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Bryan Schneider, MD

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Hematology/Oncology

Associate Professor of Medicine, Associate Professor of MMGE, Sheila D. Ward Scholar

Academic Office

Indiana Cancer Pavilion, Suite 473
535 Barnhill Dr
Indianapolis IN 46202-5289 Map

Contact Information

Phone: (317) 274-6473
Fax: (317) 278-4190
Email:

Bio

Dr. Schneider is an Assistant Professor of Medicine at the Indiana University Melvin and Bren Simon Cancer Center. He holds appointments in the Divisions of Hematology/Oncology and Clinical Pharmacology in the Department of Medicine with a secondary appointment in the Department of Medical and Molecular Genetics. Dr. Schneider completed his Medical School, Internal Medicine Residency and Hematology/Oncology Fellowship at Indiana University. Dr. Schneider devotes his clinical time caring for breast cancer patients as a Medical Oncologist and has a special interest in novel therapeutic agents. He is the model example of a translational scientist as his lab work is both an extension of and complimentary to his clinical interest. His laboratory focus is on pharmacogenetics of breast cancer therapeutics. His biomarker work to date has opened the door for the potential enrichment of patient selection for bevacizumab. Based on his early work he has designed correlative trials in collaborations with multiple groups to better guide proper patient selection for these agents. He is extensively published in the area of therapeutic individualization (i.e. "finding the right drug for each patient"). He is a recipient of the prestigious Komen Promise Award and a member of the Komen Scientific Advisory Council. Dr. Schneider is the Chair of the Educational Symposium for the Developmental Therapeutics Committee, the Vice-Chair of the Pharmacogenetics Committee, and a member of the Breast Cancer Committee for the Eastern Cooperative Oncology Group (ECOG). He is also a member of the Consortium on Breast Cancer Pharmacogenetics (CoBRA) and the Pharmacogenetics Research Network (PGRN).

Research Interests

My major research goal is translational in nature. I hope to identify critical genetic and pharmacogenetic differences that predict for etiology, aggressiveness, and therapeutic responsiveness as it relates to cancer. My current research focus is primarily involved with polymorphisms of angiogenesis as it relates to breast cancer. I also wish to participate in multiple clinical trials testing therapies in breast cancer.

Clinical Interests

Breast cancer

Education and Training

Fellowship Indiana University School of Medicine, Indianapolis, IN
Residency Indiana University School of Medicine, Indianapolis, IN
Medicine (M.D.) Indiana University
Biology, General Evansville, University Of

Publications (25)¹

Incremental Prognostic Value of Echocardiographic Strain and Its Association With Mortality in Cancer Patients.
Journal: Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography
Authors: Rhea IB; Uppuluri S; Sawada S; Schneider BP; Feigenbaum H;
Publication Date: 2015 Mar 12

Abstract

Left ventricular global longitudinal systolic strain (GLS) has been shown to be superior to ejection fraction in detecting subclinical dysfunction in patients with cancer and predicting mortality in patients with cardiovascular disease. Cancer-related fatigue is common in the later stages of neoplastic malignancies and may be indicative of nonovert heart failure. The aim of this study was to determine whether reduced strain by echocardiography was associated with all-cause mortality in a cancer cohort.
View details for PubMedID 25770665
Integrated and convenient procedure for protein extraction from formalin-fixed, paraffin-embedded tissues for LC-MS/MS analysis.
Journal: Proteomics
Authors: Lai X; Schneider BP;
Publication Date: 2014 Sep 5

Abstract

Because fresh-frozen tissue samples associated with long-term clinical data and of rare diseases are often unobtainable at the present time, formalin-fixed paraffin-embedded (FFPE) tissue samples are considered a highly valuable resource for researchers. However, protein extraction from FFPE tissues faces challenges of deparaffinization and cross-link reversion. Current procedures for protein extraction from FFPE tissue require separate steps and toxic solvents, resulting in inconvenience in protein extraction. To overcome these limitations, an integrated method was developed using nontoxic solvents in four types of FFPE tissues. The average amount of proteins from three replicates of bladder, kidney, liver, and lung FFPE tissues were 442.6, 728.9, 736.4, and 694.7 µg with CVs of 7.5, 5.8, 2.4, and 4.5%, respectively. Proteomic analysis showed that 348, 417, 607, and 304 unique proteins were identified and quantified without specification of isoform by a least two peptides from bladder, kidney, liver, and lung FFPE tissue samples, respectively. The analysis of individual protein CV demonstrated that 97-99% of the proteins were quantified with a CV = 30%, verifying the reproducibility of the integrated protein extraction method. In summary, the developed method is high-yield, reproducible, convenient, simple, low cost, nonvolatile, nonflammable, and nontoxic.
View details for PubMedID 25091982
Altered cerebral blood flow one month after systemic chemotherapy for breast cancer: a prospective study using pulsed arterial spin labeling MRI perfusion.
Journal: PloS one
Authors: Nudelman KN; Wang Y; McDonald BC; Conroy SK; Smith DJ; West JD; O'Neill DP; Schneider BP; Saykin AJ;
Publication Date: 2014 May 9

Abstract

Cerebral structural and functional alterations have been reported after chemotherapy for non-CNS cancers, yet the causative mechanism behind these changes remains unclear. This study employed a novel, non-invasive, MRI-based neuroimaging measure to provide the first direct longitudinal measurement of resting cerebral perfusion in breast cancer patients, which was tested for association with changes in cognitive function and gray matter density. Perfusion was measured using pulsed arterial spin labeling MRI in women with breast cancer treated with (N?=?27) or without (N?=?26) chemotherapy and matched healthy controls (N?=?26) after surgery before other treatments (baseline), and one month after chemotherapy completion or yoked intervals. Voxel-based analysis was employed to assess perfusion in gray matter; changes were examined in relation to overall neuropsychological test performance and frontal gray matter density changes measured by structural MRI. Baseline perfusion was not significantly different across groups. Unlike control groups, chemotherapy-treated patients demonstrated significantly increased perfusion post-treatment relative to baseline, which was statistically significant relative to controls in the right precentral gyrus. This perfusion increase was negatively correlated with baseline overall neuropsychological performance, but was not associated with frontal gray matter density reduction. However, decreased frontal gray matter density was associated with decreased perfusion in bilateral frontal and parietal lobes in the chemotherapy-treated group. These findings indicate that chemotherapy is associated with alterations in cerebral perfusion which are both related to and independent of gray matter changes. This pattern of results suggests the involvement of multiple mechanisms of chemotherapy-induced cognitive dysfunction. Additionally, lower baseline cognitive function may be a risk factor for treatment-associated perfusion dysregulation. Future research is needed to clarify these mechanisms, identify individual differences in susceptibility to treatment-associated changes, and further examine perfusion change over time in survivors.
View details for PubMedID 24816641
Nodular Regenerative Hyperplasia After Treatment With Trastuzumab Emtansine.
Journal: Journal of clinical oncology : official journal of the American Society of Clinical Oncology
Authors: Force J; Saxena R; Schneider BP; Storniolo AM; Sledge GW Jr; Chalasani N; Vuppalanchi R;
Publication Date: 2014 May 12
Genetic variant predicts bevacizumab-induced hypertension in ECOG-5103 and ECOG-2100.
Journal: British journal of cancer
Authors: Schneider BP; Li L; Shen F; Miller KD; Radovich M; O'Neill A; Gray RJ; Lane D; Flockhart DA; Jiang G; Wang Z; Lai D; Koller D; Pratt JH; Dang CT; Northfelt D; Perez EA; Shenkier T; Cobleigh M; Smith ML; Railey E; Partridge A; Gralow J; Sparano J; Davidson NE; Foroud T; Sledge GW;
Publication Date: 2014 Aug 12

Abstract

Bevacizumab has broad anti-tumour activity, but substantial risk of hypertension. No reliable markers are available for predicting bevacizumab-induced hypertension.
View details for PubMedID 25117820
Phase 1 pharmacogenetic and pharmacodynamic study of sorafenib with concurrent radiation therapy and gemcitabine in locally advanced unresectable pancreatic cancer.
Journal: International journal of radiation oncology, biology, physics
Authors: Chiorean EG; Schneider BP; Akisik FM; Perkins SM; Anderson S; Johnson CS; DeWitt J; Helft P; Clark R; Johnston EL; Spittler AJ; Deluca J; Bu G; Shahda S; Loehrer PJ; Sandrasegaran K; Cardenes HR;
Publication Date: 2014 Apr 11

Abstract

To define the safety, efficacy, and pharmacogenetic and pharmacodynamic effects of sorafenib with gemcitabine-based chemoradiotherapy (CRT) in locally advanced pancreatic cancer.
View details for PubMedID 24726286
Characterizing the heterogeneity of triple-negative breast cancers using microdissected normal ductal epithelium and RNA-sequencing.
Journal: Breast cancer research and treatment
Authors: Radovich M; Clare SE; Atale R; Pardo I; Hancock BA; Solzak JP; Kassem N; Mathieson T; Storniolo AM; Rufenbarger C; Lillemoe HA; Blosser RJ; Choi MR; Sauder CA; Doxey D; Henry JE; Hilligoss EE; Sakarya O; Hyland FC; Hickenbotham M; Zhu J; Glasscock J; Badve S; Ivan M; Liu Y; Sledge GW; Schneider BP;
Publication Date: 2013 Nov 29

Abstract

Triple-negative breast cancers (TNBCs) are a heterogeneous set of tumors defined by an absence of actionable therapeutic targets (ER, PR, and HER-2). Microdissected normal ductal epithelium from healthy volunteers represents a novel comparator to reveal insights into TNBC heterogeneity and to inform drug development. Using RNA-sequencing data from our institution and The Cancer Genome Atlas (TCGA) we compared the transcriptomes of 94 TNBCs, 20 microdissected normal breast tissues from healthy volunteers from the Susan G. Komen for the Cure Tissue Bank, and 10 histologically normal tissues adjacent to tumor. Pathway analysis comparing TNBCs to optimized normal controls of microdissected normal epithelium versus classic controls composed of adjacent normal tissue revealed distinct molecular signatures. Differential gene expression of TNBC compared with normal comparators demonstrated important findings for TNBC-specific clinical trials testing targeted agents; lack of over-expression for negative studies and over-expression in studies with drug activity. Next, by comparing each individual TNBC to the set of microdissected normals, we demonstrate that TNBC heterogeneity is attributable to transcriptional chaos, is associated with non-silent DNA mutational load, and explains transcriptional heterogeneity in addition to known molecular subtypes. Finally, chaos analysis identified 146 core genes dysregulated in >90 % of TNBCs revealing an over-expressed central network. In conclusion, use of microdissected normal ductal epithelium from healthy volunteers enables an optimized approach for studying TNBC and uncovers biological heterogeneity mediated by transcriptional chaos.
View details for PubMedID 24292813
Prognostic and predictive value of tumor vascular endothelial growth factor gene amplification in metastatic breast cancer treated with paclitaxel with and without bevacizumab; results from ECOG 2100 trial.
Journal: Clinical cancer research : an official journal of the American Association for Cancer Research
Authors: Schneider BP; Gray RJ; Radovich M; Shen F; Vance G; Li L; Jiang G; Miller KD; Gralow JR; Dickler MN; Cobleigh MA; Perez EA; Shenkier TN; Vang Nielsen K; Müller S; Thor A; Sledge GW Jr; Sparano JA; Davidson NE; Badve SS;
Publication Date: 2013 Jan 22

Abstract

Clinically validated biomarkers for anti-angiogenesis agents are not available. We have previously reported associations between candidate VEGFA single-nucleotide polymorphisms (SNP) and overall survival (OS) in E2100. The associations between tumor VEGFA amplification and outcome are evaluated here.
View details for PubMedID 23340303
Functional microRNAs in Alzheimer's disease and cancer: differential regulation of common mechanisms and pathways.
Journal: Frontiers in genetics
Authors: Holohan KN; Lahiri DK; Schneider BP; Foroud T; Saykin AJ;
Publication Date: 2013 Jan 17

Abstract

Two of the main research priorities in the United States are cancer and neurodegenerative diseases, which are attributed to abnormal patterns of cellular behavior. MicroRNAs (miRNA) have been implicated as regulators of cellular metabolism, and thus are an active topic of investigation in both disease areas. There is presently a more extensive body of work on the role of miRNAs in cancer compared to neurodegenerative diseases, and therefore it may be useful to examine whether there is any concordance between the functional roles of miRNAs in these diseases. As a case study, the roles of miRNAs in Alzheimer's disease (AD) and their functions in various cancers will be compared. A number of miRNA expression patterns are altered in individuals with AD compared with healthy older adults. Among these, some have also been shown to correlate with neuropathological changes including plaque and tangle accumulation, as well as expression levels of other molecules known to be involved in disease pathology. Importantly, these miRNAs have also been shown to have differential expression and or functional roles in various types of cancer. To examine possible intersections between miRNA functions in cancer and AD, we review the current literature on these miRNAs in cancer and AD, focusing on their roles in known biological pathways. We propose a pathway-driven model in which some molecular processes show an inverse relationship between cancer and neurodegenerative disease (e.g., proliferation and apoptosis) whereas others are more parallel in their activity (e.g., immune activation and inflammation). A critical review of these and other molecular mechanisms in cancer may shed light on the pathophysiology of AD, and highlight key areas for future research. Conclusions from this work may be extended to other neurodegenerative diseases for which some molecular pathways have been identified but which have not yet been extensively researched for miRNA involvement.
View details for PubMedID 23335942
Pharmacogenetic biomarkers for the prediction of response to antiangiogenic treatment.
Journal: The Lancet. Oncology
Authors: Schneider BP; Shen F; Miller KD;
Publication Date: 2012 Oct

Abstract

Antiangiogenic treatments have shown activity across multiple tumour types and in various settings. Despite having been approved on the basis of efficacy, the therapeutic index varies substantially in different settings for many of these agents. A major limitation is the current inability to personalise treatment a priori according to findings on measurement of a predictive biomarker. The roles of germline single-nucleotide polymorphisms have been investigated as potential biomarkers for antiangiogenic treatments. The rationale is founded on the understanding that the drugs target the vasculature rather than the tumour, which could mean that much of the variability is regulated by the host. Several single-nucleotide polymorphisms have been associated with differential outcomes and toxic effects in clinical trials. In this Review we provide an overview of available data with particular attention paid to the pitfalls and strengths of potential biomarkers. We also highlight continuing work and plans for confirmatory studies.
View details for PubMedID 23026828
Neuropathy is not associated with clinical outcomes in patients receiving adjuvant taxane-containing therapy for operable breast cancer.
Journal: Journal of clinical oncology : official journal of the American Society of Clinical Oncology
Authors: Schneider BP; Zhao F; Wang M; Stearns V; Martino S; Jones V; Perez EA; Saphner T; Wolff AC; Sledge GW Jr; Wood WC; Davidson NE; Sparano JA;
Publication Date: 2012 Jul 30

Abstract

Neuropathy is a common and potentially disabling complication of adjuvant taxane therapy. Recent studies have identified candidate single nucleotide polymorphisms associated with taxane-induced neuropathy. Therefore, we sought to determine whether neuropathy was associated with breast cancer recurrence in a clinical trial population who received adjuvant taxane therapy.
View details for PubMedID 22851566
Cancer-associated alteration of pericentromeric heterochromatin may contribute to chromosome instability.
Journal: Oncogene
Authors: Slee RB; Steiner CM; Herbert BS; Vance GH; Hickey RJ; Schwarz T; Christan S; Radovich M; Schneider BP; Schindelhauer D; Grimes BR;
Publication Date: 2011 Nov 28

Abstract

Many tumors exhibit elevated chromosome mis-segregation termed chromosome instability (CIN), which is likely to be a potent driver of tumor progression and drug resistance. Causes of CIN are poorly understood but probably include prior genome tetraploidization, centrosome amplification and mitotic checkpoint defects. This study identifies epigenetic alteration of the centromere as a potential contributor to the CIN phenotype. The centromere controls chromosome segregation and consists of higher-order repeat (HOR) alpha-satellite DNA packaged into two chromatin domains: the kinetochore, harboring the centromere-specific H3 variant centromere protein A (CENP-A), and the pericentromeric heterochromatin, considered important for cohesion. Perturbation of centromeric chromatin in model systems causes CIN. As cancer cells exhibit widespread chromatin changes, we hypothesized that pericentromeric chromatin structure could also be affected, contributing to CIN. Cytological and chromatin immunoprecipitation and PCR (ChIP-PCR)-based analyses of HT1080 cancer cells showed that only one of the two HORs on chromosomes 5 and 7 incorporate CENP-A, an organization conserved in all normal and cancer-derived cells examined. Contrastingly, the heterochromatin marker H3K9me3 (trimethylation of H3 lysine 9) mapped to all four HORs and ChIP-PCR showed an altered pattern of H3K9me3 in cancer cell lines and breast tumors, consistent with a reduction on the kinetochore-forming HORs. The JMJD2B demethylase is overexpressed in breast tumors with a CIN phenotype, and overexpression of exogenous JMJD2B in cultured breast epithelial cells caused loss of centromere-associated H3K9me3 and increased CIN. These findings suggest that impaired maintenance of pericentromeric heterochromatin may contribute to CIN in cancer and be a novel therapeutic target.
View details for PubMedID 22081068
Compliance differences between patients with breast cancer in university and county hospitals.
Journal: Clinical breast cancer
Authors: Komenaka IK; Pennington RE Jr; Schneider BP; Hsu CH; Norton LE; Clare SE; Zork NM; Goulet RJ Jr;
Publication Date: 2010 Oct 1

Abstract

Compliance with recommended breast cancer treatments outside the context of a clinical trial differs from that in study populations. The purpose of this study was to examine differences in compliance of breast cancer treatments.
View details for PubMedID 20920983
Resequencing of the vascular endothelial growth factor promoter reveals haplotype structure and functional diversity.
Journal: Angiogenesis
Authors: Radovich M; Hancock BA; Kassem N; Mi D; Skaar TC; Schneider BP;
Publication Date: 2010 Jun 16

Abstract

Our group has previously reported that SNPs in the VEGF promoter are strongly associated with efficacy and toxicity to the anti-VEGF antibody bevacizumab in breast cancer. In order to better understand the biologic mechanism for our previously reported biomarkers, we embarked on a comprehensive evaluation of genetic variation in the VEGF promoter coupled with a study of its intrinsic function. We resequenced 48 Caucasians and 48 African-Americans for the VEGF promoter to identify SNPs and elucidate its haplotype structure. We further cloned the haplotypes into reporter constructs and assessed the role of SNPs on promoter function in breast cancer cell lines. SNPs that were identified included twenty previously reported SNPs/insertions/deletions, one novel SNP, and one novel deletion. Among these variants, we identified five SNPs that tag six haplotypes capturing 74% of the genetic variation of the promoter. Subsequently, assessment of the haplotypes in reporter constructs demonstrates significant variation in promoter induced expression among the haplotypes. In particular, two haplotypes had higher expression and one haplotype had lower expression across cell lines. Haplotypes containing SNPs previously reported to be associated with increased survival with the use of bevacizumab are high-expressing haplotypes, thus lending putative functional evidence to the prior clinical finding.
View details for PubMedID 20552269
Anti-VEGF therapy as adjuvant therapy: clouds on the horizon?
Journal: Breast cancer research : BCR
Authors: Schneider BP; Sledge GW Jr;
Publication Date: 2009 May 18

Abstract

Anti-angiogenic therapies have demonstrated their value in the setting of advanced cancer, and are being explored for use in micrometastatic disease. Recent preclinical studies suggest that adjuvant anti-vascular endothelial growth factor (VEGF) therapies may increase the risk of metastasis. How concerning are these preclinical studies, and should they affect our willingness to explore anti-VEGF therapy in the adjuvant setting?
View details for PubMedID 19519950
The role of vascular endothelial growth factor genetic variability in cancer.
Journal: Clinical cancer research : an official journal of the American Association for Cancer Research
Authors: Schneider BP; Radovich M; Miller KD;
Publication Date: 2009 Aug 25

Abstract

Angiogenesis is a hallmark of tumor pathogenesis. Vascular endothelial growth factor (VEGF) is a critical regulator of angiogenesis and its inhibition has become a successful approach to antitumor therapy across tumor types. The VEGF gene is highly polymorphic with multiple common single nucleotide polymorphisms (SNPs) in the promoter, 5' untranslated region and 3' untranslated region. There is evidence that these SNPs in the regulatory regions can affect VEGF expression. In vitro and in vivo data show that genetic variability affects the activity and expression of VEGF. Case-control and cohort studies suggest that genetic variability may affect risk and outcome of a variety of disease states that are tightly regulated by angiogenesis. Recently, genetic variability in VEGF has been studied as a potential predictive biomarker for bevacizumab. The VEGF-1154 AA and -2578 AA genotypes predicted an improved median overall survival, whereas the VEGF-634 CC and -1498 TT genotypes predicted protection from grade 3-4 hypertension in the pivotal trial, E2100. If validated, these finding could help direct which subgroup of patients should receive bevacizumab.
View details for PubMedID 19706811
Exploratory study evaluating the association of polymorphisms of angiogenesis genes with hot flashes.
Journal: Breast cancer research and treatment
Authors: Schneider BP; Radovich M; Flockhart DA; Carpenter JS; Li L; Robarge JD; Storniolo AM; Hancock BA; Skaar TC; Sledge GW;
Publication Date: 2008 Sep 11

Abstract

Hot flashes are a common symptom and an important cause of decreased quality of life in women with breast cancer. Hot flashes involve vasodilatation and flushing, however, their complex etiology is not fully understood. We evaluated the association between germline polymorphisms in genes important to angiogenesis and subjective reporting of hot flashes.
View details for PubMedID 18785001
Association of vascular endothelial growth factor and vascular endothelial growth factor receptor-2 genetic polymorphisms with outcome in a trial of paclitaxel compared with paclitaxel plus bevacizumab in advanced breast cancer: ECOG 2100.
Journal: Journal of clinical oncology : official journal of the American Society of Clinical Oncology
Authors: Schneider BP; Wang M; Radovich M; Sledge GW; Badve S; Thor A; Flockhart DA; Hancock B; Davidson N; Gralow J; Dickler M; Perez EA; Cobleigh M; Shenkier T; Edgerton S; Miller KD; ECOG 2100;
Publication Date: 2008 Oct 1

Abstract

No biomarkers have been identified to predict outcome with the use of an antiangiogenesis agent for cancer. Vascular endothelial growth factor (VEGF) genetic variability has been associated with altered risk of breast cancer and variable promoter activity. Therefore, we evaluated the association of VEGF genotype with efficacy and toxicity in E2100, a phase III study comparing paclitaxel versus paclitaxel plus bevacizumab as initial chemotherapy for metastatic breast cancer.
View details for PubMedID 18824714
A 25-year single institution experience with surgery for primary mediastinal nonseminomatous germ cell tumors.
Journal: The Annals of thoracic surgery
Authors: Kesler KA; Rieger KM; Hammoud ZT; Kruter LE; Perkins SM; Turrentine MW; Schneider BP; Einhorn LH; Brown JW;
Publication Date: 2008 Feb

Abstract

The treatment of primary mediastinal nonseminomatous germ cell tumors (PMNSGCT) with cisplatin-based chemotherapy, followed by surgical resection of residual disease, has been established. We reviewed our institution's 25-year experience in the cisplatin era to determine surgical risks and predictors of survival after surgery for PMNSGCT.
View details for PubMedID 18222228
Triple-negative breast cancer: risk factors to potential targets.
Journal: Clinical cancer research : an official journal of the American Association for Cancer Research
Authors: Schneider BP; Winer EP; Foulkes WD; Garber J; Perou CM; Richardson A; Sledge GW; Carey LA;
Publication Date: 2008 Dec 15

Abstract

Triple-negative breast cancer has recently been recognized as an important subgroup of breast cancer with a distinct outcome and therapeutic approach when compared with other subgroups of breast cancer. Triple-negative breast cancer comprises primarily, but not exclusively, a molecularly distinct subtype of breast cancer, the basal-like subtype. We do not yet have an assay to identify basal-like breast cancer in clinical samples, so triple-negative breast cancer has become a commonly used proxy for this subtype. The molecular biology and pathophysiology of triple-negative breast cancer are not completely understood, but understanding is improving rapidly with the advent of sophisticated molecular biology platforms. Moreover, the established risk factors of breast cancer as a whole may not apply to this unique subgroup of patients. Finally, because triple-negative breast cancer is defined by the absence of a target, there are currently limitations to using a tailored therapeutic approach, leaving conventional cytotoxic therapies as the mainstay. Active preclinical and clinical research programs focus on defining the clinical behavior, delineating the risk factors, and more completely understanding the molecular biology of triple-negative breast cancer to improve prevention, optimize conventional agents, and unveil novel therapeutic targets. This CCR focus article will review the current state of the art on triple-negative breast cancer.
View details for PubMedID 19088017
Association of polymorphisms of angiogenesis genes with breast cancer.
Journal: Breast cancer research and treatment
Authors: Schneider BP; Radovich M; Sledge GW; Robarge JD; Li L; Storniolo AM; Lemler S; Nguyen AT; Hancock BA; Stout M; Skaar T; Flockhart DA;
Publication Date: 2007 Sep 20

Abstract

Few studies have systematically explored a pathway approach: to test the association of multiple polymorphisms from multiple genes important to angiogenesis simultaneously with risk of breast cancer. We report our preliminary data evaluating the association of polymorphisms from seven genes known to influence angiogenesis with the likelihood of having breast cancer.
View details for PubMedID 17891484
Is the blood-brain barrier relevant in metastatic germ cell tumor?
Journal: International journal of radiation oncology, biology, physics
Authors: Azar JM; Schneider BP; Einhorn LH;
Publication Date: 2007 Sep 1

Abstract

Germ cell tumors are uniquely chemosensitive and curable, even with advanced metastatic disease. Central nervous system recurrence can terminate a complete remission in other chemosensitive tumors, such as small cell lung cancer, because of the blood-brain barrier (BBB). We propose to document that the BBB is also relevant in germ cell tumors despite their dramatic chemosensitivity.
View details for PubMedID 17707269
Drug insight: VEGF as a therapeutic target for breast cancer.
Journal: Nature clinical practice. Oncology
Authors: Schneider BP; Sledge GW Jr;
Publication Date: 2007 Mar

Abstract

Angiogenesis is implicated in the pathogenesis of malignancy and metastasis. Inhibition of angiogenesis has demonstrated clinically significant improvements in outcomes in a variety of malignancies, including breast cancer. The humanized monoclonal antibody against VEGF, bevacizumab, is the clinically most mature of the antiangiogenic agents and has recently been shown to improve outcome when combined with chemotherapy in the first-line metastatic setting of breast cancer. A variety of other antiangiogenic agents are currently under investigation, including drugs that inhibit the VEGF receptor 2, the cognate receptor for VEGF found on endothelial cells. The combination of antiangiogenic drugs with one another and with other biologic agents is also being explored in an attempt to improve efficacy and to overcome the drug resistance seen with the initial studies of antiangiogenic agents. This Review will focus on the current state of therapeutics designed to inhibit this angiogenic process in breast cancer.
View details for PubMedID 17327858
Analysis of angiogenesis genes from paraffin-embedded breast tumor and lymph nodes.
Journal: Breast cancer research and treatment
Authors: Schneider BP; Skaar TC; Sledge GW; Badve S; Li L; Flockhart DA;
Publication Date: 2006 Feb 28

Abstract

Angiogenesis is important in tumor growth and metastasis. Germ-line polymorphisms critical to the angiogenesis pathway have been shown to confer prognostic information in multiple tumor types. These genes include vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS).
View details for PubMedID 16505966
Angiogenesis of breast cancer.
Journal:
Authors: Schneider BP; Miller KD;
Publication Date: 2005 Mar 10