Advances in targeted therapy for malignant lymphoma

Wang, Li; Qin, Wei; Huo, Yujia; Li, Xiao; Shi, Qingqing; Rasko, John E.J.; Janin, Anne; Zhao, Wei‐Li

doi:10.1038/s41392-020-0113-2

Cited by 70 publications

(57 citation statements)

References 501 publications

(519 reference statements)

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“…Lymphomas grow in the bone marrow and in the secondary lymphatic organs (SLOs), with a predominance of LNs and spleen, but they can also manifest in non-lymphoid tissues ( 2 ). The genetic and epigenetic alterations and the intracellular pathway dysregulations responsible for the pathogenesis and progression of lymphomas have been extensively studied and led to tremendous advancements in therapeutic intervention strategies ( 3 ). The idea of tumor dependency on cells in the surrounding of a a priori benign environment and on adapted organ properties goes back to Rudolph Virchow in the 19 th century ( 4 ).…”

Section: Introductionmentioning

confidence: 99%

Angiogenesis in Lymph Nodes Is a Critical Regulator of Immune Response and Lymphoma Growth

2020

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Tumor-induced remodeling of the microenvironment in lymph nodes (LNs) includes the formation of blood vessels, which goes beyond the regulation of metabolism, and shaping a survival niche for tumor cells. In contrast to solid tumors, which primarily rely on neo-angiogenesis, hematopoietic malignancies usually grow within pre-vascularized autochthonous niches in secondary lymphatic organs or the bone marrow. The mechanisms of vascular remodeling in expanding LNs during infection-induced responses have been studied in more detail; in contrast, insights into the conditions of lymphoma growth and lodging remain enigmatic. Based on previous murine studies and clinical trials in human, we conclude that there is not a universal LN-specific angiogenic program applicable. Instead, signaling pathways that are tightly connected to autochthonous and infiltrating cell types contribute variably to LN vascular expansion. Inflammation related angiogenesis within LNs relies on dendritic cell derived pro-inflammatory cytokines stimulating vascular endothelial growth factor-A (VEGF-A) expression in fibroblastic reticular cells, which in turn triggers vessel growth. In high-grade B cell lymphoma, angiogenesis correlates with poor prognosis. Lymphoma cells immigrate and grow in LNs and provide pro-angiogenic growth factors themselves. In contrast to infectious stimuli that impact on LN vasculature, they do not trigger the typical inflammatory and hypoxia-related stroma-remodeling cascade. Blood vessels in LNs are unique in selective recruitment of lymphocytes via high endothelial venules (HEVs). The dissemination routes of neoplastic lymphocytes are usually disease stage dependent. Early seeding via the blood stream requires the expression of the homeostatic chemokine receptor CCR7 and of L-selectin, both cooperate to facilitate transmigration of tumor and also of protective tumor-reactive lymphocytes via HEV structures. In this view, the HEV route is not only relevant for lymphoma cell homing, but also for a continuous immunosurveillance. We envision that HEV functional and structural alterations during lymphomagenesis are not only key to vascular remodeling, but also impact on tumor cell accessibility when targeted by T cell–mediated immunotherapies.

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Section: Introductionmentioning

confidence: 99%

Angiogenesis in Lymph Nodes Is a Critical Regulator of Immune Response and Lymphoma Growth

2020

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“…196 Moreover, it is a challenge to confirm treatment prescription according to clinical responses and toxic effects. 197 Thirdly, though targeting glycolysis has been testified scientific and reasonable for glioma treatment, it is still far from acheiving clinical success before entering clinical arena. Notably, metformin was verified to possess both an inhibitory effect of glioma cells and a protective effect of neurons.…”

Section: Discussionmentioning

confidence: 99%

<p>Emerging Roles and Therapeutic Interventions of Aerobic Glycolysis in Glioma</p>

Han¹,

Shi²,

Cao³

et al. 2020

OTT

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Glioma is the most common type of intracranial malignant tumor, with a great recurrence rate due to its infiltrative growth, treatment resistance, intra-and intertumoral genetic heterogeneity. Recently, accumulating studies have illustrated that activated aerobic glycolysis participated in various cellular and clinical activities of glioma, thus influencing the efficacy of radiotherapy and chemotherapy. However, the glycolytic process is too complicated and ambiguous to serve as a novel therapy for glioma. In this review, we generalized the implication of key enzymes, glucose transporters (GLUTs), signalings and transcription factors in the glycolytic process of glioma. In addition, we summarized therapeutic interventions via the above aspects and discussed promising clinical applications for glioma.

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“…Such combinations include R-GDP (NCT03373019), vinorelbine, liposomal doxorubicin, dexamethasone and thalidomide (VDDT) (NCT02733380), dexamethasone and ICE (DICE) (NCT03105596), and R-CHOP (NCT03201471) in relapsed or refractory B-NHL. A clinical trial of R-CHOP combined with chidamide (NCT02753647) in untreated elderly DLBCL patients is progressing (Wang L. et al, 2020).…”

Section: Chidamidementioning

confidence: 99%

Recent Update of HDAC Inhibitors in Lymphoma

Chen

Sethy

Liou

2020

Front. Cell Dev. Biol.

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Modulating epigenetic modification has been recognized for over a decade as an effective therapeutic approach to cancer and many studies of histone deacetylase (HDAC), one of the best known epigenetic modulators, have been published. HDAC modulates cell proliferation and angiogenesis and plays an essential role in cell growth. Research shows that up-regulated HDACs are present in many cancer types and synthetic or natural HDAC inhibitors have been used to silence overregulated HDACs. Inhibiting HDACs may cause arrest of cell proliferation, angiogenesis reduction and cell apoptosis. Recent studies indicate that HDAC inhibitors can provide a therapeutic effect in various cancers, such as B-cell lymphoma, leukemia, multiple myeloma and some virus-associated cancers. Some evidence has demonstrated that HDAC inhibitors can increase the expression of immune-related molecules leading to accumulation of CD8 + T cells and causing unresponsive tumor cells to be recognized by the immune system, reducing tumor immunity. This may be a solution for the blockade of PD-1. Here, we review the emerging development of HDAC inhibitors in various cancer treatments and reduction of tumor immunity.

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Advances in targeted therapy for malignant lymphoma

Cited by 70 publications

References 501 publications

Angiogenesis in Lymph Nodes Is a Critical Regulator of Immune Response and Lymphoma Growth

Angiogenesis in Lymph Nodes Is a Critical Regulator of Immune Response and Lymphoma Growth

<p>Emerging Roles and Therapeutic Interventions of Aerobic Glycolysis in Glioma</p>

Recent Update of HDAC Inhibitors in Lymphoma

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