1. New Study - Vitamin D and Cancer Survival - Dr. Alex Rinehart
Can the sunshine vitamin boost cancer survival?Cancer patients who had higher levels of 25-Hydroxyvitamin D were linked with better survival rates and ...
Can the sunshine vitamin boost cancer survival?Cancer patients who had higher levels of 25-Hydroxyvitamin D were linked with better survival rates and longer remission than those who are vitamin D-deficient. The findings were published in July 2014 in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism. The meta-analysis reviewed 25 studies that measured vitamin […]
2. Optical imaging of metabolism in HER2 overexpressing breast ...
Dec 9, 2011 · The optical redox ratio measures changes in tumor metabolism that reflect the oncogenic effects of HER2 activity within the cell.
3. Genome-wide association study identifies novel breast cancer ...
We aimed to identify further breast cancer susceptibility loci in a three-stage association study. In the first stage, we used a panel of 266,722 SNPs, selected ...
Breast cancer exhibits familial aggregation, consistent with variation in genetic susceptibility to the disease. Known susceptibility genes account for less than 25% of the familial risk of breast cancer, and the residual genetic variance is likely ...
4. Multicenter phase II study of the oral MEK inhibitor, CI-1040, in ...
Multicenter phase II study of the oral MEK inhibitor, CI-1040, in patients with advanced non-small-cell lung, breast, colon, and pancreatic cancer. / Rinehart, ...
Purpose: This multicenter, open-label, phase II study was undertaken to assess the antitumor activity and safety of the oral mitogen-activated extracellular signal regulated kinase kinase (MEK) inhibitor, CI-1040, in breast cancer, colon cancer, non-small-cell lung cancer (NSCLC), and pancreatic cancer. Patients and Methods: Patients with advanced colorectal, NSCLC, breast, or pancreatic cancer received oral CI-1040 continuously at 800 mg bid. All patients had measurable disease at baseline, a performance status of 2 or less, and adequate bone marrow, liver, and renal function. Expression of pERK, pAkt, and Ki-67 was assessed in archived tumor specimens by quantitative immunohistochemistry. Results: Sixty-seven patients with breast (n = 14), colon (n = 20), NSCLC (n = 18), and pancreatic (n = 15) cancer received a total of 194 courses of treatment (median, 2.0 courses; range, one to 14 courses). No complete or partial responses were observed. Stable disease (SD) lasting a median of 4.4 months (range, 4 to 18 months) was confirmed in eight patients (one breast, two colon, two pancreas, and three NSCLC patients). Treatment was well tolerated, with 81 % of patients experiencing toxicities of grade 2 or less severity. Most common toxicities included diarrhea, nausea, asthenia, and rash. A mild association (P < .055) between baseline pERK expression in archived tumor specimens and SD was observed. Conclusion: CI-1040 was generally well tolerated but demonstrated insufficient antit...
5. Breast Cancer: A Molecularly Heterogenous Disease Needing ...
Breast cancer is a heterogeneous disease, which is characterized by high genomic instability evidenced by somatic gene mutations, copy number alterations, and ...
Breast cancer is the most commonly occurring cancer in women. There were over two-million new cases in world in 2018. It is the second leading cause of death from cancer in western countries. At the molecular level, breast cancer is a heterogeneous disease, which is characterized by high genomic instability evidenced by somatic gene mutations, copy number alterations, and chromosome structural rearrangements. The genomic instability is caused by defects in DNA damage repair, transcription, DNA replication, telomere maintenance and mitotic chromosome segregation. According to molecular features, breast cancers are subdivided in subtypes, according to activation of hormone receptors (estrogen receptor and progesterone receptor), of human epidermal growth factors receptor 2 (HER2), and or BRCA mutations. In-depth analyses of the molecular features of primary and metastatic breast cancer have shown the great heterogeneity of genetic alterations and their clonal evolution during disease development. These studies have contributed to identify a repertoire of numerous disease-causing genes that are altered through different mutational processes. While early-stage breast cancer is a curable disease in about 70% of patients, advanced breast cancer is largely incurable. However, molecular studies have contributed to develop new therapeutic approaches targeting HER2, CDK4/6, PI3K, or involving poly(ADP-ribose) polymerase inhibitors for BRCA mutation carriers and immunotherapy.
6. Development of acquired resistance to lapatinib may sensitise HER2 ...
Oct 11, 2018 · ... breast cancer cells to apoptosis induction by obatoclax and TRAIL. Alex J Eustace ORCID: orcid.org/0000-0002-4092-1360,; Neil T Conlon ...
Lapatinib has clinical efficacy in the treatment of trastuzumab-refractory HER2-positive breast cancer. However, a significant proportion of patients develop progressive disease due to acquired resistance to the drug. Induction of apoptotic cell death is a key mechanism of action of lapatinib in HER2-positive breast cancer cells. We examined alterations in regulation of the intrinsic and extrinsic apoptosis pathways in cell line models of acquired lapatinib resistance both in vitro and in patient samples from the NCT01485926 clinical trial, and investigated potential strategies to exploit alterations in apoptosis signalling to overcome lapatinib resistance in HER2-positive breast cancer. In this study, we examined two cell lines models of acquired lapatinib resistance (SKBR3-L and HCC1954-L) and showed that lapatinib does not induce apoptosis in these cells. We identified alterations in members of the BCL-2 family of proteins, in particular MCL-1 and BAX, which may play a role in resistance to lapatinib. We tested the therapeutic inhibitor obatoclax, which targets MCL-1. Both SKBR3-L and HCC1954-L cells showed greater sensitivity to obatoclax-induced apoptosis than parental cells. Interestingly, we also found that the development of acquired resistance to lapatinib resulted in acquired sensitivity to TRAIL in SKBR3-L cells. Sensitivity to TRAIL in the SKBR3-L cells was associated with reduced phosphorylation of AKT, increased expression of FOXO3a and decreased expression of c...
7. Joan Garrett - Cincinnati College of Medicine
Research Interests. Mechanisms of mutant HER3 signaling in breast cancer. ERBB3, the gene encoding HER3, is mutated in ~2% of breast cancers and other ...
Mishra, Rosalin; Patel, Hima; Alanazi, Samar; Kilroy, Mary Kate; Garrett, Joan T 2021. PI3K Inhibitors in Cancer: Clinical Implications and Adverse Effects. International journal of molecular sciences, 22 7,
8. Tumor p38MAPK signaling enhances breast carcinoma vascularization ...
Sep 5, 2017 · ... Michelle Limoge, Alfiya Safina, Alexander M ... breast cancer cells would influence tumor growth and the tumor microenvironment.
// Michelle Limoge 1 , Alfiya Safina 3 , Alexander M. Truskinovsky 2 , Ieman Aljahdali 1 , Justin Zonneville 1 , Aleksandar Gruevski 5 , Carlos L. Arteaga 4 and Andrei V. Bakin 1 1 Department of Cancer Genetics, Roswell Park Cancer Institute, Buffalo, New York, USA 2 Department of Pathology, Roswell Park Cancer Institute, Buffalo, New York, USA 3 Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, New York, USA 4 Breast Cancer Research Program, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee, USA 5 State University of New York at Buffalo, Department of Biological Sciences, Buffalo, New York, USA Correspondence to: Andrei V. Bakin, email: andrei.bakin@roswellpark.org Keywords: tumor microenvironment, breast cancer, p38MAPK, angiogenesis, fibronectin Received: April 26, 2017 Accepted: May 19, 2017 Published: June 28, 2017 ABSTRACT The breast carcinoma microenvironment strikingly influences cancer progression and response to therapy. Various cell types in the carcinoma microenvironment show significant activity of p38 mitogen-activated protein kinase (MAPK), although the role of p38MAPK in breast cancer progression is still poorly understood. The present study examined the contribution of tumor p38MAPK to breast carcinoma microenvironment and metastatic capacity. Inactivation of p38MAPK signaling in metastatic breast...
9. [PDF] 2024 - October Newsletter - Yellowhawk Tribal Health Center
Oct 2, 2024 · Any person, male or female, with breast tissue can develop breast cancer. ... For more information contact James Rinehart at 541.240.8680 ...
10. Genome-wide association study identifies novel breast cancer ...
Alexander, Jinghui Zhang, Angela Cox, Ian W. ... Rinehart, Bridget Robinson, Barney Rudzki ... Dive into the research topics of 'Genome-wide association study ...
Douglas F. Easton*, Karen A. Pooley, Alison M. Dunning, Paul D.P. Pharoah, Deborah Thompson, Dennis G. Ballinger, Jeffery P. Struewing, Jonathan Morrison, Helen Field, Robert Luben, Nicholas Wareham, Shahana Ahmed, Catherine S. Healey, Richard Bowman, Kerstin B. Meyer, Christopher A. Haiman, Laurence K. Kolonel, Brian E. Henderson, Loic Le Marchand, Paul BrennanSuleeporn Sangrajrang, Valerie Gaborieau, Fabrice Odefrey, Chen Yang Shen, Pei Ei Wu, Hui Chun Wang, Diana Eccles, D. Gareth Evans, Julian Peto, Olivia Fletcher, Nichola Johnson, Sheila Seal, Michael R. Stratton, Nazneen Rahman, Georgia Chenevix-Trench, Stig E. Bojesen, Børge G. Nordestgaard, Christen K. Axelsson, Montserrat Garcia-Closas, Louise Brinton, Stephen Chanock, Jolanta Lissowska, Beata Peplonska, Heli Nevanlinna, Rainer Fagerholm, Hannaleena Eerola, Daehee Kang, Keun Young Yoo, Dong Young Noh, Sei Hyun Ahn, David J. Hunter, Susan E. Hankinson, David G. Cox, Per Hall, Sara Wedren, Jianjun Liu, Yen Ling Low, Natalia Bogdanova, Peter Schürmann, Thilo Dörk, Rob A.E.M. Tollenaar, Catharina E. Jacobi, Peter Devilee, Jan G.M. Klijn, Alice J. Sigurdson, Michele M. Doody, Bruce H. Alexander, Jinghui Zhang, Angela Cox, Ian W. Brock, Gordon MacPherson, Malcolm W.R. Reed, Fergus J. Couch, Ellen L. Goode, Janet E. Olson, Hanne Meijers-Heijboer, Ans Van Den Ouweland, André Uitterlinden, Fernando Rivadeneira, Roger L. Milne, Gloria Ribas, Anna Gonzalez-Neira, Javier Benitez, John L. Hopper, Margaret McCredie, Melissa South...
11. [PDF] FY15 Breast Cancer Research Program Peer Reviewers
Oncology, Louisiana State University. Health Sciences Center. Rinehart Ayres, Margaret. American Cancer Society. Rishi, Arun. Ph.D. Department of Oncology, ...
12. Cancer Risk Assessment | AdventHealth Medical Group
Before any tests, screenings or counseling sessions are recommended, your doctor will assess the likelihood of potential genetic disorders, such as breast ...
Search for an AdventHealth physician by name, location or services offered.
13. SHP2 is a multifunctional therapeutic target in drug resistant metastatic ...
Oct 8, 2020 · Ritter CA, Perez-Torres M, Rinehart C, Guix M, Dugger T, Engelman JA, et al. Human breast cancer cells selected for resistance to trastuzumab in ...
Metastatic breast cancer (MBC) is an extremely recalcitrant disease capable of bypassing current targeted therapies via engagement of several growth promoting pathways. SH2 containing protein tyrosine phosphatase-2 (SHP2) is an oncogenic phosphatase known to facilitate growth and survival signaling downstream of numerous receptor inputs. Herein, we used inducible genetic depletion and two distinct pharmacological inhibitors to investigate the therapeutic potential of targeting SHP2 in MBC. Cells that acquired resistance to the ErbB kinase inhibitor, neratinib, displayed increased phosphorylation of SHP2 at the Y542 activation site. In addition, higher levels of SHP2 phosphorylation, but not expression, were associated with decreased survival of breast cancer patients. Pharmacological inhibition of SHP2 activity blocked ERK1/2 and AKT signaling generated from exogenous stimulation with FGF2, PDGF, and hGF and readily prevented MBC cell growth induced by these factors. SHP2 was also phosphorylated upon engagement of the extracellular matrix (ECM) via focal adhesion kinase. Consistent with the potential of SHP2-targeted compounds as therapeutic agents, the growth inhibitory property of SHP2 blockade was enhanced in ECM-rich 3D culture environments. In vivo blockade of SHP2 in the adjuvant setting decreased pulmonary metastasis and extended the survival of systemic tumor-bearing mice. Finally, inhibition of SHP2 in combination with FGFR-targeted kinase inhibitors synergistically...
