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. Alexander K. Rinehart, CFP®, CIMA®, CEPA®, CRPS® on LinkedIn ...
A strategic partnership is required to eliminate cervical cancer by 2040. We appeal to major partners to come forward and contribute to eliminating cervical ...
According to a recent Cancer@Work study, 50% of people with cancer are afraid to tell their employers. At @UBS, we're proud to be a signatory to the…
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. Optical imaging of metabolism in HER2 overexpressing breast ...
9 dec 2011 · The optical redox ratio measures changes in tumor metabolism that reflect the oncogenic effects of HER2 activity within the cell.
6. Breast Cancer: A Molecularly Heterogenous Disease Needing ...
About 5–10% of breast cancers can be linked to gene mutations inherited from one's mother or father, such as BRCA1 or BRCA2 mutations [2]. The peak of breast ...
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.
7. Tumor p38MAPK signaling enhances breast carcinoma vascularization ...
5 sep 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...
8. Cleavage of the extracellular domain of junctional adhesion molecule-A ...
20 nov 2018 · ... Alex Eustace (Royal College of Surgeons in Ireland) and Norma O'Donovan ... Breast cancer is the most common cancer in women worldwide ...
Junctional adhesion molecule-A (JAM-A) is an adhesion molecule whose overexpression on breast tumor tissue has been associated with aggressive cancer phenotypes, including human epidermal growth factor receptor-2 (HER2)-positive disease. Since JAM-A has been described to regulate HER2 expression in breast cancer cells, we hypothesized that JAM-dependent stabilization of HER2 could participate in resistance to HER2-targeted therapies. Using breast cancer cell line models resistant to anti-HER2 drugs, we investigated JAM-A expression and the effect of JAM-A silencing on biochemical/functional parameters. We also tested whether altered JAM-A expression/processing underpinned differences between drug-sensitive and -resistant cells and acted as a biomarker of patients who developed resistance to HER2-targeted therapies. Silencing JAM-A enhanced the anti-proliferative effects of anti-HER2 treatments in trastuzumab- and lapatinib-resistant breast cancer cells and further reduced HER2 protein expression and Akt phosphorylation in drug-treated cells. Increased epidermal growth factor receptor expression observed in drug-resistant models was normalized upon JAM-A silencing. JAM-A was highly expressed in all of a small cohort of HER2-positive patients whose disease recurred following anti-HER2 therapy. High JAM-A expression also correlated with metastatic disease at the time of diagnosis in another patient cohort resistant to trastuzumab therapy. Importantly, cleavage of JAM-A was incre...
9. Targeting metastatic breast cancer: problems and potential.
4 jun 2015 · Dr Hunter's paper will certainly recalibrate the way we think about translational research in metastasis. It should inspire new generations of ...
Breast cancer is one of the leading causes of cancer-related mortality of women in the United States. Since the majority of cancer deaths are due to metastases rather than the primary tumor, a better understanding of the biological mechanisms that lead to metastatic disease is critical to reduce breast cancer associated mortality. Current adjuvant therapies use the same broadly cytotoxic and targeted strategies against metastases as are used against the primary tumor. However, resistance to chemotherapy due to the cellular dormancy, high genotypic and phenotypic heterogeneity between primary tumor and metastases as well as among individual metastases, and the limitations in detection of disseminated tumor cells and micrometastases significantly hinder the efficiency of currently available therapies. While it is crucial to directly address the issue of metastatic dormancy and evaluate for anti-metastatic therapy the relevance of molecular targets chosen based on primary tumor profiling, it is also imperative to address metastasis-specific mechanisms of growth and survival that are likely to be distinct from those of the primary tumor. We believe that a three-pronged approach to therapy will be necessary to deal with progressive disease: blocking of further dissemination after diagnosis; eradication of disseminated tumor cells and prevention of the dormant-to-proliferative switch of those remaining; and elimination of established metastatic tumors. The implementation of this st...
