Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (589 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from drug tolerance which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Resistance, Drug.
Where it fits in the MeSH classification
- Broader topics
- Pharmacological Phenomena
- Narrower topics
- Drug Resistance, Microbial; Drug Resistance, Multiple; Drug Resistance, Neoplasm; Herbicide Resistance; Insecticide Resistance; Insulin Resistance
- See also
- Pharmacogenetics
Related concepts
Research landscape
PubMed indexes 426,469 records tagged with the MeSH heading “Drug Resistance” (counts retrieved 2026-10-29). 96,329 of them (22.6%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 144,476 records.
Reviews account for 64,328 records (15.1%) and meta-analyses for 2,520. Randomized controlled trials number 9,001 (2.1%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 90,413 |
| 2000-2009 | 95,251 |
| 2010-2019 | 144,476 |
| 2020 onward | 96,329 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 64,328 | 15.1% |
| Meta-analyses | 2,520 | 0.6% |
| Randomized controlled trials | 9,001 | 2.1% |
Method: PubMed query "Drug Resistance"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in pharmacology
Drug evidence builds in layers: laboratory pharmacology describes how a compound acts, pharmacokinetic studies describe how the body handles it, and randomized trials test whether it helps and what harms it causes. Post-marketing surveillance and observational studies reveal rarer adverse effects but cannot prove causation. This page is educational and is not a recommendation to start, stop or change any medicine; decisions about treatment belong with a qualified clinician.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| RHAMM drives formation of polyploid cancer cells and confers resistance to ER-targeted therapy in breast cancer | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42748147 · DOI · PMC13598241 |
| Uncovering pan-cancer signatures of chemoresistance | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42811363 · DOI · PMC13625386 |
| Unique Genetic Clades and Frequent Zoonotic Transmission of Sporothrix brasiliensis with Reduced Itraconazole Susceptibility | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42742838 · DOI · PMC13578069 |
RHAMM drives formation of polyploid cancer cells and confers resistance to ER-targeted therapy in breast cancer [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Endocrine resistance in ER+ breast cancer remains a major clinical challenge.
- Closing excerpt
- These findings reveal RHAMM-mediated polyploidization as an adaptive mechanism underlying endocrine resistance, suggesting the therapeutic potential of targeting the RHAMM-YAP axis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (145 words)
Endocrine resistance in ER+ breast cancer remains a major clinical challenge. Here, we identify RHAMM as a key driver of resistance by orchestrating polyploid cancer cell (PCC) formation. Single-cell transcriptomics uncovered a G2/M-enriched, RHAMM+ subpopulation in endocrine-resistant tumors. Mechanistically, RHAMM binds Septin9/10 to promote aberrant cytoskeleton polymerization, activating YAP independent of Hippo signaling, which induces cytokinesis failure and facilitates PCC generation. Concurrently, RHAMM destabilizes p21 mRNA, enabling cell cycle progression despite genomic instability. The RHAMM-p21 axis serves as a bypass mechanism supporting polyploidization. Upon endocrine treatment, RHAMM is transcriptionally up-regulated by Slug. Clinically, RHAMMhigh signatures are enriched in metastatic and recurrent ER+ tumors and correlate with poor prognosis, highlighting its therapeutic relevance. Importantly, targeting RHAMM or YAP abrogates PCC formation and restores fulvestrant sensitivity. These findings reveal RHAMM-mediated polyploidization as an adaptive mechanism underlying endocrine resistance, suggesting the therapeutic potential of targeting the RHAMM-YAP axis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42748147 · DOI · PMC13598241
Uncovering pan-cancer signatures of chemoresistance [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundChemotherapy resistance remains a formidable challenge in cancer treatment, driving high mortality rates worldwide.
- Closing excerpt
- ConclusionsTo our knowledge, this is the first comprehensive study that redefines chemoresistance as a proliferative, MYC-driven state and uncover SRM as a tractable vulnerability, offering new avenues for therapeutic intervention across diverse epithelial malignancies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (246 words)
BackgroundChemotherapy resistance remains a formidable challenge in cancer treatment, driving high mortality rates worldwide. Despite significant advancements, it remains unclear whether conserved molecular programs underpin therapy resistance across cancer types.MethodsHere, we integrate single-cell RNA sequencing, spatial transcriptomics, regulatory network modeling, transcription factor binding data, and pharmacologic perturbation across multiple cancer types to define a conserved, proliferative chemoresistant tumor state.ResultsContrary to the prevailing notion that resistance arises from quiescent or EMT-like phenotypes, we find that resistant tumor cells display elevated G2/M and S-phase activity, enriched expression of E2F and MYC target genes, and activation of DNA repair and PI3K/AKT signaling pathways. We identify the transcription factor MYC as a central regulator of the resistant state, with progressive activation along the resistance trajectory and focal expression in resistant epithelial niches. A novel MYC target, SRM (Spermidine Synthase), emerges as a conserved effector of resistance, promoting polyamine biosynthesis critical for chromatin stability and metabolic resilience. SRM expression correlates with MYC binding and predicts poor patient survival. Functional validation in cell lines, patient-derived organoids and mouse models demonstrate that pharmacologic inhibition of MYC, SRM, or WNT signalling restores chemotherapy sensitivity, suppresses resistance-associated pathways, and reactivates apoptosis. Spatial and survival analyses confirm the clinical relevance of the MYC-SRM axis, establishing it as a druggable module in treatment-refractory cancers.ConclusionsTo our knowledge, this is the first comprehensive study that redefines chemoresistance as a proliferative, MYC-driven state and uncover SRM as a tractable vulnerability, offering new avenues for therapeutic intervention across diverse epithelial malignancies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42811363 · DOI · PMC13625386
Unique Genetic Clades and Frequent Zoonotic Transmission of Sporothrix brasiliensis with Reduced Itraconazole Susceptibility [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Sporothrix brasiliensis is driving a major zoonotic epidemic in Brazil, predominantly via cat-to-human transmission.
- Closing excerpt
- Our findings highlight the urgent need for antifungal stewardship and surveillance in these endemic regions.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (198 words)
Sporothrix brasiliensis is driving a major zoonotic epidemic in Brazil, predominantly via cat-to-human transmission. In the late 1990s major outbreaks were reported in Rio de Janeiro (RJ) and Rio Grande do Sul (RS), the southernmost state. We characterized the antifungal susceptibility and genetic diversity of 450 S. brasiliensis isolates collected between 2009 and 2024 in RS to better understand treatment response, emergence and transmission.A bimodal distribution of the itraconazole minimum inhibitory concentration (MIC) was observed with 24% non-wild-type (NWT) isolates. Short tandem repeat genotyping revealed three main clades: One associated with RJ strains (Clade I) and two novel clades (Clades II and III). Clade II formed large transmission clusters with < 20% of isolates being NWT for itraconazole, similar to Clade I. Clade III demonstrated less clustering, higher genetic variation and NWT MICs for 89% of isolates. Finally, all NWT strains in human patients with cat-transmitted disease and available clinical data, appeared isolated prior to azole exposure.We report the emergence of genetically distinct S. brasiliensis clades in RS with different rates of reduced itraconazole susceptibility and evidence of zoonotic transmission of NWT isolates. Our findings highlight the urgent need for antifungal stewardship and surveillance in these endemic regions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42742838 · DOI · PMC13578069
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Global prevalence of non-alcoholic fatty liver disease in type 2 diabetes mellitus: an updated systematic review and meta-analysis [4]
- Research article Triglyceride-glucose index and heart failure: a systematic review and meta-analysis [5]
- Research article The accuracy of triglyceride-glucose (TyG) index for the screening of metabolic syndrome in adults: A systematic review and meta-analysis [6]
- Research article Short-chain fatty acids and insulin sensitivity: a systematic review and meta-analysis [7]
- Research article Association of Insulin Resistance With Cardiovascular Disease and All-Cause Mortality in Type 1 Diabetes: Systematic Review and Meta-analysis [8]
- Research article Triglyceride-glucose index and obstructive sleep apnea: a systematic review and meta-analysis [9]
References
- Wu S, Chen S, Liu B, Liu Y, Yang S, Hu J, et al.. RHAMM drives formation of polyploid cancer cells and confers resistance to ER-targeted therapy in breast cancer. . 2026. PMID 42748147 · DOI · PMC13598241
- Inayatullah M, Demirdizen E, Keepers Z, Correia CM, Hashemi SM, Tripathi K, et al.. Uncovering pan-cancer signatures of chemoresistance. . 2026. PMID 42811363 · DOI · PMC13625386
- Trápaga MR, Spruijtenburg B, Hidalgo JED, Jacomel B, Madrid IM, Pereira DIB, et al.. Unique Genetic Clades and Frequent Zoonotic Transmission of Sporothrix brasiliensis with Reduced Itraconazole Susceptibility. . 2026. PMID 42742838 · DOI · PMC13578069
- En Li Cho E, Ang CZ, Quek J, Fu CE, Lim LKE, Heng ZEQ, et al.. Global prevalence of non-alcoholic fatty liver disease in type 2 diabetes mellitus: an updated systematic review and meta-analysis. Gut. 2023. PMID 37491159 · DOI
- Khalaji A, Behnoush AH, Khanmohammadi S, Ghanbari Mardasi K, Sharifkashani S, Sahebkar A, et al.. Triglyceride-glucose index and heart failure: a systematic review and meta-analysis. Cardiovasc Diabetol. 2023. PMID 37679763 · DOI · PMC10486123
- Nabipoorashrafi SA, Seyedi SA, Rabizadeh S, Ebrahimi M, Ranjbar SA, Reyhan SK, et al.. The accuracy of triglyceride-glucose (TyG) index for the screening of metabolic syndrome in adults: A systematic review and meta-analysis. Nutr Metab Cardiovasc Dis. 2022. PMID 36336547 · DOI
- Pham NHT, Joglekar MV, Wong WKM, Nassif NT, Simpson AM, Hardikar AA. Short-chain fatty acids and insulin sensitivity: a systematic review and meta-analysis. Nutr Rev. 2024. PMID 37290429 · DOI · PMC10777678
- Sun R, Wang J, Li M, Li J, Pan Y, Liu B, et al.. Association of Insulin Resistance With Cardiovascular Disease and All-Cause Mortality in Type 1 Diabetes: Systematic Review and Meta-analysis. Diabetes Care. 2024. PMID 39018337 · DOI
- Behnoush AH, Khalaji A, Ghondaghsaz E, Masrour M, Shokri Varniab Z, Khalaji S, et al.. Triglyceride-glucose index and obstructive sleep apnea: a systematic review and meta-analysis. Lipids Health Dis. 2024. PMID 38185682 · DOI · PMC10773018
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.