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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 01/09/2026

Corresponding author: Dr. Biswajit Das & Prof. Shaheen Sikandar @ssikandar.bsky.social, UC Santa Cruz. A great review to revisit for those interested in breast cancer immunity, tumor heterogeneity & plasticity.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 01/09/2026

Immune escape creates therapeutic opportunities. 📊 Table 2 surveys clinical strategies targeting PD-1/PD-L1, CTLA-4 & other immune-evasion pathways—including combination approaches across breast cancer subtypes. Understanding subtype-specific TIME biology may help guide immunotherapy strategies.

Table 2 (two panels). Therapeutic strategies targeting immune evasion in breast cancer. The table summarizes clinical trials targeting immune-evasion pathways across breast cancer subtypes, listing therapeutic targets, treatments, indications, strategies, trial status/phase, and NCT numbers. Approaches include PD-1/PD-L1 and CTLA-4 blockade, checkpoint combinations, and combinations with chemotherapy, microtubule inhibitors, tyrosine kinase inhibition, tumor-directed therapies, HER2 targeting, LAG-3 targeting, and other immunotherapeutic strategies.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 01/09/2026

Despite these differences, breast cancers converge on major immune-evasion strategies: 🔹 Suppress antigen presentation & recognition 🔹 Modulate immune checkpoints 🔹 Build an immunosuppressive TIME Together, these mechanisms enable immune escape and cancer progression.

Figure 2. Overview of immune evasion mechanisms in breast cancer. Diagram showing three major routes of immune escape: suppression of antigen presentation through altered MUC1, MHC-I and HLA molecules; modulation of PD-1/PD-L1 and CTLA-4 immune checkpoints; and formation of an immunosuppressive tumor immune microenvironment involving TAMs, MDSCs, Tregs, exhausted CD8+ T cells and γδ T cells.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 01/09/2026

Breast cancer subtypes harbor distinct tumor immune microenvironments: • HR+: relatively immune-cold • HER2+: mixed immune features • TNBC: highly immune-infiltrated, yet also enriched in immunosuppressive features 📊 Table 1 compares these subtype-specific TIME landscapes.

Table 1 (four panels). Comparison of the tumor immune microenvironment (TIME) across HR+, HER2+, and triple-negative breast cancer (TNBC). The table compares CD8+ and CD4+ T cells, B cells, dendritic cells, tumor-associated macrophages, MDSCs, NK cells, cancer-associated fibroblasts, cytokines/chemokines, and immune checkpoints. HR+ tumors generally show a relatively immune-cold environment; HER2+ tumors display intermediate or mixed immune features; and TNBC shows greater immune infiltration together with prominent immunosuppressive populations and higher immune-checkpoint expression.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 01/09/2026

📘 CHP Archive Spotlight #18 Review (2026) | Das et al. 🏛️ UC Santa Cruz How does breast cancer evade immunity? HR+, HER2+ & TNBC have distinct immune ecosystems—yet converge on shared mechanisms of immune escape. 🔗 doi.org/10.47248/chp2603010001 #BreastCancer #CancerImmunology

doi.org

The Trojan Horse Within: Mechanisms of Immune Evasion in Breast Cancer

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 09/04/2026

📢 Call for Papers — CHP Special Issue Cancer evolves. Tumors adapt. Resistance emerges. Therapies fail. 📘 Molecular Understanding & Therapeutic Targeting of Cancer Heterogeneity and Plasticity 💡 OA | No fees 📅 Apr 30, 2026 (priority; open after) 🔗 www.pivotscipub.com/chp #CancerResearch

Cartoon showing cancer plasticity (cells escaping therapy by changing) and heterogeneity (diverse tumor cell populations), emphasizing therapy resistance and the need for multiple strategies; includes call for papers for CHP special issue (deadline April 30, 2026).

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 09/04/2026

📖 Commentary Spotlight Rahul Kumar highlights: 🧠 Transcriptional plasticity drives resistance 🔗 TEAD–AP-1 cooperation sustains malignancy 💡 Supports co-targeting strategies 🔗 www.pivotscipub.com/chp/3/1/0003... #CancerHeterogeneity #TherapyResistance

Schematic of gastric cancer peritoneal metastases illustrating that YAP1 inhibition alone triggers compensatory activation of TAZ, which interacts with TEAD4 and AP-1 to sustain oncogenic signaling. This adaptive response may limit the effectiveness of YAP1-targeted therapy. In contrast, dual inhibition of YAP1 and TAZ suppresses downstream transcriptional activity and promotes tumor suppression, supporting combined targeting strategies.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 09/04/2026

YAP1 inhibition alone is insufficient: 📈 TAZ compensates to sustain oncogenic signaling 💡 Dual YAP1/TAZ targeting: • Suppresses transcriptional programs • Enhances tumor suppression 🧩 Supports combination therapeutic strategies in GCPMs

YAP1 and TAZ expression are elevated in gastric cancer versus normal tissues and show positive correlation across datasets and patient samples, including co-localization in PDX tumors.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 09/04/2026

In GCPMs: • YAP1 inhibition → ↑ TAZ activation • TAZ forms complexes with TEAD4 and AP-1 (c-JUN/FOSB) • Drives transcription of oncogenic targets (e.g., SOX9, BIRC5, CTGF, CYR61) ➡️ A key mechanism of therapy resistance via transcriptional plasticity #TumorPlasticity #TherapyResistance

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 09/04/2026

📘 CHP Archive Spotlight #12 Original Research (2026) | Wu et al. YAP1 depletion in gastric cancer peritoneal metastases (GCPM) induces compensatory TAZ activation, sustaining tumor progression and metastasis. Reveals adaptive oncogenic signaling via the YAP1–TAZ axis www.pivotscipub.com/chp/3/1/0004

Graphical abstract illustrating that in gastric cancer peritoneal metastases, YAP1 and TAZ are upregulated and act with TEAD transcription factors. Inhibition of YAP1 alone leads to compensatory upregulation of TAZ, which forms a transcriptional complex with TEAD4 and AP-1 (c-JUN/FOSB) to drive expression of oncogenic genes such as SOX9, BIRC5, CTGF, and CYR61. In contrast, co-targeting both YAP1 and TAZ suppresses this transcriptional program and reduces tumor-promoting activity.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 06/03/2026

To overcome resistance, the review highlights combination approaches: • Chemotherapy + radiotherapy • Immunotherapy + targeted therapy • Immunotherapy + vaccines • PARP inhibitors + checkpoint blockade Targeting viral, genomic, and immune pathways simultaneously may improve outcomes.

Infographic summarizing combination treatment strategies for HPV-associated cancers. Approaches include chemotherapy plus radiotherapy to increase DNA damage, immunotherapy combined with targeted therapy to enhance T-cell responses, immunotherapy with therapeutic vaccines to activate HPV-specific immunity, immunotherapy plus radiotherapy to boost systemic anti-tumor effects, and combinations with PARP inhibitors or small-molecule inhibitors to increase tumor cell lethality and block resistance pathways.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 06/03/2026

HPV integration into the host genome occurs through multiple mechanisms: • Insertional deletion • Duplication-like insertion • Translocation-like integration • Multi-breakpoint integration These diverse patterns reshape host gene regulation and contribute to tumor heterogeneity.

Diagram illustrating several mechanisms by which HPV DNA integrates into the host genome. These include insertional deletion following a double-strand DNA break, duplication-like insertion, multi-breakpoint integration involving multiple viral fragments, translocation-like integration between genomic regions, and repeat-repeat integration events. These diverse integration patterns contribute to genomic instability and heterogeneity in HPV-associated cancers.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 06/03/2026

HPV oncogenesis is driven by E6/E7 disruption of p53 and Rb, leading to: • Genomic instability • Telomerase activation • Viral genome integration • Transcriptional heterogeneity These processes generate tumor subpopulations linked to immune evasion and therapy resistance.

Diagram illustrating how HPV oncogenes E6 and E7 become dysregulated through viral genome integration or episomal persistence. Integration can occur after HPV genome linearization and may insert into host genes, disrupt tumor suppressors, activate oncogenes, or form complex multi-site integrations. Loss of the viral E2 regulatory region promotes E6/E7 overexpression. Episomal HPV can also activate E6/E7 through epigenetic silencing of E2. These mechanisms drive oncogenic transcription and malignant transformation.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 06/03/2026

📘 CHP Archive Spotlight #11 Review (2026) | Rasouli et al. HPV-driven cancers show viral integration, genomic instability, and immune escape. This review examines how HPV heterogeneity fuels therapy resistance and highlights combination therapies. 🔗 doi.org/10.47248/chp... #HPV

Graphical overview of HPV-associated cancer progression and treatment strategies. HPV infection initiates carcinogenesis through E6 and E7 oncoproteins disrupting p53 and Rb, causing genomic instability. Viral genome integration creates molecular heterogeneity leading to increased malignancy, immune evasion, and therapy resistance. Combination therapies—including chemotherapy, radiotherapy, immunotherapy, vaccines, and targeted agents—aim to overcome heterogeneity and improve treatment response.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 03/03/2026

State-of-the-art tools include: • Impedance-based assays • Elasticity mapping • Biophysical profiling platforms Toward integrating mechanical biomarkers into clinical decision-making.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 03/03/2026

Like genetic traits, physical properties show: • Intertumoral heterogeneity • Intratumoral heterogeneity • Dynamic evolution during treatment Spatial and temporal monitoring of tumor physics may improve precision oncology.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 03/03/2026

Physical and biological tumor traits reinforce each other. Biophysical abnormalities: • Promote stemness • Enhance metastatic potential • Drive therapy resistance • Correlate with prognosis Tumor mechanics are not bystanders — they are regulators.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 03/03/2026

📘 CHP Archive Spotlight #10 Review (2024) | Markl et al. Cancer is not only molecular — it is physical. Tumors reflect: • Stiffness & ECM remodeling • Cell mechanics • Electrical/thermal states • Solid stress Biophysics shapes heterogeneity. 🔗 doi.org/10.47248/chp... #TumorBiophysics #Mechanobiology

Graphical abstract divided into two halves labeled “Physical” and “Biological,” centered around a large cancer cell illustration.
Left (Physical properties):
Mechanical factors such as ECM stiffness and cell viscosity increase during tumor progression. Diagrams illustrate low, mid, and high electrical frequencies (impedance profiling), along with thermal gradients and solid stress within the tumor microenvironment.
Right (Biological consequences):
Physical properties are linked to cancer stem cell enrichment, stemness, metastatic potential, and therapy resistance. Icons show a stem cell cluster, metastatic cell invasion through epithelial layers, radiation and drug resistance, and immune interactions.
The figure emphasizes that tumor physical parameters and biological hallmarks are interconnected and mutually reinforcing, contributing to heterogeneity and clinical outcomes.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 03/03/2026

Key open questions: • What distinguishes reversible plasticity from stable lineage change? • How do epigenetic modifiers sustain reprogrammed states? • Can plasticity be therapeutically targeted? Emerging technologies may finally resolve these questions.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 03/03/2026

Across tissues: • Lung (AT2 ↔ AT1) • Intestine (CBCs, Paneth cells) • Liver & pancreas • Skin & hematopoietic systems And in cancer: • NEPC, DNPC • EMT programs • Stem-like states • Epigenetic rewiring Plasticity drives progression & therapy resistance.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 03/03/2026

Plasticity is more than “state switching.” Balk & Goodrich (CHP) distinguish: • Pathways enabling plasticity • Pathways specifying phenotype • Shared mechanisms in normal tissue & cancer • Distinct drivers of neoplastic reprogramming A framework for understanding lineage flexibility across systems.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 03/03/2026

📘 CHP Archive Spotlight #09 Review (2024) | Balk & Goodrich From development to cancer progression, phenotypic plasticity shapes cell fate. This review dissects the molecular drivers linking homeostasis to therapy resistance. 🔗 doi.org/10.47248/chp... #PhenotypicPlasticity #Epigenetics

Illustrated schematic showing phenotypic plasticity across multiple organs in normal homeostasis and injury contexts. A central human figure is surrounded by circular panels depicting:
• Lung: Alveolar type II (AT2) cells transitioning to AT1 cells after injury.
• Intestine: Crypt base columnar (CBC) stem cells and Paneth cells interacting within the intestinal niche.
• Pancreas: α and β islet cells with bidirectional plasticity under stress.
• Liver: Hepatocytes and biliary epithelial cells (BECs) showing lineage interconversion.
• Skin: Keratinocytes, fibroblasts, immune cells, and adipocytes participating in wound repair and microenvironmental remodeling.
Arrows indicate bidirectional transitions and injury-induced state changes, emphasizing that phenotypic plasticity is a conserved mechanism in tissue maintenance and regeneration.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 01/03/2026

📎 Commentary Spotlight Eversole & Chakraborty discuss how TFAP4 “unleashes” TERT activity in non-viral liver cancers and highlight therapeutic implications of targeting the TFAP4–TERT interaction. 🔗 doi.org/10.47248/chp... #HCC #CancerBiology

Illustration of TFAP4-mediated reactivation of TERT in non-HBV-associated hepatocellular carcinoma. Alcohol exposure increases CTCF expression, which promotes transcription of TFAP4. TFAP4 binds the TERT promoter (at approximately −111 nt), enhancing TERT gene transcription. Elevated TERT expression increases telomerase activity, stabilizes telomeres, and supports hepatocellular carcinoma progression and metastasis. The pathway is depicted within the nucleus of an HCC cell, leading to tumor growth in non-viral-associated liver cancer.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 01/03/2026

Using luciferase & ChIP assays, Lim et al. show: • TFAP4 binds the TERT promoter (−111 nt site) • CTCF promotes TFAP4 transcription • TFAP4 knockdown reduces TERT expression & telomere length • Ethanol enhances the TFAP4–TERT axis in non-HBV HCC A mutation-independent telomerase rewiring mechanism.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 01/03/2026

📘 CHP Archive Spotlight #08 Original Research (2024) | Lim et al. TFAP4 directly reactivates TERT in non-HBV HCC — independent of promoter mutation. CTCF → TFAP4 → TERT axis drives telomerase activation, especially in alcohol-related tumors. 🔗 doi.org/10.47248/chp... #HCC #TERT #Telomerase

Schematic model of telomerase reactivation in non-HBV-associated hepatocellular carcinoma. CTCF binds to the TFAP4 promoter and increases TFAP4 expression. TFAP4 then binds directly to the TERT promoter, enhancing TERT mRNA transcription. Increased TERT expression leads to elevated telomerase activity and stabilization of telomeres. Ethanol exposure further upregulates TFAP4 and TERT in non-HBV HCC cells, while this regulatory pathway appears limited in HBV-associated HCC.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 01/03/2026

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 28/02/2026

📘 CHP Archive Spotlight #07 Review (2024) | Her et al. How do noncoding RNAs drive cancer plasticity? miRNAs, lncRNAs, circRNAs & tRNA fragments regulate stemness, EMT, epigenetics & therapy resistance — with emerging roles as biomarkers & targets. 🔗 doi.org/10.47248/chp... #ncRNA #CancerStemCells

Schematic overview of noncoding RNA functions in cancer cell plasticity. The figure is organized by RNA type: miRNAs regulate pluripotency inhibition, translational repression, mRNA degradation, EMT transition, cancer stem cell initiation, and metastasis; lncRNAs modulate epigenetic regulation, transcription, signaling pathways, chromatin architecture, alternative splicing, and dedifferentiation; circRNAs function as miRNA sponges, regulate transcription, interact with RNA-binding proteins, and influence self-renewal and apoptosis; tRNAs and tRNA-derived fragments regulate translation, mRNA stability, mitochondrial homeostasis, metabolic reprogramming, and hormone-dependent signaling.

Illustration of therapeutic strategies targeting noncoding RNAs in cancer. Approaches include synthetic miRNA mimics and lentiviral delivery for oncogene suppression, antisense oligonucleotides and RNA sponges for tumor suppressor restoration, CRISPR-based activation or repression of lncRNAs, synthetic circRNA sponges and Cas13-mediated cleavage, siRNA-loaded nanoparticles, and inhibition of tRNA methyltransferases to block translation and tumor growth.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 28/02/2026

📘 CHP Archive Spotlight #06 Perspective (2024) | Kondo Targeting cancer stem cell heterogeneity & plasticity with a miRNA-dependent AAV system designed to eradicate diverse CSC populations while minimizing side effects. 🔗 doi.org/10.47248/chp... #CancerStemCells #Heterogeneity #AAV

Graphical abstract illustrating cancer stem cell (CSC) heterogeneity driven by genetic, epigenetic, and environmental factors, and a proposed miRNA-dependent AAV strategy selectively eradicating heterogeneous CSCs to prevent recurrence.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 27/02/2026

📘 CHP Archive Spotlight #05 Perspective (2024) | Jamroze, Liu & Tang AR signaling inhibitors induce lineage plasticity in prostate cancer, promoting stem-like, mesenchymal & neural states driving CRPC & NEPC progression. 🔗 doi.org/10.47248/chp... #LineagePlasticity #CRPC #CancerStemCells

Graphical abstract illustrating ARSI-induced lineage plasticity in prostate cancer. Androgen receptor signaling inhibition promotes transition from prostate adenocarcinoma (PRAD) to aggressive CRPC variants with increased mesenchymal, basal, stem-like, and neural cell states, highlighting reversibility and tumor heterogeneity.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 26/02/2026

📘 CHP Archive Spotlight #04 Review (2024) | Chen et al. Linking phenotype ↔ genotype at single-cell resolution. Reviews tools for isolating and profiling individual cells — key to understanding plasticity, metastasis & therapy resistance. 🔗 doi.org/10.47248/chp... #SingleCell #CancerHeterogeneity

Graphical abstract illustrating single-cell isolation and labeling techniques linking cell phenotype to genotype. Methods such as robotic aspiration, laser detachment, microraft arrays, optical tweezers, droplet microfluidics, and spatial omics enable selective retrieval and molecular analysis of individual cells to study cancer heterogeneity.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 26/02/2026

📖 Commentary Spotlight In the inaugural issue, Liu discusses how SMLR1 reshapes the liver metastatic niche through macrophage polarization, highlighting its role in cancer plasticity and immune modulation. 🔗 www.pivotscipub.com/chp/1/1/0002... #CancerHeterogeneity #TumorMicroenvironment

Graphical summary of SMLR1 in colorectal cancer liver metastasis. Primary colon tumor cells metastasize to the liver, where SMLR1 expression increases. SMLR1 interacts with macrophage receptors MRC1 (CD206) and SIGLEC1 (CD169), promoting macrophage polarization toward an immunosuppressive, pro-tumoral phenotype. The diagram highlights immune suppression and enhanced tumor growth within the liver-specific metastatic niche.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 26/02/2026

SMLR1 engages TAM markers MRC1 (CD206) & SIGLEC1 (CD169), linking metastatic CRC cells to immunosuppressive macrophages in the liver niche. A potential immune-evasion mechanism in CRLM. CHP 2024;1(1):0003 #TumorPlasticity #ImmuneEvasion

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 26/02/2026

📘 CHP Archive Spotlight #02 Original Research (2024) | Wong et al. 📢 New mechanistic insight in CRC liver metastasis: Cancer cells upregulate SMLR1 to engage immunosuppressive TAMs, reshaping the liver niche. 🔗 www.pivotscipub.com/chp/1/1/0003... #ColorectalCancer #TumorMicroenvironment

Graphical abstract illustrating colorectal cancer liver metastasis. Cancer cells in the colon metastasize to the liver, where they upregulate SMLR1. SMLR1 interacts with macrophage receptors MRC1 (CD206) and SIGLEC1 (CD169), promoting tumor–macrophage interactions within the liver microenvironment. Legend indicates cancer cells (green), macrophages (beige), and molecular interactions.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 26/02/2026

📘 CHP Archive Spotlight #01 Inaugural Editorial (2024) EIC Dean Tang outlines CHP’s mission: dissecting how cancer heterogeneity, plasticity & tumor microenvironment interactions drive therapy resistance, metastasis & recurrence. 📖 CHP 2024;1(1):0001 🔗 doi.org/10.47248/chp... #TumorPlasticity

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Reposted by Cancer Heterogeneity and Plasticity

Shaheen Sikandar @ssikandar.bsky.social · 09/12/2025

📢 We review the mechanisms of immune evasion in breast cancer, focusing on how cellular plasticity and the tumor immune microenvironment cooperate to suppress detection. 🧬 @chp-pivot.bsky.social www.pivotscipub.com/chp/3/1/0001... #breastcancer #ImmuneEvasion #TumorMicroenvironment #CellPlasticity

pivotscipub.com

The Trojan Horse Within: Mechanisms of Immune Evasion in Breast Cancer

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Reposted by Cancer Heterogeneity and Plasticity

Juan Carlos López-Gil @juancarloslpz13.bsky.social · 17/06/2025

Fresh from the oven!! Our latest review published in @chp-pivot.bsky.social about the origin of PDAC CSCs and their inner and outer determinants by Diego Navarro and myself. A little bit of inflammation, a little bit of CIN, tons of stemness!! Enjoy!! www.pivotscipub.com/chp/2/2/0010

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 20/02/2026

Considering submission? CHP welcomes research articles, reviews, perspectives, and methodological advances relevant to cancer heterogeneity and plasticity. The editorial team aims for a transparent and efficient review process with constructive feedback. Questions: chp@pivotscipub.com

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 20/02/2026

Why consider CHP? • Focused readership in tumor plasticity • Expert peer review • Open access & permanent archiving • Fees waived in 2026 If your work addresses cell state transitions, lineage plasticity, or microenvironment-driven evolution, CHP may be a good fit. Submission guidelines:

pivotscipub.com

Cancer Heterogeneity and Plasticity-Submission Instructions

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 20/02/2026

What distinguishes CHP? • Focused on cancer plasticity & heterogeneity • Cross-disciplinary scope (genomics, stem cell biology, tumor evolution) • Mechanistic insight into state transitions As lineage reprogramming is increasingly linked to therapy resistance, a focused venue matters.

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Cancer Heterogeneity and Plasticity @chp-pivot.bsky.social · 20/02/2026

CHP focuses on cancer cell states, lineage plasticity, and tumor microenvironment dynamics. Since 2024, we’ve published research and reviews advancing this area. Explore: www.pivotscipub.com/chp Looking forward to engaging with the cancer plasticity and heterogeneity community here on Bluesky.

Editorial board slide for Cancer Heterogeneity and Plasticity (CHP) listing seven editors with headshots and affiliations across USA, Germany, Japan, China, and Canada, including Dean G. Tang (Roswell Park), Anna Dubrovskа (OncoRay), Toru Kondo (Hokkaido), Jinsong Liu (MD Anderson), Suling Liu (Zhejiang University), Amina Zoubeidi (UBC), and Ping Mu (Yale).

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