraordinary planetary nebula lies in the constellation Draco and has captivated astronomers for decades with its elaborate and multilayered structure. Observations with ESA’s Gaia mission place the nebula at 4,400 light-years away.

Planetary nebulae, so-called because of their round shape, which made them appear to look like planets when viewed through early telescopes, are in fact expanding gas thrown off by stars in their final stages of evolution. It was the Cat’s Eye Nebula itself where this fact was first discovered in 1864 — examining the spectrum of its light reveals the emission from individual molecules that’s characteristic of a gas, distinguishing planetary nebulae from stars and galaxies. 

Hubble also revolutionized our understanding of planetary nebulae; its detailed images showed that the simple, circular appearance of a planetary nebula seen from the ground belies a very complex morphology. This was particularly true of the Cat’s Eye Nebula, where Hubble images in 1995 revealed never-before-seen structures that broadened our understanding of how planetary nebulae come to be.

In this new image, Hubble captures the very core of billowing gas with the High Resolution Channel sub-instrument on its Advanced Camera for Surveys (ACS). This instrument is optimized for taking very sharp images of fine details in a small area, such as the complex features at the heart of the Cat’s Eye Nebula. The data reveal a tapestry of concentric shells, jets of high-speed gas and dense knots sculpted by shock interactions, features that appear almost surreal in their intricacy. These structures are believed to record episodic mass loss from the dying star at the nebula’s center, creating a kind of cosmic “fossil record” of its final evolutionary stages. Part of these data were also used in a previous image of the Cat’s Eye Nebula, released in 2004. Previously unused data from ACS is combined with state-of-the-art image processing to create this new image, the sharpest yet taken of this nebula.

ESA/Hubble & NASA, Z. Tsvetanov

This time, Hubble is joined by ESA’s Euclid space telescope to create a new image of NGC 6543. The combined eyes of Hubble and Euclid reveal the remarkable complexity of stellar death in this object. Though primarily designed to map the distant universe, Euclid captures the Cat’s Eye Nebula as part of its deep imaging surveys. In Euclid’s wide, near-infrared, and visible light view, the arcs and filaments of the nebula’s bright central region are situated within a halo of colorful fragments of gas zooming away from the star. This ring was ejected from the star at an earlier stage, before the main nebula at the center formed. The whole nebula stands out against a backdrop teeming with distant galaxies, demonstrating how local astrophysical beauty and the farthest reaches of the cosmos can be seen together with Euclid.

In Euclid’s wide, near-infrared, and visible light view, the arcs and filaments of the nebula’s bright central region are situated within a halo of colorful fragments of gas zooming away from the star. This ring was ejected from the star at an earlier stage, before the main nebula at the center formed. Hubble captures the very core of the billowing gas with high-resolution visible-light images, adding extra detail in the center of this image. The whole nebula stands out against a backdrop teeming with distant galaxies, demonstrating how local astrophysical beauty and the farthest reaches of the cosmos can be seen together in modern astronomical surveys. Together, these missions provide a rich and complementary view of NGC 6543 — revealing the delicate interplay between stellar end-of-life processes and the vast cosmic tapestry beyond.

ESA/Hubble & NASA, ESA Euclid/Euclid Consortium/NASA/Q1-2025, J.-C. Cuillandre & E. Bertin (CEA Paris-Saclay), Z. Tsvetanov

Within this broad view of the nebula and its surroundings, Hubble captures the very core of the billowing gas with a new high-resolution visible-light image, adding extra detail in the center of this image. The data reveal a tapestry of concentric shells, jets of high-speed gas and dense knots sculpted by shock interactions, features that appear almost surreal in their intricacy. These structures are believed to record episodic mass loss from the dying star at the nebula’s center, creating a kind of cosmic “fossil record” of its final evolutionary stages.

Combining the focused view of Hubble with Euclid’s deep field observations not only highlights the nebula’s exquisite structure but also places it within the broader context of the universe that both space telescopes explore. Together, these missions provide a rich and complementary view of NGC 6543 — revealing the delicate interplay between stellar end-of-life processes and the vast cosmic tapestry beyond. 

Source: Scoria Cones on Earth and Mars - NASA Science 

Preventing breast cancer resistance to CDK4/6 inhibitors using genomic findings - medicalxpress

Germline–somatic interactions in breast cancer. Credit: Nature (2026). DOI: 10.1038/s41586-026-10197-0

Researchers at Memorial Sloan Kettering Cancer Center (MSK) have made an important discovery about how genetic mutations in breast cancer patients can interact and drive resistance to certain drugs called CDK4/6 inhibitors. This finding, published in Nature, suggests a new strategy for predicting and preventing resistance to specific therapies based on the tumor's genetic profile.

"This represents a major advance in understanding and predicting cancer behavior in response to treatment," says physician-scientist Pedram Razavi, MD, Ph.D., who led the study with physician-scientist Sarat Chandarlapaty, MD, Ph.D. The study's first author was Anton Safonov, MD, a physician-scientist in the MSK Breast Translational Program.

"To our knowledge, this is the first example showing that a complete genomic analysis of breast cancer, including both inherited and tumor-specific alterations, can predict the precise biological mechanism of resistance before therapy even begins," Dr. Razavi adds.

Predicting gene loss and breast cancer therapy resistance

Many patients with breast cancer eventually develop resistance to CDK4/6 inhibitor combinations. But about 10% do so in a specific way: Their cancer cells lose a protective gene called RB1. The new study found two warning signs before treatment that a patient may develop resistance:

• DNA repair problems, especially one called homologous recombination deficiency (HRD), where cancer cells can't fix broken DNA properly.
• The initial genetic makeup of the tumor, which can help doctors predict which cancers might lose the RB1 gene.

These findings provide a path toward identifying high-risk tumors and guiding more personalized treatment decisions.

Based on the discovery, a global, randomized phase 3 clinical trial called EvoPAR-Breast01 is now enrolling patients to test the new approach for their first treatment, which replaces CDK4/6 inhibitors and instead uses therapies targeting HRD. Patients in the trial will have newly diagnosed ER-positive, HRD-positive metastatic breast cancer.

"Cancers don't have endless ways to escape treatment," Dr. Razavi says. "They are one- or two-trick ponies, and those tricks are often determined by their inherited or tumor-specific genetic features. If we can predict what they're capable of, we can intercept it before the resistance happens. That's what we're trying to do in this trial—forecast the mechanism of resistance and hopefully improve the outcomes for our patients."

Key findings:

The research involved analyzing data from more than 5,800 MSK breast cancer patients to understand how inherited (germline) and acquired (somatic) genetic changes affect how a breast tumor grows and responds to therapy. This analysis revealed:

• Patients born with mutations in the BRCA2 gene are more likely to have additional mutations in another gene called RB1.
• These patients do poorly when they are treated with the standard CDK4/6 inhibitor–based therapy.
• Tumors carrying only a single copy of the RB1 gene before starting CDK4/6 inhibitor treatment are much more likely to develop complete RB1 loss.
• Underlying DNA repair defects—especially HRD—further drive the resistance mechanism.
• In preclinical models supported by clinical data, drugs called PARP inhibitors resulted in better outcomes than CDK4/6 inhibitors in tumors with HRD.
• Importantly, some tumors developed "reversion mutations" that restore DNA repair function. Once HRD is reversed, these tumors may regain sensitivity to CDK4/6 inhibitors. This suggests that using PARP inhibitors early may not only improve initial outcomes, but also potentially restore responsiveness to CDK4/6 inhibitors later.

The research is part of a broader effort at MSK to anticipate and counteract breast cancer treatment resistance, led by Dr. Razavi, Dr. Chandarlapaty, and other MSK experts from many disciplines.

Since 2018, research efforts led by Dr. Chandarlapaty and Dr. Razavi have uncovered multiple mechanisms by which breast cancers develop resistance to CDK4/6 inhibitors, including loss of RB1 function and alterations in another tumor suppressor, TP53.

In this latest study, the researchers found that inheriting a BRCA2 mutation—and certain other genes linked to HRD—can cause DNA problems that make it more likely for the RB1 gene to mutate as well. This explains why these patients don't respond well to CDK4/6 inhibitors—losing both tumor suppressor genes is like a car with failed brakes smashing through a barrier.

In addition, the researchers showed that defective DNA repair through HRD independently increases the likelihood of acquiring RB1 alterations. To extend the analogy, this is akin to a car with a frayed brake line: It may appear functional at first but is particularly vulnerable to failing under stress.

"This study gives us the opportunity to address drug resistance proactively, rather than reactively," Dr. Safonov says. "This will allow us to stay one step ahead of breast cancer by gaining the ability to peek at its 'battle plans.'"

In a series of lab experiments conducted in Dr. Chandarlapaty's laboratory, co-first author Minna Lee, MD, used patient-derived xenograft models from BRCA2-mutant breast cancers. She found that CDK4/6 inhibitors did not work as well on these tumors, which were prone to losing the RB1 gene during treatment.

These laboratory results confirmed and explained what doctors were seeing in patients: There was a biological reason why these treatments failed. Importantly, collaborating with international research partners, the team showed that PARP inhibitors consistently worked better than CDK4/6 inhibitors in HRD-positive tumors.

The lab evidence strongly supported giving patients with DNA repair problems (HRD-positive) PARP inhibitors first instead of CDK4/6 inhibitors.

The convergence of genomic, laboratory, and clinical evidence led to quick approval to launch the global phase 3 EvoPAR-Breast01 clinical trial.

"This highlights the strength of our program and how we are able to very quickly translate our findings to a potentially practice-changing clinical trial," Dr. Razavi says. "There aren't many examples where translational data were compelling enough to move directly into a phase 3 study without developing earlier clinical evidence."

"This study underscores how critical it is to integrate clinical observations with rigorous laboratory modeling," Dr. Chandarlapaty says. "The ability to test hypotheses generated from data in patient-derived models and engineered cell lines allows us to move beyond correlation and establish biological causality. This gives us the confidence to design trials that meaningfully change patient care."

The trial will evaluate whether the combination of the highly selective PARP inhibitor drug saruparib and the hormonal therapy camizestrant is more effective than treatments with standard-of-care CDK4/6 inhibitors and hormonal therapy. 

Provided by Memorial Sloan Kettering Cancer Center 

by Jim Stallard, Memorial Sloan Kettering Cancer Center

edited by Stephanie Baum, reviewed by Robert Egan 

Source: Preventing breast cancer resistance to CDK4/6 inhibitors using genomic findings