Evidence map›Paper›PMID 42218676›Full record

ReviewMagyar onkologia2026

Reframing cancer drug resistance: transporters, persister cells, senescence, and emerging therapeutic strategies.

Péter Nagy, Anna Kamilla Kis, Eszter Bajtai, Ines Lidia Haffaressas, Balázs Gombos, Dóra Bereczki, Kornélia Szebényi, Gergely Szakács, Szilárd Tóth, András Füredi

Abstract readReview
In one paragraph

Review in Magyar onkologia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Péter NagyCenter of Excellence of the Hungarian Academy of Sciences, HUN-REN Research Centre for Natural Sciences, Institute of Molecular Life Sciences, Budapest, Hungary. furedi.andras@ttk.hu.
Anna Kamilla KisCenter of Excellence of the Hungarian Academy of Sciences, HUN-REN Research Centre for Natural Sciences, Institute of Molecular Life Sciences, Budapest, Hungary. furedi.andras@ttk.hu.
Eszter BajtaiCenter of Excellence of the Hungarian Academy of Sciences, HUN-REN Research Centre for Natural Sciences, Institute of Molecular Life Sciences, Budapest, Hungary. furedi.andras@ttk.hu.
Ines Lidia HaffaressasCenter of Excellence of the Hungarian Academy of Sciences, HUN-REN Research Centre for Natural Sciences, Institute of Molecular Life Sciences, Budapest, Hungary. furedi.andras@ttk.hu.
Balázs GombosCenter of Excellence of the Hungarian Academy of Sciences, HUN-REN Research Centre for Natural Sciences, Institute of Molecular Life Sciences, Budapest, Hungary. furedi.andras@ttk.hu.
Dóra BereczkiCenter of Excellence of the Hungarian Academy of Sciences, HUN-REN Research Centre for Natural Sciences, Institute of Molecular Life Sciences, Budapest, Hungary. furedi.andras@ttk.hu.
Kornélia SzebényiCenter of Excellence of the Hungarian Academy of Sciences, HUN-REN Research Centre for Natural Sciences, Institute of Molecular Life Sciences, Budapest, Hungary. furedi.andras@ttk.hu.
Gergely SzakácsCenter of Excellence of the Hungarian Academy of Sciences, HUN-REN Research Centre for Natural Sciences, Institute of Molecular Life Sciences, Budapest, Hungary. furedi.andras@ttk.hu.
Szilárd TóthCenter of Excellence of the Hungarian Academy of Sciences, HUN-REN Research Centre for Natural Sciences, Institute of Molecular Life Sciences, Budapest, Hungary. furedi.andras@ttk.hu.
András FürediCenter of Excellence of the Hungarian Academy of Sciences, HUN-REN Research Centre for Natural Sciences, Institute of Molecular Life Sciences, Budapest, Hungary. furedi.andras@ttk.hu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer drug resistance remains one of the greatest barriers to durable therapeutic success. Here, we reframe resistance as a dynamic landscape shaped by transporter‑mediated efflux, reversible drug‑tolerant persister states, and therapy‑induced senescence. This review highlights areas where our group has made substantial contributions, with a particular focus on our own experimental and conceptual advances. We show how P‑glycoprotein (P-gp) overexpression, traditionally viewed as an obstacle sustaining cancer multidrug resistance (MDR), creates exploitable metabolic vulnerabilities, enabling the development of MDR‑selective compounds. We demonstrate that persister cells rely on transient P‑gp-mediated detoxification, revealing a therapeutic window during drug‑free intervals. We further show that senescence is not a terminal fate but a relapse‑initiating state requiring targeted intervention. Finally, we illustrate how pharmacokinetics and dosing schedules can be harnessed to reshape tumor evolution, culminating in LiPyDau, a next‑generation liposomal anthracycline with durable activity against resistant tumors. Together, these insights outline a unified strategy for anticipating, intercepting, and ultimately overcoming cancer drug resistance.

Indexed as

Antineoplastic AgentsCellular SenescenceDrug Resistance, MultipleDrug Resistance, NeoplasmNeoplasmsAnimalsAnthracyclinesATP Binding Cassette Transporter, Subfamily B, Member 1HumansAnthracyclinesAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily B, Member 1

Identifiers

PMID42218676
PMCPMC13233020

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.