New murine models of aggressive lymphoma

Flümann, Ruth; Nieper, Pascal; Reinhardt, Hans Christian; Knittel, Gero

doi:10.1080/10428194.2019.1691200

Cited by 4 publications

(2 citation statements)

References 76 publications

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“…Many patients do not respond to cisplatin‐based chemotherapy. Immunotherapy has provided an alternative approach; however, only about 20% of patients respond, and molecular sub‐typing of tumors means that those who respond to cisplatin and those who respond to immunotherapy may have substantial overlap (Flümann, Nieper, Reinhardt, & Knittel, 2020). The restoration of cisplatin sensitivity remains a significant barrier to better patient treatment.…”

Section: Curcumin–cisplatin Co‐therapymentioning

confidence: 99%

Curcumin–cisplatin chemotherapy: A novel strategy in promoting chemotherapy efficacy and reducing side effects

Hussain

Islam

Khan

et al. 2021

Phytotherapy Research

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The efficacy of chemotherapy in cancer therapy is limited due to resistance, treatment selectivity, and severe adverse effects. Immunotherapy, chemotherapy, targeted therapy, radiation, and surgery are the most common therapeutic strategies for treatment, with chemotherapy being the most successful. Nonetheless, these treatments exhibit poor effectiveness due to toxicity and resistance. Therefore, combination therapies of natural products may be used as an effective and novel strategy to overcome such barriers. Cisplatin is a platinum‐based chemotherapy agent, and when administered alone, it can lead to severe adverse effects and resistance mechanism resulting in therapeutic failure. Curcumin is a polyphenolic compound extracted from turmeric (Curcuma longa) exhibiting anticancer potential with minimal adverse effects. The combination therapy of curcumin and cisplatin is a novel strategy to mitigate/attenuate cisplatin‐related adverse effects and improve the barrier of resistance reducing unwanted effects. However, there are uncertainties on the efficacy of curcumin, and more in depth and high‐quality studies are needed. This review aims to explain the adverse effects related to individual cisplatin delivery, the positive outcome of individual curcumin delivery, and the combination therapy of curcumin and cisplatin from nano platform as a novel strategy for cancer therapy.

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Section: Curcumin–cisplatin Co‐therapymentioning

confidence: 99%

Curcumin–cisplatin chemotherapy: A novel strategy in promoting chemotherapy efficacy and reducing side effects

Hussain

Islam

Khan

et al. 2021

Phytotherapy Research

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“…Among others, mouse models of lymphoid malignancies have advanced our understanding of lymphomagenesis [reviewed in (57)(58)(59)(60)] and currently support the biological investigations on the most common putative driver mutations alone or in combination. The limited access to (pre)malignant biopsies during the initiating stage of lymphoma development, the difficulties to recapitulate in in vitro experimental systems the complexity of the GC reaction during an immune response (61), the spatial and (epi)genetic heterogeneity across and within human lymphomas make the development of genetically engineered mice models the most suitable tool i) to characterize the molecular mechanisms by which candidate lymphoma mutations contribute in vivo to lymphomagenesis either alone or in combination and ii) to trace how tumours grow and evolve over time by recapitulating the precise timing at which the genetic lesions happens in human settings iii) to test the effects of targeted pharmacological agents and iv) the synergy between co-occurring genetic alterations.…”

Section: Introductionmentioning

confidence: 99%

Human B Lymphomas Reveal Their Secrets Through Genetic Mouse Models

et al. 2021

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Lymphomas are cancers deriving from lymphocytes, arising preferentially in secondary lymphoid organs, and represent the 6th cancer worldwide and the most frequent blood cancer. The majority of B cell Non-Hodgkin lymphomas (B-NHL) develop from germinal center (GC) experienced mature B cells. GCs are transient structures that form in lymphoid organs in response to antigen exposure of naive B cells, and where B cell receptor (BCR) affinity maturation occurs to promote B cell differentiation into memory B and plasma cells producing high-affinity antibodies. Genomic instability associated with the somatic hypermutation (SHM) and class-switch recombination (CSR) processes during GC transit enhance susceptibility to malignant transformation. Most B cell differentiation steps in the GC are at the origin of frequent B cell malignant entities, namely Follicular Lymphoma (FL) and GCB diffuse large B cell lymphomas (GCB-DLBCL). Over the past decade, large sequencing efforts have provided a great boost in the identification of candidate oncogenes and tumor suppressors involved in FL and DLBCL oncogenesis. Mouse models have been instrumental to accurately mimic in vivo lymphoma-specific mutations and interrogate their normal function in the GC context and their oncogenic function leading to lymphoma onset. The limited access of biopsies during the initiating steps of the disease, the cellular and (epi)genetic heterogeneity of individual tumors across and within patients linked to perturbed dynamics of GC ecosystems make the development of genetically engineered mouse models crucial to decipher lymphomagenesis and disease progression and eventually to test the effects of novel targeted therapies. In this review, we provide an overview of some of the important genetically engineered mouse models that have been developed to recapitulate lymphoma-associated (epi)genetic alterations of two frequent GC-derived lymphoma entities: FL and GCB-DLCBL and describe how those mouse models have improved our knowledge of the molecular processes supporting GC B cell transformation.

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An Overview on Diffuse Large B-Cell Lymphoma Models: Towards a Functional Genomics Approach

Yanguas‐Casás¹,

Pedrosa

Fernández‐Miranda

et al. 2021

Cancers

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Lymphoma research is a paradigm of the integration of basic and clinical research within the fields of diagnosis and therapy. Clinical, phenotypic, and genetic data are currently used to predict which patients could benefit from standard treatment. However, alternative therapies for patients at higher risk from refractoriness or relapse are usually empirically proposed, based on trial and error, without considering the genetic complexity of aggressive B-cell lymphomas. This is primarily due to the intricate mosaic of genetic and epigenetic alterations in lymphomas, which are an obstacle to the prediction of which drug will work for any given patient. Matching a patient’s genes to drug sensitivity by directly testing live tissues comprises the “precision medicine” concept. However, in the case of lymphomas, this concept should be expanded beyond genomics, eventually providing better treatment options for patients in need of alternative therapeutic approaches. We provide an overview of the most recent findings in diffuse large B-cell lymphomas genomics, from the classic functional models used to study tumor biology and the response to experimental treatments using cell lines and mouse models, to the most recent approaches with spheroid/organoid models. We also discuss their potential relevance and applicability to daily clinical practice.

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New murine models of aggressive lymphoma

Cited by 4 publications

References 76 publications

Curcumin–cisplatin chemotherapy: A novel strategy in promoting chemotherapy efficacy and reducing side effects

Curcumin–cisplatin chemotherapy: A novel strategy in promoting chemotherapy efficacy and reducing side effects

Human B Lymphomas Reveal Their Secrets Through Genetic Mouse Models

An Overview on Diffuse Large B-Cell Lymphoma Models: Towards a Functional Genomics Approach

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