Cancer / Oncology/Non-Hodgkin lymphoma
Hematologic · type
Non-Hodgkin lymphoma
Clinical / Scientific
NHL is a family (DLBCL, follicular, mantle, Burkitt, T-cell). Shared maps include B-cell /NF-κB, BCL-2, MYC and . Subtype genetics differ enough that adjuncts should be read as class-level hypotheses unless specified.
Core Biological Drivers
BCR / NF-κB
Especially ABC-DLBCL.
BCL-2
Follicular and double-hit biology.
MYC
Burkitt and high-grade transformations.
Key Pathways
Scientific explanation
NF-κB factors link inflammatory cytokines and innate sensors to survival, production and sometimes therapy resistance.
Scientific explanation
BCL-2, BCL-XL, MCL-1 and BAX/BAK control outer-membrane permeabilization, a core checkpoint frequently skewed toward survival in lymphoid and solid tumours.
Scientific explanation
MYC factors coordinate biomass accumulation, ribosome biogenesis, and glutamine use. Amplification or pathway activation is common.
Scientific explanation
phosphorylates PIP2 to PIP3, recruiting . supports growth, survival, glucose uptake and mTORC1 input. Pathway activation is common via PIK3CA mutation, PTEN loss or -tyrosine- signalling.
Scientific explanation
mTORC1 integrates growth-factor and nutrient signals to drive protein synthesis, lipid synthesis and suppression. It sits downstream of PI3K/AKT and amino-acid sensing.
Scientific explanation
receptors signal through JAKs to STATs. in particular supports survival, invasion and inflammatory gene programmes in many solid and hematologic tumours.
Scientific explanation
Intrinsic and extrinsic apoptotic programmes remove damaged cells. Evasion of is a hallmark, via BCL-2 family imbalance, death- decoys, or p53 loss.
Scientific explanation
Aerobic (Warburg metabolism) supports ATP, biomass and redox buffering even when oxygen is available. Hexokinase, PKM2 and lactate export are frequent nodes.
Pathway Convergence
Target → pathway → downstream effect → biological consequence. Shared intersections are mechanistic maps, not protocols.
Growth-factor signalling
Ligand or mutation-driven RTK input feeds PI3K/AKT and mTORC1, supporting anabolic growth. This is a map of signalling, not a treatment protocol.
Inflammatory survival
Chronic cytokine tone activates NF-κB and STAT3 transcriptional programmes that favour survival, invasion and sometimes immune evasion.
Energy stress
Energetic stress activates AMPK, which can restrain mTORC1. Biguanides and related tools map onto this axis in models.
Metabolic Vulnerabilities
Aerobic supports ATP, biomass and acidification even when oxygen is available. Extent varies by tumour and remains a vulnerability hypothesis rather than a uniform target.
Glutamine anaplerosis and nucleotide nitrogen demand are prominent in MYC-high and rapidly proliferating tumours. Dependence is heterogeneous.
Tumor Microenvironment
Tumour-associated macrophages and myeloid-derived suppressor cells secrete cytokines that support invasion and blunt cytotoxic T cells.
Metastasis Module
Leukemias and related neoplasms disseminate by trafficking rather than classical -driven carcinoma . Marrow, blood and lymphoid niches dominate.
Resistance Biology
BCL-2 persistence, BCR bypass and efflux.
Cancer Stemness
Wnt, Notch, Hedgehog, ALDH and CD44-associated programmes can mark stem-like fractions with quiescence and therapy tolerance. These markers are not interchangeable across tumour types.
Mechanism-Based Adjunctive Strategies
Compounds appear only where a mechanistic overlap exists for this cancer. Evidence tiers are not equivalent. Nothing here is a treatment recommendation.
Curcumin
Target / Mechanism
Polyphenol with promiscuous in-vitro NF-κB, and ROS effects. Bioavailability is poor; dish activity does not establish clinical anticancer efficacy.
Cancer relevance
In-vitro NF-κB/ effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Inflammatory-signalling dish models. Convergence: NF-κB, JAK/STAT.
Target / Mechanism
Modest complex I inhibition raises AMP:ATP, activating and restraining hepatic and -linked anabolism. Direct antineoplastic efficacy is not established from that pharmacology alone.
Cancer relevance
activation and restraint provide a metabolic rationale in - and -linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Metabolic adjunctive research context. Convergence: AMPK, mTOR, Glycolysis.
Target / Mechanism
Benzimidazole that binds β-. Mammalian disruption, mitotic arrest and related signalling in cancer models are preclinical and are not an approved anticancer use.
Cancer relevance
disruption can trigger mitotic stress and in cell and animal models. This is not an established oncology use.
Experimental antimitotic / microtubule stress. Convergence: Apoptosis, p53.
Disulfiram
Target / Mechanism
ALDH ; copper-complexed forms can inhibit proteasome and NF-κB-related survival programmes in models. Clinical oncology evidence remains limited.
Cancer relevance
ALDH and copper-dependent proteasome/NF-κB stress in models; clinical oncology remains limited.
ALDH / redox experimental context. Convergence: Cancer stemness, NF-κB, Oxidative stress.
Target / Mechanism
Lysosomotropic agent that raises endosomal/autophagosomal pH, impairing flux. Combination trials in oncology have been mixed; blockade is not equivalent to proven benefit.
Cancer relevance
Lysosomal pH elevation impairs flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
Autophagy-modulation research combinations. Convergence: Autophagy.
Research Context
- Hallmarks. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646-674. https://doi.org/10.1016/j.cell.2011.02.013
- NF-κB. Karin M. NF-κB as a critical link between inflammation and cancer. Cold Spring Harb Perspect Biol. 2009;1(5):a000141. https://doi.org/10.1101/cshperspect.a000141
This oncology atlas is educational. Pathway maps, adjunctive strategies, and compound listings describe mechanistic relevance. They do not establish clinical efficacy, do not recommend treatment, and are not a substitute for oncology care. Evidence tiers are not equivalent.