Dogus M. AltintasMolecular biology · Cancer adaptation

Molecular biology · Cancer adaptation

Dogus M. Altintas, PhD

How cancer cells
adapt. Persist.
Invade.

I study how translational control shapes cancer adaptation — connecting stress-responsive MET expression, oncogene priming and the persistence of invasive growth.

THE RESEARCH THREAD01 — 03
01

Environmental stress

Stress-responsive MET translation
02

Oncogene priming

Rewiring the 5′ untranslated region
03

Persistent invasive growth?

A framework for the next questions
Three connected research themes.
A conceptual map, not a demonstrated causal sequence.

Selected discoveries / 2025—2026

Three discoveries, at a glance.

All publications ↗

The EMBO Journal · 2025

Stress activates the ISR, which can increase MET translation.

Stress can drive
MET translation.

Connecting the integrated stress response to MET-dependent invasive growth.

Cell Reports · 2026

Replacing a 5′UTR can change translational output without changing the coding sequence.

Oncogene priming
through UTR rewiring.

Oncogenic fusions can alter translational regulation while preserving protein structure.

Trends Open · 2026 / Opinion

An adaptive programme can resolve, while the proposed cancer framework emphasizes persistence.

What if progression
is failed resolution?

A framework for cancer as the chronic stabilization of invasive growth.

Life Science Alliance · 2026 / Review

The Janus framework.
From homeostasis to maladaptation.

When does a protective stress response become a persistent, disease-associated state? The Janus framework connects the molecular discoveries to this broader question.

Explore Janus and the original figure →
Published Janus framework figure contrasting acute homeostasis and chronic maladaptation.

The researcher behind the questions

From gene regulation
to cancer adaptation.

My work connects molecular mechanisms with a broader question: how does a temporary response become a lasting cellular state?

Explore my scientific trajectory, recent publications and the direction of my proposed independent research programme.

The next chapter / Proposed independent programme

SATURN

When does adaptation
stop being reversible?

SATURN extends these research questions toward the persistence of adaptive cellular states: how they begin, what sustains them, and whether they can resolve.

  1. Initiation
  2. Stabilization
  3. Reversibility
Explore the research vision ↗

Proposed research programme · funding not confirmed.

Scientific discussion & opportunities

Working on a related question?

I welcome conversations about translational control, oncogene regulation and persistent adaptive states.

Get in touch ↗

The people & support behind the work

Collaborations & support

Science grows through shared questions, complementary expertise and collective effort. I am grateful to the colleagues, research platforms and funders who contributed to the work presented here.

Lab alumni

  • Paolo M. ComoglioIFOM ETS, Milan
  • Marina CerquaIFOM ETS, Milan

Research support

Support acknowledged in the featured publications.

With thanks to Fondazione Umberto Veronesi for supporting my research.

With thanks to Fondazione AIRC for supporting the collaborative work presented here.

Research platforms & collaborators

With thanks to the IFOM Cell Biology and Imaging Units, and the Cogentech teams providing genome editing, sequencing, quantitative PCR and genomics support.

I am also grateful to all the collaborators and colleagues whose expertise, discussions and generosity have contributed to this work.