Evidence map›Paper›PMID 40913249›Full record

ArticleMolecular pain

Exacerbation of paclitaxel-induced neuropathic pain behaviors in breast tumor-bearing mice.

Hee Kee Kim, Juping Xing, Youn-Sang Jung, Jae-Il Park, Hee Young Kim, Jimin Kim, Salahadin Abdi

Abstract read
In one paragraph

Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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.

Hee Kee KimSouthern Reformed College & Seminary, Houston, TX, USA.
Juping XingDepartment of Physiology, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID 0009-0001-3259-4347
Youn-Sang JungThe Department of Life Science, Chung-Ang University, Seoul, Republic of Korea.
Jae-Il ParkThe Department of Experimental Radiation Oncology, Division of Radiation Oncology; Graduate School of Biomedical Sciences; Program in Genetics and Epigenetics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Hee Young KimDepartment of Physiology, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0002-2495-9115
Jimin KimUniversity of the Incarnate Word School of Osteopathic Medicine, San Antonio, TX, USA.
Salahadin AbdiDivision of Anesthesiology, Critical Care & Pain Medicine, The Department of Pain Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.

Funding

PAF-Remodeled DREAM Complex in Cancer and RegenerationR01CA193297 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PARK, JAE-IL · 2015 to 2024
$3.6M
NCI NIH HHS R01 CA193297
6 · The paper itself

Abstract

backgroundChronic pain and cancer interact bidirectionally, with pain enhancing sensory peptides and potentially promoting tumor growth. Despite this, most chemotherapy-induced neuropathic pain (CIPN) studies overlook the contribution of cancer itself to neuropathy, focusing instead on chemotherapy-induced mechanisms. Animal models of chemotherapy-induced neuropathic pain (CINP) have been developed by injecting chemotherapeutic drugs such as paclitaxel into normal animals without cancer. This study aimed to develop a new model in mouse mammary tumor virus-polyomavirus middle T antigen (MMTV-PyMT) mice, a widely used breast cancer model with normal immune function.

resultsThe percentage of positive response (PPR) of paclitaxel-injected MMTV-PyMT mice increased (about 20%; baseline, 10%) on day 4, reached the highest levels (50%-60%) on days 6-9, and then plateaued by day 29. In comparison, the PPR of paclitaxel-injected C57BL/6 was less than 10% on days 0-6, was about 40% on day 9, and then plateaued by day 29. Breast tumor-bearing mice exhibited an earlier onset and greater severity of paclitaxel-induced pain behaviors than tumor-free C57BL/6 mice. Systemic LGK-974 ameliorated paclitaxel-induced pain behaviors in MMTV-PyMT mice. Active β-catenin was detected in neurons and satellite cells of the dorsal root ganglia.

conclusionsPaclitaxel-induced neuropathic pain model in breast tumor-bearing female MMTV-PyMT mice may be a useful animal model for investigating the analgesic effects and underlying mechanisms for CINP in breast cancer patients as well as the interplay between CINP development and cancer progression.

Indexed as

Antineoplastic Agents, PhytogenicBehavior, AnimalBreast NeoplasmsMammary Neoplasms, ExperimentalNeuralgiaPaclitaxelAnimalsDisease Models, AnimalFemaleGanglia, SpinalMiceMice, Inbred C57BLAntineoplastic Agents, PhytogenicPaclitaxelbreast tumorneuropathic painPaclitaxel

Identifiers

PMID40913249
PMCPMC12536134

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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.