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Article: Anti-CD47 immunotherapy as a therapeutic strategy for the treatment of breast cancer brain metastasis.

Mackert, Jessica D / Stirling, Elizabeth R / Wilson, Adam S / Westwood, Brian / Zhao, Dawen / Lo, Hui-Wen / Metheny-Barlow, Linda / Cook, Katherine L / Lesser, Glenn J / Soto-Pantoja, David R

bioRxiv : the preprint server for biology

2023

Abstract: The presence of cell surface protein CD47 allows cancer cells to evade innate and adaptive immune surveillance resulting in metastatic spread. CD47 binds to and activates SIRPα on the surface of myeloid cells, inhibiting their phagocytic activity. On the ...

Abstract	The presence of cell surface protein CD47 allows cancer cells to evade innate and adaptive immune surveillance resulting in metastatic spread. CD47 binds to and activates SIRPα on the surface of myeloid cells, inhibiting their phagocytic activity. On the other hand, CD47 binds the matricellular protein Thrombospondin-1, limiting T-cell activation. Thus, blocking CD47 is a potential therapeutic strategy for preventing brain metastasis. To test this hypothesis, breast cancer patient biopsies were stained with antibodies against CD47 to determine differences in protein expression. An anti-CD47 antibody was used in a syngeneic orthotopic triple-negative breast cancer model, and CD47 null mice were used in a breast cancer brain metastasis model by intracardiac injection of the E0771-Br-Luc cell line. Immunohistochemical staining of patient biopsies revealed an 89% increase in CD47 expression in metastatic brain tumors compared to normal adjacent tissue (p ≤ 0.05). Anti-CD47 treatment in mice bearing brain metastatic 4T1br3 orthotopic tumors reduced tumor volume and tumor weight by over 50% compared to control mice (p ≤ 0.05) and increased IBA1 macrophage/microglia marker 5-fold in tumors compared to control (p ≤ 0.05). Additionally, CD47 blockade increased the M1/M2 macrophage ratio in tumors 2.5-fold (p ≤ 0.05). CD47 null mice had an 89% decrease in metastatic brain burden (p ≤ 0.05) compared to control mice in a brain metastasis model. Additionally, RNA sequencing revealed several uniquely expressed genes and significantly enriched genes related to tissue development, cell death, and cell migration tumors treated with anti-CD47 antibodies. Thus, demonstrating that CD47 blockade affects cancer cell and tumor microenvironment signaling to limit metastatic spread and may be an effective therapeutic for triple-negative breast cancer brain metastasis.
Language	English
Publishing date	2023-07-25
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.07.25.550566
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Article ; Online: Collagen deposition within brain metastases is associated with leptomeningeal failure after  cavity-directed radiosurgery.

Abdulhaleem, Mohammed / Ruiz, Jimmy / O'Neill, Stacey / Hughes, Ryan T / Qasem, Shadi / Strowd, Roy E / Furdui, Cristina / Watabe, Konousuke / Miller, Lance D / Debinski, Waldemar / Tatter, Stephen / Metheny-Barlow, Linda / White, Jaclyn J / Lee, Jingyun / McTyre, Emory R / Laxton, Adrian / Chan, Michael D / Su, Jing / Soike, Michael H

Neuro-oncology advances

2023 Volume 5, Issue 1, Page(s) vdac186

Abstract: Background: Leptomeningeal failure (LMF) represents a devastating progression of disease following resection of brain metastases (BrM). We sought to identify a biomarker at time of BrM resection that predicts for LMF using mass spectrometry-based ... ...

Abstract	Background: Leptomeningeal failure (LMF) represents a devastating progression of disease following resection of brain metastases (BrM). We sought to identify a biomarker at time of BrM resection that predicts for LMF using mass spectrometry-based proteomic analysis of resected BrM and to translate this finding with histochemical assays. Methods: We retrospectively reviewed 39 patients with proteomic data available from resected BrM. We performed an unsupervised analysis with false discovery rate adjustment (FDR) to compare proteomic signature of BrM from patients that developed LMF versus those that did not. Based on proteomic analysis, we applied trichrome stain to a total of 55 patients who specifically underwent resection and adjuvant radiosurgery. We used competing risks regression to assess predictors of LMF. Results: Of 39 patients with proteomic data, FDR revealed type I collagen-alpha-1 (COL1A1, Conclusion: The degree of trichrome staining correlated with COL1A1 and portended a higher risk of LMF in patients with resected brain metastases treated with adjuvant radiosurgery. Collagen deposition and degree of fibrosis may be able to serve as a biomarker for LMF.
Language	English
Publishing date	2023-01-06
Publishing country	England
Document type	Journal Article
ZDB-ID	3009682-0
ISSN	2632-2498 ; 2632-2498
ISSN (online)	2632-2498
ISSN	2632-2498
DOI	10.1093/noajnl/vdac186
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Article ; Online: Correction: Loss of XIST in Breast Cancer Activates MSN-c-Met and Reprograms Microglia via Exosomal miRNA to Promote Brain Metastasis.

Cancer research

2021 Volume 81, Issue 21, Page(s) 5582

Language	English
Publishing date	2021-11-01
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-21-3056
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Article ; Online: Correction: TGLI1 transcription factor mediates breast cancer brain metastasis via activating metastasis-initiating cancer stem cells and astrocytes in the tumor microenvironment.

Sirkisoon, Sherona R / Carpenter, Richard L / Rimkus, Tadas / Doheny, Daniel / Zhu, Dongqin / Aguayo, Noah R / Xing, Fei / Chan, Michael / Ruiz, Jimmy / Metheny-Barlow, Linda J / Strowd, Roy / Lin, Jiayuh / Regua, Angelina T / Arrigo, Austin / Anguelov, Marlyn / Pasche, Boris / Debinski, Waldemar / Watabe, Kounosuke / Lo, Hui-Wen

Oncogene

2021 Volume 40, Issue 12, Page(s) 2338

Language	English
Publishing date	2021-03-02
Publishing country	England
Document type	Published Erratum
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-020-01620-5
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Article ; Online: Tumor-induced loss of mural Connexin 43 gap junction activity promotes endothelial proliferation.

Choudhary, Mayur / Naczki, Christine / Chen, Wenhong / Barlow, Keith D / Case, L Douglas / Metheny-Barlow, Linda J

BMC cancer

2015 Volume 15, Page(s) 427

Abstract: Background: Proper functional association between mural cells and endothelial cells (EC) causes EC of blood vessels to become quiescent. Mural cells on tumor vessels exhibit decreased attachment to EC, which allows vessels to be unstable and ... ...

Abstract	Background: Proper functional association between mural cells and endothelial cells (EC) causes EC of blood vessels to become quiescent. Mural cells on tumor vessels exhibit decreased attachment to EC, which allows vessels to be unstable and proliferative. The mechanisms by which tumors prevent proper association between mural cells and EC are not well understood. Since gap junctions (GJ) play an important role in cell-cell contact and communication, we investigated whether loss of GJ plays a role in tumor-induced mural cell dissociation. Methods: Mural cell regulation of endothelial proliferation was assessed by direct co-culture assays of fluorescently labeled cells quantified by flow cytometry or plate reader. Gap junction function was assessed by parachute assay. Connexin 43 (Cx43) protein in mural cells exposed to conditioned media from cancer cells was assessed by Western and confocal microscopy; mRNA levels were assessed by quantitative real-time PCR. Expression vectors or siRNA were utilized to overexpress or knock down Cx43. Tumor growth and angiogenesis was assessed in mouse hosts deficient for Cx43. Results: Using parachute dye transfer assay, we demonstrate that media conditioned by MDA-MB-231 breast cancer cells diminishes GJ communication between mural cells (vascular smooth muscle cells, vSMC) and EC. Both protein and mRNA of the GJ component Connexin 43 (Cx43) are downregulated in mural cells by tumor-conditioned media; media from non-tumorigenic MCF10A cells had no effect. Loss of GJ communication by Cx43 siRNA knockdown, treatment with blocking peptide, or exposure to tumor-conditioned media diminishes the ability of mural cells to inhibit EC proliferation in co-culture assays, while overexpression of Cx43 in vSMC restores GJ and endothelial inhibition. Breast tumor cells implanted into mice heterozygous for Cx43 show no changes in tumor growth, but exhibit significantly increased tumor vascularization determined by CD31 staining, along with decreased mural cell support detected by NG2 staining. Conclusions: Our data indicate that i) functional Cx43 is required for mural cell-induced endothelial quiescence, and ii) downregulation of Cx43 GJ by tumors frees endothelium to respond to angiogenic cues. These data define a novel and important role for maintained Cx43 function in regulation of vessel quiescence, and suggest its loss may contribute to pathological tumor angiogenesis.
MeSH term(s)	Animals ; Breast Neoplasms/blood supply ; Breast Neoplasms/metabolism ; Cell Communication ; Cell Line, Tumor ; Cell Proliferation ; Connexin 43/antagonists & inhibitors ; Connexin 43/genetics ; Connexin 43/metabolism ; Culture Media, Conditioned ; Endothelial Cells/physiology ; Endothelium, Vascular/physiopathology ; Gap Junctions/metabolism ; Humans ; Mice ; Myocytes, Smooth Muscle/metabolism ; Neovascularization, Pathologic/physiopathology ; RNA, Messenger/metabolism
Chemical Substances	Connexin 43 ; Culture Media, Conditioned ; GJA1 protein, human ; RNA, Messenger
Language	English
Publishing date	2015-05-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1471-2407
ISSN (online)	1471-2407
DOI	10.1186/s12885-015-1420-9
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Article: Pericytes on the tumor vasculature: jekyll or hyde?

Barlow, Keith D / Sanders, Anne M / Soker, Shay / Ergun, Suleyman / Metheny-Barlow, Linda J

Cancer microenvironment : official journal of the International Cancer Microenvironment Society

2012 Volume 6, Issue 1, Page(s) 1–17

Abstract: The induction of tumor vasculature, known as the 'angiogenic switch', is a rate-limiting step in tumor progression. Normal blood vessels are composed of two distinct cell types: endothelial cells which form the channel through which blood flows, and ... ...

Abstract	The induction of tumor vasculature, known as the 'angiogenic switch', is a rate-limiting step in tumor progression. Normal blood vessels are composed of two distinct cell types: endothelial cells which form the channel through which blood flows, and mural cells, the pericytes and smooth muscle cells which serve to support and stabilize the endothelium. Most functional studies have focused on the responses of endothelial cells to pro-angiogenic stimuli; however, there is mounting evidence that the supporting mural cells, particularly pericytes, may play key regulatory roles in both promoting vessel growth as well as terminating vessel growth to generate a mature, quiescent vasculature. Tumor vessels are characterized by numerous structural and functional abnormalities, including altered association between endothelial cells and pericytes. These dysfunctional, unstable vessels contribute to hypoxia, interstitial fluid pressure, and enhanced susceptibility to metastatic invasion. Increasing evidence points to the pericyte as a critical regulator of endothelial activation and subsequent vessel development, stability, and function. Here we discuss both the stimulatory and inhibitory effects of pericytes on the vasculature and the possible utilization of vessel normalization as a therapeutic strategy to combat cancer.
Language	English
Publishing date	2012-03-31
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2422345-1
ISSN	1875-2284 ; 1875-2292
ISSN (online)	1875-2284
ISSN	1875-2292
DOI	10.1007/s12307-012-0102-2
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Article ; Online: Angiotensin-(1-7) prevents radiation-induced inflammation in rat primary astrocytes through regulation of MAP kinase signaling.

Moore, Elizabeth D / Kooshki, Mitra / Metheny-Barlow, Linda J / Gallagher, Patricia E / Robbins, Mike E

Free radical biology & medicine

2013 Volume 65, Page(s) 1060–1068

Abstract: About 500,000 new cancer patients will develop brain metastases in 2013. The primary treatment modality for these patients is partial or whole brain irradiation which leads to a progressive, irreversible cognitive impairment. Although the exact ... ...

Abstract	About 500,000 new cancer patients will develop brain metastases in 2013. The primary treatment modality for these patients is partial or whole brain irradiation which leads to a progressive, irreversible cognitive impairment. Although the exact mechanisms behind this radiation-induced brain injury are unknown, neuroinflammation in glial populations is hypothesized to play a role. Blockers of the renin-angiotensin system (RAS) prevent radiation-induced cognitive impairment and modulate radiation-induced neuroinflammation. Recent studies suggest that RAS blockers may reduce inflammation by increasing endogenous concentrations of the anti-inflammatory heptapeptide angiotensin-(1-7) [Ang-(1-7)]. Ang-(1-7) binds to the AT(1-7) receptor and inhibits MAP kinase activity to prevent inflammation. This study describes the inflammatory response to radiation in astrocytes characterized by radiation-induced increases in (i) IL-1β and IL-6 gene expression; (ii) COX-2 and GFAP immunoreactivity; (iii) activation of AP-1 and NF-κB transcription factors; and (iv) PKCα, MEK, and ERK (MAP kinase) activation. Treatment with U-0126, a MEK inhibitor, demonstrates that this radiation-induced inflammation in astrocytes is mediated through the MAP kinase pathway. Ang-(1-7) inhibits radiation-induced inflammation, increases in PKCα, and MAP kinase pathway activation (phosphorylation of MEK and ERK). Additionally Ang-(1-7) treatment leads to an increase in dual specificity phosphatase 1 (DUSP1). Furthermore, treatment with sodium vanadate (Na3VO4), a phosphatase inhibitor, blocks Ang-(1-7) inhibition of radiation-induced inflammation and MAP kinase activation, suggesting that Ang-(1-7) alters phosphatase activity to inhibit radiation-induced inflammation. These data suggest that RAS blockers inhibit radiation-induced inflammation and prevent radiation-induced cognitive impairment not only by reducing Ang II but also by increasing Ang-(1-7) levels.
MeSH term(s)	Angiotensin I/pharmacology ; Animals ; Astrocytes/immunology ; Astrocytes/radiation effects ; Cells, Cultured ; Drug Evaluation, Preclinical ; Dual Specificity Phosphatase 1/metabolism ; Inflammation/metabolism ; MAP Kinase Signaling System ; Peptide Fragments/pharmacology ; Primary Cell Culture ; Radiation-Protective Agents/pharmacology ; Rats
Chemical Substances	Peptide Fragments ; Radiation-Protective Agents ; Angiotensin I (9041-90-1) ; Dual Specificity Phosphatase 1 (EC 3.1.3.48) ; Dusp1 protein, rat (EC 3.1.3.48) ; angiotensin I (1-7) (IJ3FUK8MOF)
Language	English
Publishing date	2013-09-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2013.08.183
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Article ; Online: Fibronectin Produced by Cerebral Endothelial and Vascular Smooth Muscle Cells Contributes to Perivascular Extracellular Matrix in Late-Delayed Radiation-Induced Brain Injury.

Andrews, Rachel N / Caudell, David L / Metheny-Barlow, Linda J / Peiffer, Ann M / Tooze, Janet A / Bourland, J Daniel / Hampson, Robert E / Deadwyler, Samuel A / Cline, J Mark

Radiation research

2018 Volume 190, Issue 4, Page(s) 361–373

Abstract: Late-delayed radiation-induced brain injury (RIBI) is a major adverse effect of fractionated whole-brain irradiation (fWBI). Characterized by progressive cognitive dysfunction, and associated cerebrovascular and white matter injury, RIBI deleteriously ... ...

Abstract	Late-delayed radiation-induced brain injury (RIBI) is a major adverse effect of fractionated whole-brain irradiation (fWBI). Characterized by progressive cognitive dysfunction, and associated cerebrovascular and white matter injury, RIBI deleteriously affects quality of life for cancer patients. Despite extensive morphological characterization of the injury, the pathogenesis is unclear, thus limiting the development of effective therapeutics. We previously reported that RIBI is associated with increased gene expression of the extracellular matrix (ECM) protein fibronectin (FN1). We hypothesized that fibronectin contributes to perivascular ECM, which may impair diffusion to the dependent parenchyma, thus contributing to the observed cognitive decline. The goal of this study was to determine the localization of fibronectin in RIBI and further characterize the composition of perivascular ECM, as well as identify the cell of origin for FN1 by in situ hybridization. Briefly, fibronectin localized to the vascular basement membrane of morphologically normal blood vessels from control comparators and animals receiving fWBI, and to the perivascular space of edematous and fibrotic vascular phenotypes of animals receiving fWBI. Additional mild diffuse parenchymal staining in areas of vascular injury suggested blood-brain-barrier disruption and plasma fibronectin extravasation. Perivascular ECM lacked amyloid and contained lesser amounts of collagens I and IV, which localized to the basement membrane. These changes occurred in the absence of alterations in microvascular area fraction or microvessel density. Fibronectin transcripts were rarely expressed in control comparators, and were most strongly induced within cerebrovascular endothelial and vascular smooth muscle cells after fWBI. Our results demonstrate that fibronectin is produced by cerebrovascular endothelial and smooth muscle cells in late-delayed RIBI and contributes to perivascular ECM, which we postulate may contribute to diffusion barrier formation. We propose that pathways that antagonize fibronectin deposition and matrix assembly or enhance degradation may serve as potential therapeutic targets in RIBI.
MeSH term(s)	Animals ; Brain/blood supply ; Brain/radiation effects ; Brain Injuries/etiology ; Brain Injuries/metabolism ; Brain Injuries/pathology ; Cerebrovascular Circulation ; Endothelium, Vascular/metabolism ; Extracellular Matrix/metabolism ; Fibronectins/biosynthesis ; Fibronectins/physiology ; Gene Expression ; Macaca mulatta ; Male ; Muscle, Smooth, Vascular/metabolism ; Radiation Injuries, Experimental/metabolism ; Radiation Injuries, Experimental/pathology
Chemical Substances	Fibronectins
Language	English
Publishing date	2018-07-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80322-4
ISSN	1938-5404 ; 0033-7587
ISSN (online)	1938-5404
ISSN	0033-7587
DOI	10.1667/RR14961.1
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Article ; Online: Differential expression of Homer1a in the hippocampus and cortex likely plays a role in radiation-induced brain injury.

Moore, Elizabeth D / Kooshki, Mitra / Wheeler, Kenneth T / Metheny-Barlow, Linda J / Robbins, Mike E

Radiation research

2013 Volume 181, Issue 1, Page(s) 21–32

Abstract: Fractionated partial or whole-brain irradiation is the primary treatment for metastatic brain tumors. Despite reducing tumor burden and increasing lifespan, progressive, irreversible cognitive impairment occurs in >50% of the patients who survive >6 ... ...

Abstract	Fractionated partial or whole-brain irradiation is the primary treatment for metastatic brain tumors. Despite reducing tumor burden and increasing lifespan, progressive, irreversible cognitive impairment occurs in >50% of the patients who survive >6 months after fractionated whole-brain irradiation. The exact mechanism(s) responsible for this radiation-induced brain injury are unknown; however, preclinical studies suggest that radiation modulates the extracellular receptor kinase signaling pathway, which is associated with cognitive impairment in many neurological diseases. In the study reported here, we demonstrated that the extracellular receptor kinase transcriptionally-regulated early response gene, Homer1a, was up-regulated transiently in the hippocampus and down-regulated in the cortex of young adult male Fischer 344 X Brown Norway rats at 48 h after 40 Gy of fractionated whole-brain irradiation. Two months after fractionated whole-brain irradiation, these changes in Homer1a expression correlated with a down-regulation of the hippocampal glutamate receptor 1 and protein kinase Cγ, and an up-regulation of cortical glutamate receptor 1 and protein kinase Cγ. Two drugs that prevent radiation-induced cognitive impairment in rats, the angiotensin type-1 receptor blocker, L-158,809, and the angiotensin converting enzyme inhibitor, ramipril, reversed the fractionated whole-brain irradiation-induced Homer1a expression at 48 h in the hippocampus and cortex and restored glutamate receptor 1 and protein kinase Cγ to the levels in sham-irradiated controls at 2 months after fractionated whole-brain irradiation. These data indicate that Homer1a is, (1) a brain region specific regulator of radiation-induced brain injury, including cognitive impairment and (2) potentially a druggable target for preventing it.
MeSH term(s)	Animals ; Brain Injuries/genetics ; Brain Injuries/metabolism ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Cognition/drug effects ; Cognition/radiation effects ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/radiation effects ; Hippocampus/drug effects ; Hippocampus/metabolism ; Hippocampus/physiopathology ; Hippocampus/radiation effects ; Homer Scaffolding Proteins ; Imidazoles/pharmacology ; Male ; Protein Kinase C/metabolism ; Radiation Injuries/genetics ; Radiation Injuries/metabolism ; Ramipril/pharmacology ; Rats ; Receptors, Metabotropic Glutamate/metabolism ; Signal Transduction/drug effects ; Signal Transduction/radiation effects ; Tetrazoles/pharmacology ; Time Factors
Chemical Substances	Carrier Proteins ; Homer Scaffolding Proteins ; Imidazoles ; Receptors, Metabotropic Glutamate ; Tetrazoles ; metabotropic glutamate receptor type 1 ; L 158809 (608GM1WHMG) ; protein kinase C gamma (EC 2.7.1.-) ; Protein Kinase C (EC 2.7.11.13) ; Ramipril (L35JN3I7SJ)
Language	English
Publishing date	2013-12-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80322-4
ISSN	1938-5404 ; 0033-7587
ISSN (online)	1938-5404
ISSN	0033-7587
DOI	10.1667/RR13475.1
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Article ; Online: Identification of CD37, cystatin A, and IL-23A gene expression in association with brain metastasis: analysis of a prospective trial.

Dohm, Ammoren / Su, Jing / McTyre, Emory R / Taylor, James M / Miller, Lance D / Petty, W Jeffrey / Xing, Fei / Lo, Hui-Wen / Metheny-Barlow, Linda J / O'Neill, Stacey / Bellinger, Christina / Dotson, Travis / Pasche, Boris / Watabe, Kounosuke / Chan, Michael D / Ruiz, Jimmy

The International journal of biological markers

2019 Volume 34, Issue 1, Page(s) 90–97

Abstract: Purpose/objectives: We aimed to assess the predictive value of a lung cancer gene panel for the development of brain metastases.: Materials/methods: Between 2011 and 2015, 102 patients with lung cancer were prospectively enrolled in a clinical trial ... ...

Abstract	Purpose/objectives: We aimed to assess the predictive value of a lung cancer gene panel for the development of brain metastases. Materials/methods: Between 2011 and 2015, 102 patients with lung cancer were prospectively enrolled in a clinical trial in which a diagnostic fine-needle aspirate was obtained. Gene expression was conducted on all samples that rendered a diagnosis of non-small cell lung cancer (NSCLC). Subsequent retrospective analysis of brain metastases-related outcomes was performed by reviewing patient electronic medical records. A competing risk multivariable regression was performed to estimate the adjusted hazard ratio for the development of brain metastases and non-brain metastases from NSCLC. Results: A total of 49 of 102 patients had died by the last follow-up. Median time of follow-up was 13 months (range 0.23-67 months). A total of 17 patients developed brain metastases. Median survival time after diagnosis of brain metastases was 3.58 months (95% confidence interval (CI) 2.17, not available). A total of 30 patients developed metastases without any evidence of brain metastases until the time of death or last follow-up. Competing risk analysis identified three genes that were downregulated differentially in the patients with brain metastases versus non-brain metastatic disease: CD37 (0.017), cystatin A (0.022), and IL-23A (0.027). Other factors associated with brain metastases include: stage T ( P ⩽ 8.3e Conclusions: We have identified three genes, CD37, cystatin A, and IL-23A, for which downregulation of gene expression was associated with a greater propensity for developing brain metastases. Validation of these biomarkers could have implications on surveillance patterns in patients with brain metastases from NSCLC.
MeSH term(s)	Adenocarcinoma/metabolism ; Adenocarcinoma/secondary ; Aged ; Antigens, Neoplasm/metabolism ; Biomarkers, Tumor/metabolism ; Brain Neoplasms/metabolism ; Brain Neoplasms/secondary ; Carcinoma, Non-Small-Cell Lung/metabolism ; Carcinoma, Non-Small-Cell Lung/pathology ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/secondary ; Cystatin A/metabolism ; Female ; Follow-Up Studies ; Humans ; Interleukin-23 Subunit p19/metabolism ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Male ; Middle Aged ; Prognosis ; Prospective Studies ; Retrospective Studies ; Survival Rate ; Tetraspanins/metabolism
Chemical Substances	Antigens, Neoplasm ; Biomarkers, Tumor ; CD37 protein, human ; Cystatin A ; IL23A protein, human ; Interleukin-23 Subunit p19 ; Tetraspanins ; CSTA protein, human (80209-89-8)
Language	English
Publishing date	2019-03-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	645113-5
ISSN	1724-6008 ; 0393-6155
ISSN (online)	1724-6008
ISSN	0393-6155
DOI	10.1177/1724600818803104
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