B Lymphocytes and Cancer: A Love–Hate Relationship

Yuen, Grace J.; Demissie, Ezana; Pillai, Shiv

doi:10.1016/j.trecan.2016.10.010

Cited by 336 publications

(280 citation statements)

References 109 publications

Supporting

Mentioning

270

Contrasting

Unclassified

Order By: Relevance

“…This is interesting to note in regards to work characterizing autoantibodies as a major factor in driving the pro‐tumoral response . Immune complexes that are against intracellular tumor associated antigens presumably do not prime immune responses against tumors but instead might facilitate the differentiation of myeloid cells in the tumor milieu into myeloid‐derived suppressor cells, thus promoting tumorigenesis …”

Section: Tuning B Cell Receptor Signaling Within the Tumor Environmentmentioning

confidence: 99%

“…[121][122][123] Immune complexes that are against intracellular tumor associated antigens presumably do not prime immune responses against tumors but instead might facilitate the differentiation of myeloid cells in the tumor milieu into myeloid-derived suppressor cells, thus promoting tumorigenesis. 121,124 In adapter. Its inhibitory functions are therefore likely not to be direct.…”

Section: Siglecs and The Capture Of Tumor-derived Vesiclesmentioning

confidence: 99%

See 1 more Smart Citation

Viewing Siglecs through the lens of tumor immunology

Fraschilla

Pillai

2017

Immunological Reviews

Self Cite

106

View full text Add to dashboard Cite

Summary Many Siglecs function as inhibitory receptors on innate and adaptive immune cells and may contribute to the attenuation of immune responses to tumors. Siglec 9 on neutrophils and Siglec 7 on NK cells are prominent examples of inhibitory Siglecs that can potentially dampen anti-tumor immunity. CD169 is a Siglec that may function as an adhesion molecule and a facilitator of the recognition and internalization of sialic acid decorated apoptotic bodies and exosomes derived from tumors. It can potentially contribute to both the attenuation as well as the facilitation of anti-tumor immunity. Siglecs have been best studied in the tumor context in animal models of cancer. Modulators of Siglec function are likely to be developed and investigated clinically in a cancer context over the next few years.

show abstract

Section: Tuning B Cell Receptor Signaling Within the Tumor Environmentmentioning

confidence: 99%

Section: Siglecs and The Capture Of Tumor-derived Vesiclesmentioning

confidence: 99%

Viewing Siglecs through the lens of tumor immunology

Fraschilla

Pillai

2017

Immunological Reviews

Self Cite

106

View full text Add to dashboard Cite

show abstract

“…However, preclinical studies also indicated some tumor-promoting roles of B cells [62,63]. It is well characterized that TIL B cells can produce lymphotoxin, which is a survival factor that induce angiogenesis [64]. In prostate cancer models, the secreted lymphotoxin activates non-canonical and canonical NF-κB signaling and STAT3 in cancer cells, resulting in androgen-refractory growth and tumor progression [65][66][67].…”

Section: Double-edged Cellular Componentsmentioning

confidence: 99%

Complex interplay between tumor microenvironment and cancer therapy

Shen

Kang

2018

Front. Med.

View full text Add to dashboard Cite

Tumor microenvironment (TME) is comprised of cellular and non-cellular components that exist within and around the tumor mass. The TME is highly dynamic and its importance in different stages of cancer progression has been well recognized. A growing body of evidence suggests that TME also plays pivotal roles in cancer treatment responses. TME is significantly remodeled upon cancer therapies, and such change either enhances the responses or induces drug resistance. Given the importance of TME in tumor progression and therapy resistance, strategies that remodel TME to improve therapeutic responses are under developing. In this review, we provide an overview of the essential components in TME and the remodeling of TME in response to anti-cancer treatments. We also summarize the strategies that aim to enhance therapeutic efficacy by modulating TME.

show abstract

“…Therefore, although it may be speculated that in the PyMT-BO1 BrCa model B cells play an (early) anti-tumourigenic role, further studies are required to probe this in more detail. Notably, previous studies have indicated B cells can both promote and inhibit cancer progression (46), and mice specifically lacking B cells had no impact on primary tumour latency or progression in the MMTV-PyMT model (33), highlighting the complexity and dynamic nature of specific immune cell populations in cancer models.…”

Section: Discussionmentioning

confidence: 92%

Antibiotic-induced disturbances of the gut microbiota result in accelerated breast tumour growth via a mast cell-dependent pathway

Madgwick

et al. 2020

Preprint

View full text Add to dashboard Cite

One Sentence Summary:We show that breast cancer progression is accelerated through a unique/novel immune response involving mast cells as a result of an antibiotic induced perturbation of the gut microbiota in a mouse model. AbstractThe diverse community of commensal microbes that comprise the gut microbiota is known to play an integral role in human health, not least through its ability to regulate host immune responses and metabolic pathways. Alterations to the homeostasis of this community, including through the use of broad-spectrum antibiotics, have already been associated with the progression of several cancers, namely melanoma and liver. The aggressive nature of breast cancer (BrCa), largely due to its ability to metastasize early, has ranked the disease with the second highest mortality rate of all cancers globally. Yet the body of research into the complex relationship between the microbiota and BrCa is still limited. This study found that a depletion of the microbiota, through the administration of antibiotics, significantly increased the rate of primary tumour progression in mouse BrCa models. We show that antibiotic-induced microbiota disturbances lead to changes in behaviour of a relatively obscure tumour-immune cell population: mast cells. We observed increases in tumour stroma-associated mast cells in antibiotic treated animals. Moreover, inhibition of mast cell degranulation, via cromolyn, slowed tumour progression in antibiotic treated animals but not in control animals. Thus, it appears that a perturbed microbiota drives stroma-associated mast cell recruitment and activation, which in turn promotes primary tumour growth through an as yet unknown mechanism.

show abstract

B Lymphocytes and Cancer: A Love–Hate Relationship

Cited by 336 publications

References 109 publications

Viewing Siglecs through the lens of tumor immunology

Viewing Siglecs through the lens of tumor immunology

Complex interplay between tumor microenvironment and cancer therapy

Antibiotic-induced disturbances of the gut microbiota result in accelerated breast tumour growth via a mast cell-dependent pathway

Contact Info

Product

Resources

About