Prognostic role of B7-H4 in patients with non-small cell lung cancer: A meta-analysis

Tan, Zhibo; Shen, Weitao

doi:10.18632/oncotarget.15648

Cited by 12 publications

(11 citation statements)

References 35 publications

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“…Following injection of the CT26 [B7x] tumor cells i.v., we demonstrated that B7x accelerated the development of pulmonary metastases compared to the CT26 [MSCV] controls. This is in accord with a majority of current clinical studies highlighting that tumor-expressed B7x associates with a poor clinical outcome [ 21 , 38 , 39 ].…”

Section: Discussionsupporting

confidence: 88%

Tumor-expressed immune checkpoint B7x promotes cancer progression and antigen-specific CD8 T cell exhaustion and suppressive innate immune cells

et al. 2017

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B7x (B7-H4 or B7S1) is a coinhibitory member of the B7 immune checkpoint ligand family that regulates immune function following ligation with its unknown cognate receptors. B7x has limited expression on normal tissues, but is up-regulated on solid human tumors to inhibit anti-tumor immunity and associates with poor clinical prognosis. We assessed the contribution of cytokine stimuli to induce surface B7x expression on cancer cells and the role of tumor-expressed B7x in a murine pulmonary metastasis model, and finally evaluated the potential interaction between B7x and Neuropilin-1, a suggested potential cognate receptor. We showed that pro-inflammatory and anti-inflammatory cytokines IFNγ, TNFα, and IL-10 did not induce expression of B7x on human or murine cancer cells. Following i.v. injection of CT26, a murine colon cancer cell line in the BALB/c background, we observed a significant increase in tumor burden in the lung of B7x-expressing CT26 mice compared to B7x-negative parental CT26 control mice. This was marked by a significant increase in M2 tumor associated macrophages and antigen-specific CD8 T cell exhaustion. Finally, we found through multiple systems that there was no evidence for B7x and Neuropilin-1 direct interaction. Thus, the B7x pathway has an essential role in modulating the innate and adaptive immune cell infiltrate in the tumor microenvironment with its currently unknown cognate receptor(s).

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Section: Discussionsupporting

confidence: 88%

Tumor-expressed immune checkpoint B7x promotes cancer progression and antigen-specific CD8 T cell exhaustion and suppressive innate immune cells

et al. 2017

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“…Increases in B7-H4 would attenuate the presentation of glioma antigens and result in a poor immune response. The prognostic value of elevated levels of B7-H4 expression has been reported in gastric 39,40 , pancreatic 40 , and non-small-cell lung cancers 41,42 . Expression positively associates with progression in prostate cancer 43 .…”

Section: Discussionmentioning

confidence: 98%

Measuring Cancer Hallmark Mediation of the TET1 Glioma Survival Effect with Linked Neural-Network Based Mediation Experiments

Luechtefeld¹,

Lin²,

Paller

et al. 2020

Sci Rep

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This paper examines the effect of TET1 expression on survival in glioma patients using open-access data from the Genomic Data Commons. A neural network-based survival model was built on expression data from a selection of genes most affected by TET1 knockdown with a median cross-validated survival concordance of 82.5%. A synthetic experiment was then conducted that linked two separately trained neural networks: a multitask model estimating cancer hallmark gene expression from TET1 expression, and a survival neural network. This experiment quantified the mediation of the TET1 survival effect through eight cancer hallmarks: apoptosis, cell cycle, cell death, cell motility, DNA repair, immune response, two phosphorylation pathways, and a randomized gene sets. Immune response, DNA repair, and apoptosis displayed greater mediation than the randomized gene set. Cell motility was inversely associated with only 12.5% mediated concordance. We propose the neural network linkage mediation experiment as an approach to collecting evidence of hazard mediation relationships with prognostic capacity useful for designing interventions. Gliomas represent approximately 75% of primary brain tumors in adults. The median survival of adult patients with gliomas is less than five years, with overall survival of 8-14 months for patients with glioblastoma multiforme (GBM) 1. The current standard of care includes surgery followed by radiation therapy and treatment with temozolomide. The therapy causes cells to die as a result of extensive DNA damage. Factors that contribute to recurrence are glioma invasiveness, the growth of cell populations resistant to radiation and temozolomide, and the blood brain barrier 2,3. Classifications of gliomas have been adding molecular features to histology for better diagnosis, especially under circumstances when histological phenotype is unclear. For example, the revised World Health Organization classifications now include 1p/19q co-deletion as a defining feature of oligodendroglial tumors 4. The use of molecular features will result in more precise prognosis and in the design of treatments tailored to the tumor. Resistance to the alkylating agent temozolomide is associated with promoter methylation of the gene encoding the DNA repair protein O6-methylguanine-DNA methyltransferase 5. We recently reported that glioma cell lines deficient with Tet methylcytosine dioxygenase 1 (TET1) exhibited greater genomic instability and were more resistant to ionizing radiation therapy 6. TET1 belongs to a family of enzymes comprised of three members that catalyzes the conversion of 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC), which is the initial step of DNA demethylation 7. We found that TET1-deficient cells displayed an attenuated DNA damage response (DDR). TET1-deficient cells fail to undergo apoptosis in response to ionizing radiation and have attenuated DNA repair resulting in high numbers of DNA strand breaks in the survival cell population 6,8. There has also been evidence indicating the involvem...

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“…By reviewing the literature, we also find that some authors use meta-analysis to investigate the correlation between B7-H4 and prognosis of cancer patients. [ 34 – 36 ] Their research also suggests that the high expression of B7-H4 is associated with worse OS in different cancer. However, different studies suggest that the level of B7-H4 expression is associated with different clinical pathological features in various cancers.…”

Section: Discussionmentioning

confidence: 99%

“…However, different studies suggest that the level of B7-H4 expression is associated with different clinical pathological features in various cancers. For example, Tan and Shen [ 34 ] reported that the correlation between B7-H4 and lymph node metastasis, advanced TNM stage and poor differentiation in patients with nonsmall cell lung cancer. But our study reveals that it correlates with lymph node metastasis and higher TNM tumor staging in PC.…”

Section: Discussionmentioning

confidence: 99%

The prognostic value of B7-H4 in pancreatic cancer

Chen

Luan²,

Yuan³

et al. 2018

Medicine

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Background:There were many reports suggesting that different kinds of tumors can express B7-H4; however, the prognostic value in cancer was still unclearly. Therefore, we conducted a meta-analysis to investigate the relationship between overexpression of B7-H4 with the prognostic value in pancreatic cancer patients.Materials and Methods:The Pubmed, Embase, Cochrane Library, Ovid, Web of Science, and Chinese research database (including CBM, CNKI, and WAN FANG) were searched for related literature published until October 12, 2017. The pooled odds ratios (ORs) and/or pooled hazard ratios (HRs) for clinical pathological factors and overall survival (OS) were calculated and analyzed using Stata software. To assess whether an individual study had an impact on the result, sensitivity analysis was performed for all included individual studies using the fixed-effects model. Publication bias was evaluated using Egger's and Begg's tests.Results:Data from 6 observational studies including 442 patients were summarized in this meta-analysis, and each study was eligible for inclusion based on included and exclude criteria. The pooled results indicated that the B7-H4 overexpression could predict the presentation of lymph node metastasis (OR = 3.94, 95% CI: 1.22–12.66, P = .022), advanced TNM stage (T = the extent of the primary tumor, N = regional lymph nodes, M = distant metastases) (III+IV vs I+II; OR = 7.63, 95% CI: 2.46–23.66, P < .001), and the poor OS (HR = 3.00, 95%CI = 2.20–4.10, P < .001) in PC patients.Conclusions:This study reveals that high expression of B7-H4 is an unfavorable prognostic factor for patients with pancreatic cancer. These results may guide the clinical management of this patient population.

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Prognostic role of B7-H4 in patients with non-small cell lung cancer: A meta-analysis

Cited by 12 publications

References 35 publications

Tumor-expressed immune checkpoint B7x promotes cancer progression and antigen-specific CD8 T cell exhaustion and suppressive innate immune cells

Tumor-expressed immune checkpoint B7x promotes cancer progression and antigen-specific CD8 T cell exhaustion and suppressive innate immune cells

Measuring Cancer Hallmark Mediation of the TET1 Glioma Survival Effect with Linked Neural-Network Based Mediation Experiments

The prognostic value of B7-H4 in pancreatic cancer

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