Utah Department of Emergency Medical Services reiterate the importance of staying safe in extreme heat
The Utah Department of Emergency Medical Services reminded that simple tips like drinking water, wearing sunscreen, and making sure you take breaks can be key to survival during extreme heat.
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Gizmodo
29 minutes ago
- Gizmodo
Bats Have Cancer-Fighting ‘Superpowers'—Here's What That Means for Humans
When you think of longevity in animals, chances are that the Greenland shark will immediately come up. After all, researchers estimate that the enigmatic animal can live for at least 250 years. It turns out, however, that bats also hold their own when it comes to lifespan, with some species living up to 25 years—equivalent to 180 human years—and they tend to do it cancer-free. Researchers from the University of Rochester (UR) have investigated anti-cancer 'superpowers,' as described in a UR statement, in four bat species: the little brown bat, the big brown bat, the cave nectar bat, and the Jamaican fruit bat. The results of their investigation could have important implications for treating cancer in humans. 'Longer lifespans with more cell divisions, and longer exposure to exo- [external] and endogenous [internal] stressors increase cancer incidence,' the researchers wrote in a study published last month in the journal Nature Communications. 'However, despite their exceptional lifespans, few to no tumors have been reported in long-lived wild and captive populations of bats.' Led by biologists Vera Gorbunova and Andrei Seluanov from the UR Department of Biology and Wilmot Cancer Institute, the team identified a number of biological defenses that help bats avoid the disease. For example, bats have a tumor-suppressor gene, called p53. Specifically, little brown bats carry two copies of the gene, and have high p53 activity, which can get rid of cancer cells during apoptosis, a biological process that eliminates unwanted cells. 'We hypothesize that some bat species have evolved enhanced p53 activity as an additional anti-cancer strategy, similar to elephants,' the researchers explained. Too much p53, though, runs the risk of killing too many cells. Clearly, bats are able to find the right apoptosis balance. Humans also have p53, but mutations in the gene—which disrupt its anti-cancer properties—exist in around 50% of human cancers. The researchers also analyzed the enzyme telomerase. In bats, the telomerase expression allows bat cells to multiply endlessly. That means they don't undergo replicative senescence: a feature that restricts cell proliferation to a certain number of divisions. Since, according to the study, senescence 'promotes age-related inflammation contributing to the aging process,' bats' lack thereof would seem to promote longevity. And while indefinite cell proliferation might sound like the perfect cancer hotbed, bats' high p53 activity can kill off any cancer cells. Furthermore, 'bats have unique immune systems which allows them to survive a wide range of deadly viruses, and many unique immune adaptations have been described in bats,' the researchers wrote. 'Most knowledge of the bat immune systems comes from studies of bat tolerance to viral infections deadly to humans. However, these or similar immune adaptations may also recognize and eliminate tumors,' as well as 'temper inflammation, which may have an anticancer effect.' Cells have to go through several steps, or 'oncogenic hits,' to become harmful cancerous cells. Surprisingly, the researchers also found that it only takes two hits for normal bat cells to become malignant, meaning bats aren't naturally resistant to cancer—they just have 'robust tumor-suppressor mechanisms,' as described in the statement. The team's findings carry important implications for treating cancer. Specifically, the study confirms that increased p53 activity—which is already targeted by some anti-cancer drugs—can eliminate or slow cancer growth. More broadly, their research is yet another example of scientists turning to nature for solutions to human challenges on all scales. Though the study focuses on bats, the ultimate aim is, always, finding a cure for cancer in humans.
Medscape
39 minutes ago
- Medscape
IRONMAN: Can PSA Guide Metastatic Prostate Cancer Care?
CHICAGO — Prostate-specific antigen (PSA) levels could help guide treatment decisions for patients with metastatic hormone-sensitive prostate cancer, according to real-world findings from the IRONMAN study. Specifically, an undetectable PSA nadir — defined as PSA level < 0.2 ng/mL — predicted a good prognosis and a PSA level ≥ 0.2 ng/mL predicted poor prognosis among patients receiving androgen deprivation therapy (ADT) or androgen receptor pathway inhibitor (ARPI) therapy for 6-12 months, according to Michael Ong, MD, who presented the findings at the 2025 American Society of Clinical Oncology annual meeting. In other words, this real-world study found that absolute PSA at 6 and 12 months is prognostic in this patient population, said Ong, a medical oncologist at Ottawa Hospital Research Institute, Canada. Patients with a poor prognosis could then be considered for clinical trials offering therapy escalation, whereas those with a better prognosis — particularly those with PSA < 0.1 ng/mL — could be considered for de-escalation, said Ong. Ong explained that prior phase 3 studies have demonstrated that PSA > 0.2 ng/mL is associated with poor prognosis in patients receiving ADT and ARPI. However, data in real-world settings remain limited. Some patients with rapid PSA decline never progress, whereas others develop early resistance despite intensive therapy, he explained. The IRONMAN study set out to answer two main questions: When should PSA cutoffs be interpreted for prognostic significance? And how may PSA cutoffs differ in real-world patients? To this end, Ong and his colleagues included 1219 patients from the prospective IRONMAN cohort with metastatic hormone-sensitive prostate cancer who had received ADT and ARPI therapy, with or without docetaxel, and had PSA data available. PSA was stratified into three groups: ≥ 0.2 ng/mL, 0.10-0.19 ng/mL, and < 0.10 ng/mL. The research team constructed a 12-month landmark population to assess conditional overall survival (OS) and progression-free survival (PFS) at 6 and 12 months across each PSA level. The 12-month analysis was the primary study outcome. Patients were a median age of 70 years, 58% had Gleason score of 8-10, and 75% had de novo metastatic disease. Overall, most (74%) were White and just over half were enrolled from centers outside US or Canada. ARPI agents included abiraterone acetate (44%), apalutamide (21%), enzalutamide (22%), or darolutamide (13%), and 12% of patients received docetaxel in addition to doublet therapy with ADT plus ARPI. PSA levels shifted across the two time points. At 6 months, 52% of patients had a PSA < 0.2 ng/mL, whereas 48% had a PSA level ≥ 0.2 ng/mL. At 12 months, 68% had PSA levels < 0.2 ng/mL and 32% had levels ≥ 0.2 ng/mL. Both the 6- and 12-month landmark analyses showed that PSA ≥ 0.2 ng/mL was associated with worse conditional OS and PFS compared with PSA < 0.2 ng/mL. Ong broke down conditional OS and PFS at 12 months — the primary study outcome —by absolute PSA levels. Absolute PSA 3-year overall survival 3-year progression-free survival OS mortality risk (adjusted hazard ratio) ≥ 0.2 ng/mL 45% 41% 4.85 (3.36-7.01) 0.10-0.19 ng/mL 79% 62% 1.34 (0.82-2.20) < 0.1 ng/mL 84% 80% Reference After adjustment for confounders, PSA ≥ 0.2 ng/mL was associated with an almost fivefold higher risk for death at 12 months (adjusted hazard ratio, 4.85). Ong noted that PSA was prognostic of overall survival regardless of ARPI class or whether patients received doublet or triplet therapy with docetaxel. Invited discussant Rahul Aggarwal, MD, agreed that a PSA nadir between 6 and 12 months 'is strongly prognostic for progression-free and overall survival.' However, Aggarwal cautioned, although 'it is tempting to use PSA nadir to guide treatment decisions in clinical practice,' the approach has not been validated. Plus, other factors and biomarkers may play a role in treatment decisions and help optimize outcomes, including quality of life, treatment and financial toxicity, and the role of the tumor suppressor gene PTEN , added Aggarwal, of the University of California, San Francisco. 'We await randomized trial data to know, in fact, whether we should use this to guide treatment decision-making,' said Aggarwal. Such trials are underway. Ong is co-chair of a phase 3 study assessing survival after treatment escalation for patients with PSA ≥ 0.2 ng/mL after 6-12 months of ADT and ARPI therapy. Another phase 3 study will assess treatment de-escalation in those with PSA ≤ 0.2 ng/mL at 6-12 months after treatment initiation. This study's principal funder was the Movember Foundation; the Prostate Cancer Clinical Trials Consortium was a trial sponsor, plus Amgen, Astellas, AstraZeneca, Bayer, Janssen, Merck, Novartis and Sanofi provided funding support. Ong disclosed relationships with AstraZeneca, Bayer, Bristol-Myers Squibb, EMD Serono, Janssen, Merck, Novartis/AAA, Pfizer, Sanofi, and Ipsen. Aggarwal disclosed relationships with Alessa Therapeutics, Amgen, AstraZeneca, Bayer, BioXcel Therapeutics, Boxer Capital, Curio Science, and others.
Associated Press
an hour ago
- Associated Press
GeoVax to Participate in BIO International Convention 2025
ATLANTA, GA - June 12, 2025 ( NEWMEDIAWIRE ) - GeoVax Labs, Inc. (Nasdaq: GOVX), a clinical-stage biotechnology company developing multi-antigen vaccines and immunotherapies, today announced that company representatives will attend the 2025 BIO International Convention being held June 16-19, 2025 at the Boston Convention and Exhibition Center in Boston, Massachusetts. The BIO International Convention is the world's largest gathering of the biotechnology industry, attracting thousands of biotechnology and pharmaceutical executives from around the globe. The event provides an ideal venue for companies to engage with potential partners, investors, and policymakers. During the convention, GeoVax will participate in business development and partnering meetings to discuss its expanding pipeline of infectious disease and cancer immunotherapies, including GEO-MVA, a Modified Vaccinia Ankara (MVA)-based vaccine targeting Mpox and smallpox; GEO-CM04S1, a multi-antigen COVID-19 vaccine candidate; and Gedeptin(R), a gene-directed enzyme prodrug therapy for the treatment of solid tumors. GeoVax's participation at BIO 2025 supports its broader business development strategy, including ongoing efforts to establish strategic partnerships, expand manufacturing capabilities, and align with public and private sector priorities in pandemic preparedness, oncology, and biodefense. About GeoVax GeoVax Labs, Inc. is a clinical-stage biotechnology company developing novel vaccines against infectious diseases and therapies for solid tumor cancers. The Company's lead clinical program is GEO-CM04S1, a next-generation COVID-19 vaccine currently in three Phase 2 clinical trials, being evaluated as (1) a primary vaccine for immunocompromised patients such as those suffering from hematologic cancers and other patient populations for whom the current authorized COVID-19 vaccines are insufficient, (2) a booster vaccine in patients with chronic lymphocytic leukemia (CLL) and (3) a more robust, durable COVID-19 booster among healthy patients who previously received the mRNA vaccines. In oncology the lead clinical program is evaluating a novel oncolytic solid tumor gene-directed therapy, Gedeptin(R), having recently completed a multicenter Phase 1/2 clinical trial for advanced head and neck cancers. The Company is also developing GEO-MVA, a vaccine targeting Mpox and smallpox. GeoVax has a strong IP portfolio in support of its technologies and product candidates, holding worldwide rights for its technologies and products. For more information about the current status of our clinical trials and other updates, visit our website: Company Contact: [email protected] 678-384-7220 Investor Relations [email protected] 212-698-8696 Contact: Media Contact: Jessica Starman [email protected] View the original release on
