Oncology Drug– category –

Seeing What Matters — Composite Diagnostics (Imaging × Transcriptome × CNV) Therapy moves only when we can answer “for whom, when, and what.” This chapter maps a beginner-friendly framework for composite diagnostics across imaging, trans...

Plasticity & Escape — A Gentle Guide to OPC/AC/MES State Transitions Why do single agents rarely suffice? Because GBM has plasticity—it can shift among OPC-like, AC-like, and MES-like faces. Let’s build intuition and turn it into a p...

The Moving Tumor — Intuitive Guide to ECM, Adhesion, and White-Matter Tract Invasion Why does GBM come back even after “maximal” surgery? This beginner-first chapter explains the mobility of GBM via ECM, adhesion signaling, and the highw...

Extinguishing the Spark — Microenvironment & Immunity (MIF–CD74 Primer) This beginner-friendly chapter looks beyond the tumor mass to the “place” that makes GBM easier to grow: the microenvironment. We introduce brain immunity, ECM, ...

Where It Begins — SVZ Hypothesis and Precancerous Cells (pre-CC) Beyond the tumor mass: a beginner’s map of how GBM may arise, diversify, and interact with its “niche”. Today’s Goals (3-Minute Preview) Understand what the SVZ (subventric...

A gentle, beginner-friendly walkthrough of GBM care from first symptoms to initial therapy and what to consider at recurrence—using clear, minimal jargon. Today’s Goals (3-Minute Preview) Recognize common presenting symptoms that trigger...

A beginner-friendly introduction: understand the brain’s building blocks and a simple, number-based overview of GBM (incidence, prognosis, and quality of life). Series Table of Contents Part 0 | GBM Primer: Brain Basics and By-the-Number...

This Part focuses on how extrachromosomal DNA (ecDNA) shapes spatial heterogeneity and evolution in glioblastoma (GBM). We outline the extreme copy-number gains of drivers (EGFR/PDGFRA/CDK4) on ecDNA, region-to-region response gaps, and ...

Extrachromosomal DNA (ecDNA) reshapes oncogene dosage, transcription, phenotypes, and spatial organization, thereby accelerating intratumor heterogeneity and therapy resistance. In Part 1, we briefly introduce non-GBM evidence up front a...

For over four decades, KRAS symbolized the “undruggable.” By the mid-2020s, it became the flagship of precision oncology. This final chapter summarizes that evolution—from structural biology to AI-driven therapeutics—and looks ahead to h...

The race to drug KRAS is reshaping not only science but the entire biotech ecosystem. Once deemed “undruggable,” KRAS became a proving ground for startups, academic spinouts, and AI-driven discovery. This part reviews key players—Revolut...

The rise of KRAS inhibitors marked the end of the “undruggable” era—but tumors adapt swiftly. Resistance often stems from a cooperative reactivation between mutant and wild-type RAS. This sixth installment dissects the molecular basis of...

KRAS has evolved from the icon of “undruggable” to the engine of next-generation oncology. Building on the success of allele-selective inhibitors (e.g., G12C), the mid-2020s ushered in three powerful paradigms: RAS(ON) inhibition, pan-KR...

KRAS research has now transcended oncology. Recent studies reveal that KRAS signaling interconnects with immunity, cellular aging, and even regenerative medicine. In this fourth installment, we redefine KRAS as a “life regulator” rather ...

As KRAS-targeted therapy enters a new era, one unexpected player has captured the spotlight: Wild-type KRAS (WT-KRAS). While mutant KRAS has long been seen as the dominant oncogenic driver, emerging evidence shows that its wild-type coun...

In Part 1, we traced the long struggle to target KRAS and the breakthrough that made the “undruggable” druggable. Now we turn to a crucial question: how do different KRAS alleles shape tumor biology, signaling behavior, and clinical outc...

Few oncogenes have shaped the landscape of cancer research as profoundly as KRAS. Since the first RAS mutation was identified in human bladder cancer cells in 1982, this small GTP-binding protein has fascinated scientists as both a myste...

Takeaway: Lymph-node–targeted amphiphile delivery achieved robust dual CD4/CD8 responses. A data-driven ~9.17× immune threshold aligned with RFS/OS gains and ctDNA negativity in the adjuvant MRD setting. Contents 1. One-Minute Summary 2....

Takeaway: the field is coalescing around shared neoantigens × off-the-shelf × adjuvant MRD. Elicio (ELI-002 7P) leads the pack; academic SLP + poly-ICLC programs and Gritstone’s SLATE-KRAS follow. With V941 halted, the landscape is clear...

In Part 1, we reviewed mechanisms by which NK cells contribute to resistance against immune checkpoint blockade (ICB). In this follow-up article (Part 2), we discuss the clinical implications, potential strategies, and future directions ...