Evidence map›Paper›PMID 35247928›Full record

ArticleMolecular cancer therapeutics2022

Optimal Strategy and Benefit of Pulsed Therapy Depend On Tumor Heterogeneity and Aggressiveness at Time of Treatment Initiation.

Deepti Mathur, Bradford P Taylor, Walid K Chatila, Howard I Scher, Nikolaus Schultz, Pedram Razavi, Joao B Xavier

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 42% of its field
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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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

7 authors at 1 institution in 1 country.

Deepti MathurProgram for Computational and Systems Biology, Memorial Sloan Kettering Cancer Center, New York, New York.
Bradford P TaylorProgram for Computational and Systems Biology, Memorial Sloan Kettering Cancer Center, New York, New York.ORCID 0000-0001-7808-955X
Walid K ChatilaHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York.
Howard I ScherGenitourinary Oncology Service, Memorial Sloan Kettering Cancer Center, New York, New York.
Nikolaus SchultzHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York.
Pedram RazaviDepartment of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York.
Joao B XavierProgram for Computational and Systems Biology, Memorial Sloan Kettering Cancer Center, New York, New York.
Memorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Tumor-specific T cell state dynamics and heterogeneity in early tumorigenesisU54CA209975 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI LESLIE, CHRISTINA S, RUDENSKY, ALEXANDER Y · 2016 to 2021
$11.8M
Dissecting the complexity of metastasis with mathematical models and quantitative experiments with in zebrafishR01CA229215 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI WHITE, RICHARD MARK, XAVIER, JOAO · 2018 to 2022
$3.1M
Metabolic determinants of metastatic heterogeneity: quantitative experiments and mathematical modelsF32CA260841 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI MATHUR, DEEPTI · 2021 to 2023
$223k
NCI NIH HHS F32 CA260841NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA229215NCI NIH HHS U54 CA209975
6 · The paper itself

Abstract

Therapeutic resistance is a fundamental obstacle in cancer treatment. Tumors that initially respond to treatment may have a preexisting resistant subclone or acquire resistance during treatment, making relapse theoretically inevitable. Here, we investigate treatment strategies that may delay relapse using mathematical modeling. We find that for a single-drug therapy, pulse treatment-short, elevated doses followed by a complete break from treatment-delays relapse compared with continuous treatment with the same total dose over a length of time. For tumors treated with more than one drug, continuous combination treatment is only sometimes better than sequential treatment, while pulsed combination treatment or simply alternating between the two therapies at defined intervals delays relapse the longest. These results are independent of the fitness cost or benefit of resistance, and are robust to noise. Machine-learning analysis of simulations shows that the initial tumor response and heterogeneity at the start of treatment suffice to determine the benefit of pulsed or alternating treatment strategies over continuous treatment. Analysis of eight tumor burden trajectories of breast cancer patients treated at Memorial Sloan Kettering Cancer Center shows the model can predict time to resistance using initial responses to treatment and estimated preexisting resistant populations. The model calculated that pulse treatment would delay relapse in all eight cases. Overall, our results support that pulsed treatments optimized by mathematical models could delay therapeutic resistance.

Indexed as

Breast NeoplasmsFemaleHumansRecurrenceTumor Burden

Identifiers

PMID35247928
PMCPMC9081172
OpenAlexW4220929855

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.