Topics and Trends in Most Cited Cancer-related Molecular Pathways Papers

Ranked by citations 18 months after publication

Class of 2026 (Papers Published in 2024)

What topics and trends defined most-cited Cancer-related Molecular Pathways research in the Class of 2026?

The Class of 2026 in Cancer-related Molecular Pathways is defined by a deep focus on targeted therapies for breast cancer, particularly CDK4/6 inhibitors and endocrine therapy. However, the field is rapidly pivoting toward novel resistance mechanisms, marked by a surge in research on CDK2 and post-translational modifications.

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Updated September 13, 2026

At a glance

Field
Cancer-related Molecular Pathways
Cohort label
Class of 2026 (2024 publications)
Papers analyzed
3,171
Papers ranked
20
Top topics in ranked papers
CDK4/6 inhibitors, TP53 mutation, endocrine therapy, breast cancer
Publication window
Jan 1, 2024 – Dec 31, 2024
Eligibility
Research articles; reviews excluded
Citation window
18 months post-publication
18m citation range
39–272
Data source
OpenAlex · Retrieved June 2026
License
CC BY 4.0

Rankings

20 papers ranked by 18-month citation count

#1 of 3,171
27218m citations

Alanyl-tRNA synthetase, AARS1, is a lactate sensor and lactyltransferase that lactylates p53 and contributes to tumorigenesis

Zhi Zong et al.Cell202410.1016/j.cell.2024.04.002

Fangfang ZhouSoochow University, China

AARS1lactate sensorlactyltransferasep53 lactylationtumorigenesislactate metabolismpost-translational modificationLactylationtumor microenvironmentmetabolic reprogramminglactate signalingaminoacyl-tRNA synthetasenon-canonical enzyme functioncancer metabolism
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#2 of 3,171
15318m citations

Imlunestrant with or without Abemaciclib in Advanced Breast Cancer

Komal L Jhaveri et al.New England Journal of Medicine202410.1056/nejmoa2410858

Komal L JhaveriMemorial Sloan Kettering Cancer Center, United States

imlunestrantabemaciclibselective estrogen-receptor degraderESR1 mutationsER-positive breast cancerHER2-negative breast canceradvanced breast canceraromatase inhibitorCDK4/6 inhibitorprogression-free survivalbrain-penetrant oral agentendocrine monotherapyrestricted mean survival timeimlunestrant-abemaciclib combinationEMBER-3 trial
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#3 of 3,171
11518m citations

Abemaciclib plus a nonsteroidal aromatase inhibitor as initial therapy for HR+, HER2− advanced breast cancer: final overall survival results of MONARCH 3

M P Goetz et al.Annals of Oncology202410.1016/j.annonc.2024.04.013

M.P. GoetzMayo Clinic, United States

abemaciclibnonsteroidal aromatase inhibitorHR+ HER2− advanced breast cancerMONARCH 3overall survivalprogression-free survivalanastrozoleletrozolepostmenopausal womeninitial therapyvisceral diseasechemotherapy-free survivalCDK4/6 inhibitorendocrine therapyPhase 3 trialfulvestrant
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#4 of 3,171
9718m citations

Overall Survival With Palbociclib Plus Letrozole in Advanced Breast Cancer

Dennis J Slamon et al.Journal of Clinical Oncology202410.1200/jco.23.00137

Dennis J SlamonUniversity of California Los Angeles, United States

palbociclibletrozoleoverall survivalprogression-free survivalER-positive breast cancerHER2-negative breast canceradvanced breast cancerpostmenopausal womenPALOMA-2CDK4/6 inhibitorendocrine therapyhazard ratiosurvival outcome imbalancemedian follow-up 90.1 monthsfirst-line systemic therapy
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#6 of 3,171
7118m citations

PACE: A Randomized Phase II Study of Fulvestrant, Palbociclib, and Avelumab After Progression on Cyclin-Dependent Kinase 4/6 Inhibitor and Aromatase Inhibitor for Hormone Receptor–Positive/Human Epidermal Growth Factor Receptor–Negative Metastatic Breast Cancer

Erica L Mayer et al.Journal of Clinical Oncology202410.1200/jco.23.01940

Erica L MayerDana-Farber Cancer Institute, United States

CDK4/6 inhibitorpalbociclibfulvestrantavelumabhormone receptor-positive breast cancerHER2-negative metastatic breast canceraromatase inhibitorimmune checkpoint inhibitorsprogression-free survivalESR1 alterationsPIK3CA alterationsCDK4/6 inhibitor resistanceendocrine therapypost-progression treatmentde novo metastatic breast cancer
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#7 of 3,171
6918m citations

Discovery of WRN inhibitor HRO761 with synthetic lethality in MSI cancers

Stephane Ferretti, Jacques Hamon, Ruben de Kanter, Clemens Scheufler et al.Nature202410.1038/s41586-024-07350-y

Henrik Möbitz, Marta Cortés-CrosNovartis BioMedical Research, Switzerland

WRN helicaseHRO761microsatellite instabilitysynthetic lethalityAllosteric inhibitionD1 and D2 helicase domainsDNA damagep53-independent mechanismWRN degradationmicrosatellite-stable cellspatient-derived xenograftcolorectal cancerimmune checkpoint inhibitorsRecQ helicasepharmacological WRN inhibitiongenetic screens
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#8 of 3,171
6718m citations

Direct and selective pharmacological disruption of the YAP–TEAD interface by IAG933 inhibits Hippo-dependent and RAS–MAPK-altered cancers

Emilie A Chapeau et al.Nature Cancer202410.1038/s43018-024-00754-9

Emilie A. Chapeau, Tobias SchmelzleNovartis BioMedical Research, Switzerland

YAP-TEAD protein-protein interactionHippo pathwayIAG933direct interface disruptionTEAD lipid pocketYAP eviction from chromatinTEAD paralogsmesotheliomaRAS-MAPK pathwayKRAS mutationRTK inhibitorsMAPK inhibitorscombination therapylung cancerpancreatic cancercolorectal cancerHippo-mediated transcriptionTumor regressionYAP oncogenic functions
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#9 of 3,171
6518m citations

Cell cycle dysregulation in cancer

Antonino Glaviano et al.Pharmacological Reviews202410.1016/j.pharmr.2024.100030

Antonino GlavianoUniversity of Palermo, Italy

cell cycle dysregulationcancercyclinscyclin-dependent kinaseCDK inhibitorcheckpoint controlG1/S transitionG2/M transitionp53 pathwayRb-E2F pathwayoncogenestumor suppressorcell cycle progressionMitotic checkpointDNA damage response
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#10 of 3,171
6318m citations

Abemaciclib Plus Fulvestrant in Advanced Breast Cancer After Progression on CDK4/6 Inhibition: Results From the Phase III postMONARCH Trial

Kevin Kalinsky et al.Journal of Clinical Oncology202410.1200/jco-24-02086

Kevin KalinskyWinship Cancer Institute, United States

abemaciclibfulvestrantCDK4/6 inhibitorendocrine therapyhormone receptor-positive breast cancerHER2-negative breast canceradvanced breast cancerprogression-free survivalaromatase inhibitorESR1 mutationsPIK3CA mutationOverall response rateblinded independent central reviewpostMONARCH trialtreatment rechallengeacquired resistance
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#11 of 3,171
5718m citations

Final Results of RIGHT Choice: Ribociclib Plus Endocrine Therapy Versus Combination Chemotherapy in Premenopausal Women With Clinically Aggressive Hormone Receptor–Positive/Human Epidermal Growth Factor Receptor 2–Negative Advanced Breast Cancer

Yen-Shen Lu et al.Journal of Clinical Oncology202410.1200/jco.24.00144

Yen-Shen LuNational Taiwan University Hospital, Taiwan

ribociclibCDK4/6 inhibitorendocrine therapycombination chemotherapyhormone receptor-positive breast cancerHER2-negative breast canceradvanced breast cancerpremenopausal womenclinically aggressive diseaseletrozoleanastrozolegoserelindocetaxel plus capecitabinepaclitaxel plus gemcitabinecapecitabine plus vinorelbinevisceral diseasevisceral crisisprogression-free survivalOverall response ratetime to response
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#12 of 3,171
5318m citations

p53 at the crossroads of tumor immunity

Gizem Efe et al.Nature Cancer202410.1038/s43018-024-00796-z

Anil K. Rustgi, Carol PrivesColumbia University Irving Medical Center, United States

p53 tumor suppressortumor immunityimmune checkpointT cell responsetumor microenvironmentimmunosurveillancecancer immunotherapyantigen presentationimmune evasioncytokine signalingtumor-infiltrating lymphocytesMHC class Iinterferon responseimmunogenic cell deathPD-L1 regulation
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#13 of 3,171
5218m citations

TSPAN8 <sup>+</sup> myofibroblastic cancer–associated fibroblasts promote chemoresistance in patients with breast cancer

Guangjian Fan et al.Science Translational Medicine202410.1126/scitranslmed.adj5705

Guangjian Fan, Bo Yu, Lei Tang, Rongxuan Zhu, Hongxia WangShanghai General Hospital, China

TSPAN8+ myofibroblastic CAFscancer-associated fibroblastschemotherapy resistancebreast cancersingle-cell high-dimensional flow cytometrysenescence-associated secretory phenotypeIL-6IL-8cancer stem cell stemnessSIRT6RBBP6MAPK11RBBP6 Ser772 phosphorylationGLS1PYCR1aspartate secretionproline secretionmetabolic nicheanti-TSPAN8 antibodyMDL-800
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#14 of 3,171
5218m citations

Relocalizing transcriptional kinases to activate apoptosis

Roman C Sarott, Sai Gourisankar, Basel Karim et al.Science202410.1126/science.adl5361

Roman C. Sarott, Sai Gourisankar, Basel A. Karim, Michael R. Green, Gerald R. Crabtree, Nathanael S. GrayStanford University, United States

chemically induced proximitykinase inhibitorstranscriptional activationBCL6cyclin-dependent kinaseCDK9bivalent moleculesRNA polymerase II phosphorylationpro-apoptotic gene expressiondiffuse large B-cell lymphomagerminal center responsekinase relocalizationBCL6-target genesgain-of-functioncontext-specific transcription
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#16 of 3,171
4518m citations

Mechanisms of Response and Tolerance to Active RAS Inhibition in <i>KRAS</i> -Mutant Non–Small Cell Lung Cancer

Haniel A Araujo, Ximo Pechuan-Jorge, Teng Zhou et al.Cancer Discovery202410.1158/2159-8290.cd-24-0421

Ferdinandos SkoulidisThe University of Texas MD Anderson Cancer Center, United States

RMC-7977KRASG12C-mutant NSCLCinactive state-selective RASG12C inhibitorsRASGTP accumulationactive RAS inhibitionRASG12C(ON) inhibitor resistanceRASG12C(OFF) inhibitor resistancesingle-cell transcriptional responsesmucinous transcriptional programtumor cell persistencesotorasibadagrasibmucinous histologic featuresRAS pathway inhibitioncovalent targeting of active RASG12Creversible RASGTP inhibitioncomutational models
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#17 of 3,171
4218m citations

Control of cell proliferation by memories of mitosis

Franz Meitinger et al.Science202410.1126/science.add9528

Franz Meitinger, Karen Oegema, Arshad DesaiUniversity of California San Diego, United States

mitotic durationmitotic extensionChromosome missegregationGenomic instability53BP1USP28p53 tumor suppressor53BP1-USP28-p53 protein complexesPolo-like kinase 1G1 phase p53 responsecell proliferation controlmitotic memoryTP53 mutationwild-type TP53antimitotic agent sensitivity
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#18 of 3,171
4018m citations

Lactate enhances NMNAT1 lactylation to sustain nuclear NAD+ salvage pathway and promote survival of pancreatic adenocarcinoma cells under glucose-deprived conditions

Huimin Huang et al.Cancer Letters202410.1016/j.canlet.2024.216806

Huimin Huang, Huajun Yu, Xiaoqun Zheng, Haishan Huang, Linhua LanWenzhou Medical University, China

lactateNMNAT1Lactylationnuclear NAD+ salvage pathwaypancreatic adenocarcinoma cellsglucose deprivationNAD+ metabolismpost-translational modificationmetabolic adaptationcancer cell survivalnutrient stress
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#19 of 3,171
4018m citations

Sonrotoclax overcomes BCL2 G101V mutation–induced venetoclax resistance in preclinical models of hematologic malignancy

Jiuyang Liu et al.Blood202410.1182/blood.2023019706

Jiuyang LiuBeiGene (Beijing) Co, Ltd, China

sonrotoclaxvenetoclaxBCL-2G101V mutationvenetoclax resistanceBCL2 inhibitorchronic lymphocytic leukemiahematologic malignancyapoptosisPro-apoptotic proteinsP2 pocketCrystal structureDrug resistanceBCL2 variantsbinding modetumor growth inhibitionsecond-generation inhibitor
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#20 of 3,171
3918m citations

Checkpoint Inhibition in Addition to Dabrafenib/Trametinib for BRAF <sup>V600E</sup> -Mutated Anaplastic Thyroid Carcinoma

Sarah Hamidi et al.Thyroid202410.1089/thy.2023.0573

Maria E. CabanillasThe University of Texas MD Anderson Cancer Center, United States

BRAF V600E mutationAnaplastic thyroid carcinomadabrafenibtrametinibpembrolizumabimmune checkpoint inhibitorsanti-PD-1 inhibitorspartalizumabBRAF/MEK inhibitorsneoadjuvant therapyoverall survivalprogression-free survivalDrug resistanceimmune-related adverse eventscombination immunotherapyhepatitiscolitis
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Dominant research themes and year-over-year shifts in Cancer-related Molecular Pathways

What Topics Define the Class of 2026?

The research landscape for the Class of 2026 is heavily anchored in targeted therapies and biomarker-driven treatments, particularly for breast cancer. The most prominent theme is the continued focus on CDK4/6 inhibitors and their clinical application in advanced, hormone receptor-positive, and HER2-negative breast cancers. Complementing this is a strong emphasis on endocrine therapy and specific agents like fulvestrant. Beyond targeted inhibitors, the molecular underpinnings of cancer progression remain critical areas of investigation, with significant attention given to TP53 mutations and the mechanisms of metabolic reprogramming. Furthermore, post-translational modifications are emerging as important focal points for understanding signaling pathways and potential therapeutic targets. Together, these topics underscore a mature but evolving field dedicated to refining precision medicine and overcoming therapeutic resistance in oncology.

Leading research themes
Leading research themes

How Did Topics Shift from the Class of 2025 to the Class of 2026?

A comparison between the Class of 2025 and 2026 reveals a notable maturation in research priorities, marked by shifts from established targets to novel resistance mechanisms. While CDK4/6 inhibitors remain dominant, their relative frequency experienced a slight decline, alongside a decreased focus on generic TP53 mutations. In their place, we observe a sharp, four-fold increase in studies investigating CDK2 and post-translational modifications. This suggests a strategic pivot toward addressing resistance pathways that emerge following initial CDK4/6 inhibition. Additionally, clinical classifications such as advanced breast cancer and hormone receptor-positive breast cancer saw significant growth, reflecting an increasing dedication to specific patient stratifications. Overall, the field is transitioning from initial pathway characterization toward a more nuanced understanding of secondary targets and metabolic reprogramming in advanced disease states.

How topics shifted year over year
How topics shifted year over year
Methodology

PRI identifies high-impact research using a transparent, topic-agnostic framework applied consistently across scientific domains. Bibliographic records are drawn from OpenAlex, including publication dates, citation relationships, and document types.

This ranking covers the Class of 2026 cohort: journal articles published in 2024. Reviews and other non-article document types are excluded to ensure comparability.

Research impact is quantified with an 18-month post-publication citation window—the number of citing works published within 18 months of each paper's publication date. This metric captures early impact while controlling for publication age.

An LLM-based relevance classifier then reviews each candidate's title and abstract to confirm substantive alignment with the target domain. Only papers classified as relevant appear in the final ranking.

Zheng Su, Tinsley Li, Thematic Shifts in Early-High-Impact Cancer Genomics and Diagnostics Research: A Bibliometric and Semantic Analysis. bioRxiv 2026.07.04.736459; doi: https://doi.org/10.64898/2026.07.04.736459

Full methodologyGitHubbioRxiv preprint

Cite this ranking

Pepkio Research Index (PRI). Topics and Trends in Most Cited Cancer-related Molecular Pathways Papers, Class of 2026. https://pri.pepkio.com/top-papers/cancer-related-molecular-pathways/2026. Accessed 2026-10-24.

Methodology
Zheng Su, Tinsley Li, Thematic Shifts in Early-High-Impact Cancer Genomics and Diagnostics Research: A Bibliometric and Semantic Analysis. bioRxiv 2026.07.04.736459; doi: https://doi.org/10.64898/2026.07.04.736459