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Biochemistry, Genetics and Molecular Biology · Research topic

Open research questions in Cancer, Lipids, and Metabolism

527 gap statements mined from Cancer, Lipids, and Metabolism papers in our 7.9M-paper local library, which holds 1,547 papers on the topic — drawn mostly from each paper's own stated research gap, future-work, challenge and limitation notes, and its abstract. The ones listed below are a selection still marked open; each names the study that raised it, with a DOI link where the paper has one.

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What the literature leaves open

  • It highlights the need for causal models and multi-omics integration to better understand the endocrine-microbiome axis. The paper also discusses the challenges of translating findings from experimental models to human populations, including the need for longitudinal sampling and prespecified confounder control.

    Beyond estrobolome 1.0: unraveling endocrine-microbiome axis as a driver and therapeutic target in hormone-driven cancers · 2026 · DOI

  • The next challenge is to move from association to causality and to apply methodological rigor to probe disease-stage-specific mechanisms. Future work should define how lipid flux is translated into locus-specific chromatin remodeling, which of these changes are reversible, and when they become sufficiently stable to lock cells into maladaptive states.

    Epigenomic Remodeling by Lipid Metabolism: A Cross-Disease Perspective on Cancer and Brain Disorders · 2026 · DOI

  • While there is a noted clinical correlation between hypercholesterolemia and the progression of PCa, the precise role of extracellular LDL in this context remains unclear.

    Elevated low-density lipoprotein cholesterol levels and prostate cancer risk: UK Biobank evidence · 2026 · DOI

  • Limited understanding of the role of fatty acid metabolism in PDAC. Need for effective pharmacological approaches to target fatty acid metabolism in PDAC.

    Fatty acids metabolic reprogramming and tumor microenvironment in pancreatic cancer: targeting pathways · 2026 · DOI

  • The underlying molecular mechanisms driving liver cancer initiation and progression remain incompletely understood. The metabolic reprogramming events that facilitate aggressive phenotypes in liver cancer are not well understood. The role of TAF3 in liver cancer progression is not well understood.

    The TAF3/SREBP2/cholesterol axis drives tumor progression in hepatocellular carcinoma · 2026 · DOI

  • Further longitudinal and mechanistic studies are warranted to determine whether LCN2 actively contributes to cachexia pathophysiology or primarily reflects inflammatory stress, and to evaluate its potential utility in patient stratification and therapeutic monitoring.

    Circulating lipocalin-2 is associated with systemic inflammation and cachexia-related features in patients with gastrointestinal cancer · 2026 · DOI

  • PLA2G16 may therefore represent a candidate molecular link between lipid metabolism, autophagy regulation, and OXA sensitivity, although whether its effects on the OXA response depend on lipophagy remains to be established.

    Lipid metabolism mediating oxaliplatin resistance in colorectal cancer · 2026 · DOI

  • However, the specific mechanisms linking FFAR1/4 signaling to CDDP sensitivity in lung cancer remain unclear. Cytokines, growth factors, and lipid mediators may contribute to these effects, but their roles remain to be determined.

    Differential responsiveness to stromal fibroblasts in highly invasive lung cancer cells is associated with free fatty acid receptor 1 (FFAR1) and FFAR4 signaling · 2026 · DOI

  • 3-Hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2), a mitochondrial enzyme involved in ketogenesis, has been linked to tumor progression, but its role in CCA remains unclear.

    SIRT3 Regulates HMGCS2 Deacetylation and Influences Cholangiocarcinoma Progression via the Metabolism of Ketone Bodies · 2026 · DOI

  • Deep-phenotyping approaches that integrate Mendelian randomisation with multi-omic readouts should clarify whether on-target (HMGCR-dependent) or off-target pathways, such as TLR4/MyD88, NLRP3 or PAR-2, drive the clinically relevant immunomodulation seen in disparate diseases.

    Molecular and Immunomodulatory Mechanisms of Statins in Inflammation and Cancer Therapeutics with Emphasis on the NF-κB, NLRP3 Inflammasome, and Cytokine Regulatory Axes · 2025 · DOI

  • Due to limited data and sometimes contradictory results, a deeper understanding of the molecular interrelationship between cancer cells and PRAT may provide the foundation of future personalized therapy development, favoring the establishment of an anti-tumor microenvironment and leading to improved oncologic patient prognosis.

    The Role of Perirenal Adipose Tissue in Carcinogenesis—From Molecular Mechanism to Therapeutic Perspectives · 2025 · DOI

  • Nonetheless, the associated molecular mechanisms remain unclear. Few previous studies using a very low number of DLBCL cell lines suggested that the ABC DLBCL subset may be more sensitive to FASN inhibition, although with seemingly contradictory results.

    Fatty Acid Metabolism Provides an Essential Survival Signal in OxPhos and BCR DLBCL Cells · 2025 · DOI

  • Our previous study also revealed that CD36 was abundantly expressed by OSCCs and involved in the proliferation and migration of the tumor cells, whereas little is known about the role of CD36 in the host immune responses in OSCCs.

    Targeting CD36-Mediated Lipid Metabolism by Selective Inhibitor-Augmented Antitumor Immune Responses in Oral Cancer · 2024 · DOI

  • The regulation of CD36 expression by peripheral adipocytes, as well as the specific enhancement of metastatic potential in CD36+ metastasis-initiating cells through a high-fat diet, suggests the need to control the quantity and composition of dietary lipids.

    CD36: The Bridge between Lipids and Tumors · 2024 · DOI

  • As the field of lipidomics is still in its early stages, additional research across the spectrum of glioblastoma, from diagnosis, prognosis, and targeted therapies, would be beneficial. There is particular promise in the discovery of lipid biomarkers that are reliable as early biomarkers, or perhaps that can denote risk factors of disease.

    The Lipidomic Signature of Glioblastoma: A Promising Frontier in Cancer Research · 2024 · DOI

  • The paper identifies a need for further exploration into the key genes that regulate lipid metabolism.

    The Critical Role of Lipid Metabolism in Health and Diseases · 2024 · DOI

  • Few studies have reported the ability of the classical NF-κB pathway to promote either mitochondrial respiration or Warburg effect in cancer cells.

    The alternative NF-κB RelB subunit is a novel critical sensor of lipid metabolism to promote tumor development · 2026 · DOI

  • Validate TAF3 expression across etiologically diverse HCC cohorts (e.g., HBV, HCV, NAFLD) to determine whether our findings are universal or subtype-specific. Investigate whether circulating cholesterol levels or a TAF3/SREBP2 gene signature in tumor tissue can serve as predictive or prognostic biomarkers. Explore the downstream mechanisms through which elevated cholesterol promotes HCC invasion and metastasis.

    The TAF3/SREBP2/cholesterol axis drives tumor progression in hepatocellular carcinoma · 2026 · DOI

  • Lipid metabolic reprogramming is histotype- and context-dependent across tumor cells, host metabolism, immune-spatial niches and treatment response. PTC evidence supports altered fatty acid acquisition, synthesis, desaturation, oxidation and membrane remodeling linked to recurrence and metastasis. In aggressive tumors, cholesterol synthesis, FAO adaptation and ferroptosis defense are plausible resistance mechanisms.

    Lipid Metabolic Reprogramming in Thyroid Cancer: Systemic Biomarkers, Tumor Dependencies and Therapeutic Resistance · 2026 · DOI

  • An integrative therapeutic strategy that simultaneously engages apoptosis, ACD, necroptosis, pyroptosis, and ferroptosis in OSCC could, in principle, yield more complete tumor eradication than single-pathway approaches, as recent comprehensive analyses have underscored the complex interplay and potential synergy among these regulated cell death modalities in oral cancer.

    Therapeutic Targeting of Apoptosis, Autophagic Cell Death, Necroptosis, Pyroptosis, and Ferroptosis Pathways in Oral Squamous Cell Carcinoma: Molecular Mechanisms and Potential Strategies · 2025 · DOI

  • The reprogramming of lipid metabolism in cancer cells is extremely closely related to redox homeostasis. Increased metabolic activity is accompanied by ROS production, which in turn affects lipid metabolic homeostasis at multiple levels.

    Oxidative Stress and Reprogramming of Lipid Metabolism in Cancers · 2025 · DOI

  • Emerging technologies in spatial metabolomics and single-cell metabolomics are revolutionizing our understanding of metabolic heterogeneity within tumours, which is essential in tumour progression, tumour microenvironment, and therapeutic response.

    Unveiling Metabolic Signatures as Potential Biomarkers in Common Cancers: Insights from Lung, Breast, Colorectal, Liver, and Gastric Tumours · 2025 · DOI

  • During the early stages of CRC development, oncogenic APC/b-catenin signaling promotes de novo lipogenesis, providing transformed intestinal epithelial cells with increased lipid availability for membrane biogenesis, energy production, and signal transduction.

    Lipid metabolism: a potential checkpoint for cGAS-STING regulation in colorectal cancer · 2026 · DOI

  • AML exhibits a coordinated reprogramming of cholesterol metabolism that extends far beyond increased lipid availability.

    Cholesterol Reprogramming in Acute Myeloid Leukemia: Integrating Tumor-Intrinsic Metabolism and Immune Crosstalk · 2026 · DOI

  • Future studies should explore the extrapolation of oxLDL-targeted strategies developed for CRC to other oxidative stress-rich tumors, while multidisciplinary approaches integrating technological innovations…

    Oxidized Low-Density Lipoprotein as a Potential Target for Enhancing Immune Checkpoint Inhibitor Therapy in Microsatellite-Stable Colorectal Cancer · 2025 · DOI

Most-cited papers in Cancer, Lipids, and Metabolism

Most recent work

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Open questions raised by papers listed on this page include: (1) Future work should define how lipid flux is translated into locus-specific chromatin remodeling, which of these changes are reversible, and when they become sufficiently stable to lock cells into maladaptive states (“Epigenomic Remodeling by Lipid Metabolism: A Cross-Disease Perspective on…”, 2026); (2) While there is a noted clinical correlation between hypercholesterolemia and the progression of PCa, the precise role of extracellular LDL in this context remains unclear (“Elevated low-density lipoprotein cholesterol levels and prostate cancer risk:…”, 2026); (3) The underlying molecular mechanisms driving liver cancer initiation and progression remain incompletely understood (“The TAF3/SREBP2/cholesterol axis drives tumor progression in hepatocellular…”, 2026); (4) PLA2G16 may therefore represent a candidate molecular link between lipid metabolism, autophagy regulation, and OXA sensitivity, although whether its effects on the OXA response depend on lipophagy remains to be established (“Lipid metabolism mediating oxaliplatin resistance in colorectal cancer”, 2026); (5) The specific mechanisms linking FFAR1/4 signaling to CDDP sensitivity in lung cancer remain unclear (“Differential responsiveness to stromal fibroblasts in highly invasive lung…”, 2026). 527 gap statements have been mined from Cancer, Lipids, and Metabolism papers in our 7.9M-paper local library, which holds 1,547 papers on the topic; the gaps come from whichever of those papers state one. They are mostly the research gaps the authors state and the papers' abstracts, plus future-work, limitations and challenges passages. The ones listed below are a selection still marked open; each names the study that raised it, with a DOI link where the paper has one, so you can read the original claim in context.

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