Evidence map›Paper›PMID 34308274›Full record

ArticleCancer drug resistance (Alhambra, Calif.)2021

Proteasomal adaptations to FDA-approved proteasome inhibitors: a potential mechanism for drug resistance?

Kyung Bo Kim

Open access · diamondAbstract read
In one paragraph

Article in Cancer drug resistance (Alhambra, Calif.), 2021. 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 38% 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, 8 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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

1 author at 1 institution in 1 country.

Kyung Bo KimDepartment of Pharmaceutics, College of Pharmacy, University of Kentucky, Lexington, KY 40536-0596, USA.
University of Kentucky · US

Funding

Non-peptide proteasome inhibitors as a novel anticancer agentR01CA188354 · NCI · UNIVERSITY OF KENTUCKY · PI KIM, KYUNG BO · 2014 to 2018
$1.5M
NCI NIH HHS R01 CA188354
6 · The paper itself

Abstract

With proteasome inhibitors (PIs) becoming clinically available since 2003, outcomes for patients with multiple myeloma (MM) have dramatically changed, improving quality of life and survival. Despite the impressive treatment success, however, almost all MM patients who initially respond to these PIs eventually develop resistance. Furthermore, a portion of MM patients is inherently unresponsive to the PIs. Extensive mechanistic investigations identified several non-proteasomal signaling pathways suspected to be linked to the PI resistance, for which several excellent reviews are currently available. On the other hand, it is still unclear how cancer cells under high PI environments adapt to spare proteasome activity essential for survival and proliferation regardless of cancer evolution stages. This review outlines current progress towards understanding the proteasomal adaptations of cells in response to PI treatment to maintain necessary proteasome activity. A better understanding of cellular proteasomal changes in response to the PIs could provide a rationale to develop new therapeutics that could be used to overcome resistance to existing PI drugs.

Indexed as

bortezomibcarfilzomibConstitutive proteasomedrug resistanceimmunoproteasome

Identifiers

PMID34308274
PMCPMC8297691
OpenAlexW3172299255

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.