ISLAMABAD:
Prime Minister Shehbaz Sharif on Monday ordered to immediate…

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The webcast, as with other selected presentations regarding developments in Amgen’s business given by management at certain investor and medical conferences, can be found on Amgen’s website, www.amgen.com, under Investors. Information regarding presentation times, webcast availability and webcast links are noted on
About Amgen
Amgen discovers, develops, manufactures and delivers innovative medicines to help millions of patients in their fight against some of the world’s toughest diseases. More than 40 years ago, Amgen helped to establish the biotechnology industry and remains on the cutting-edge of innovation, using technology and human genetic data to push beyond what’s known today. Amgen is advancing a broad and deep pipeline that builds on its existing portfolio of medicines to treat cancer, heart disease, osteoporosis, inflammatory diseases and rare diseases.
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In August 2025, artist Liam Gillick spoke with photographer and filmmaker Michel Auder. The transcript of their conversation was edited for the present publication.
Liam Gillick: All your work evokes a peculiar consciousness. There is also…

Vorasidenib (Voranigo) was associated with lower volumetric tumor growth rates (TGR) compared with placebo in patients with grade 2 glioma harboring IDH1/2 mutations, according to data from exploratory analyses from the phase 3 INDIGO trial (NCT04164901) presented at the
Across linear, biexponential, and velocity of diametric expansion (VDE) modeling approaches, patients receiving vorasidenib exhibited substantially lower on-treatment TGRs than those receiving placebo, with these differences translating into clinically meaningful improvements in progression-free survival (PFS) and time to next intervention (TTNI).
Using linear TGR, vorasidenib produced a mean on-treatment tumor growth of 0.4 mL per 6 months (95% CI, –0.2 to 1.0) compared with 2.7 mL per 6 months (95% CI, 1.9-3.4) for placebo (difference, –2.3; 95% CI, –3.3 to –1.4; P < .001). Multivariable Cox modeling showed that each 1-mL per 6-month increase in TGR increased the risk of progression by 4.6% and the risk of requiring next intervention by 5.1%. Within this study, vorasidenib significantly reduced the risks of PFS (HR, 0.376; 95% CI, 0.268-0.526) and TTNI (HR, 0.276; 95% CI, 0.177-0.431).
“On-treatment TGR is a strong predictor of PFS and TTNI,” lead study investigator Benjamin M. Ellingson, PhD, MS, and colleagues wrote in a poster presentation of the data. “In patients with IDH1/2[-mutant] glioma enrolled into the INDIGO trial, on-treatment TGR was substantially lower in those receiving vorasidenib than in those receiving placebo, as measured using 3 different approaches.”
Ellingson currently serves as director of MRI Research and a professor of radiology, psychiatry, bioengineering, and neurosurgery within the David Geffen School of Medicine at the University of California, Los Angeles.
In August 2024,
This analysis utilized volumetric TGR modeling to evaluate whether early tumor growth dynamics could help predict clinical outcomes in patients with grade 2, IDH1/2-mutated diffuse glioma treated in the phase 3 INDIGO trial. The randomized, placebo-controlled study enrolled adults with grade 2 glioma harboring IDH1/2 mutations, and investigators compared vorasidenib, an oral brain-penetrant IDH1/2 inhibitor, with placebo. Tumor volume data from patients assigned to vorasidenib (n = 168) or placebo (n = 163) were analyzed.
Investigators assessed tumor growth using 3 distinct modeling approaches: a linear regression model measuring growth in mL per six months, a biexponential model incorporating a tumor growth parameter, and a velocity of diametric expansion model quantifying millimeters per year.3 Individual TGRs were derived from volumetric measures obtained during the first 6 months of on-treatment imaging. These TGR metrics were then correlated with PFS and TTNI to determine their predictive relevance for treatment outcomes in this molecularly defined glioma population.
Consistent findings were observed using biexponential modeling: mean tumor growth (g-value) was lower with vorasidenib (0.00097; 95% CI, 0.00079-0.00114) vs placebo (0.00125; 95% CI, 0.00110-0.00141; P = .0197), and slower-growing tumors were associated with superior PFS and TTNI.1 VDE analysis similarly demonstrated a marked difference in tumor expansion velocity between treatment arms, with a mean on-treatment VDE of 0.2 mm/year (95% CI, –0.3 to 0.6) for vorasidenib vs 3.1 mm/year (95% CI, 2.6-3.6) for placebo (P < .001).
The VDE analysis further demonstrated that on-treatment tumor growth dynamics strongly correlate with clinical outcomes in the INDIGO trial. Using linear regression modeling to characterize individual tumor expansion rates, vorasidenib markedly reduced on-treatment VDE compared with placebo, with a mean VDE of 0.2 mm per year (95% CI, –0.3 to 0.6) in the vorasidenib arm vs 3.1 mm per year (95% CI, 2.6-3.6) in the placebo, reflecting a significant mean difference of –2.9 mm per year (P < .001).
When VDE values were stratified into clinically relevant categories, slower expansion rates consistently aligned with improved PFS and TTNI. Patients with the lowest VDE (≤ –0.50 mm/year) demonstrated the most favorable outcomes, whereas those with rapid tumor expansion (>3.13 mm/year) experienced markedly shorter PFS (median, 8.4 months) and TTNI (median, 12.0 months). Intermediate ranges (>1.27 to ≤3.13 mm/year) also conveyed reduced benefit, with a median TTNI of 28.8 months.
