Sentences with phrase «er +»

One enthusiastic and very amateur DIY - er + a Pinterest obsession + a flat in need of a serious makeover = one pin left in.
These associations were primarily limited to hormone receptor — positive tumors as migraine was associated with a 0.65-fold (95 % CI, 0.51 - 0.83) reduced risk of estrogen receptor — positive (ER +) / progesterone receptor — positive (PR +) ductal carcinoma.
Finally, I am ER + BC HER2 Neg with Mets in bones and liver....
Tamoxifen often is prescribed as part of the treatment for ER + breast cancer.
Bottom line While research has shown some benefits with regards to ER + breast cancer cell death and prevention of metastases within mice and cellular models, it is recommended that human intake should be through diet only, not supplementation.
The sesame seed lignan sesamin has been found to reduce breast tumor area in rats with hormone receptor positive (ER + / PR +) tumors.
Several studies have found that sesame seed components can stimulate the growth of estrogen - dependent (ER +) breast cancer cells.
Another study published in the journal Cancer Biotherapy and Biopharmaceuticals found that FWGE in conjunction with the ER + breast cancer chemotherapy drug Tamoxifen «significantly increased apoptosis already 24 hours after starting treatment.»
But when European researchers recently looked at breast cancer by subtype, they found a connection between dietary fat intake and ER + / progesterone - receptor - positive (PR +) breast cancer, the most common type.
«We found a strong reduction in the risk of estrogen - receptor - negative [ER --RSB- breast cancer in particular, which is exciting because that type of tumor, while rarer than estrogen - receptor - positive [ER +] tumors, tends to be aggressive.»
And in a series of studies last year, Duke University researchers showed that a by - product of cholesterol known as 27HC mimics estrogen and can drive the growth of ER + breast cancer.
Women in the study who consumed the most had a 28 % higher risk of ER + / PR + cancer than those who ate the least.
Development of gene signatures to predict treatment efficacy in endocrine resistant ER + breast cancers
Dr. Mack's research has focused primarily on the use of novel antitumor agents in human estrogen receptor negative breast tumor cells, and more recently, on the use of bioflavonoids in the regulation of estrogen receptor positive (ER +) and estrogen receptor negative (ER --RRB- breast tumor cell proliferation.
Specifically, my research proposal addresses the mechanisms by which the kinase 3 - phosphoinoside dependent protein kinase - 1 (PDK1) mediates resistance to cell cycle related CDK4 / 6 inhibition in ER + breast cancer and explores the in vivo effects of inhibiting PDK1 in combination with CDK4 / 6 inhibitors toward ER + breast cancer growth.
Additionally for patients with ER + or PR + breast cancer who are refractory to endocrine therapy, or patients who have triple negative breast cancer, targeted therapeutic options remain quite limited.
In estrogen - receptor positive (ER +) breast cancer, breast cancer cells receive growth signals from the female hormone estrogen.
SLC6A14 is induced in colon cancer [12], cervical cancer [13], pancreatic cancer [11] and estrogen receptor positive (ER +) breast cancer [14].
She has also obtained a Breast Cancer Research Foundation American Association for Cancer Research (BCRF - AACR) Grant for Translational Breast Cancer Research to explore combined endocrine and ErbB inhibition in ER + / HER2 + breast cancers in 2007, a K23 Career Development Award to explore targeted therapies in breast cancer, and is also co-Leader in three of the four research projects of the NCI - funded Vanderbilt Breast Cancer Specialized Program of Research Excellence (SPORE; Carlos Arteaga, Director).
This model should be a powerful tool for testing therapies for aggressive ER + breast cancers and for studying luminal cancers — the most prevalent and deadliest forms of breast cancer.
Not only is the progesterone receptor an «essential modulator of estrogen - receptor - regulated genes,» but it also significantly contributes to the «prognostic value of estrogen receptors in ER + / PR + breast cancers.»
PHIb Trial of Fulvestrant, Palbociclib (CDK4 / 6 inhibitor) and Erdafitinib (JNJ - 42756493, pan-FGFR Tyrosine Kinase Inhibitor) in ER + / HER2 - / FGFR - amplified Metastatic Breast Cancer (MBC)
The researchers, including scientists from The Genome Institute at Washington University School of Medicine, presented the research titled, «Patient - derived xenograft study reveals endocrine therapy resistance of ER + breast cancer caused by distinct ESR1 gene aberrations.»
They also show increased expression of the estrogen receptor alpha [ER +] gene that drives cell division,» says Koshy.
«Never before has PTK6 inhibition been shown to inhibit growth and induce cell death of ER + breast cancer cells, including those resistant to standard treatments for this subtype such as tamoxifen,» said Hanna Irie, MD, PhD, Assistant Professor of Medicine (Hematology and Medical Oncology) and Oncological Sciences at The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, and senior author of the study.
«Novel therapeutic target discovered for estrogen receptor positive (ER +) breast cancer.»
Approximately 65 percent of all breast cancers express the estrogen receptor (ER +) and / or the progesterone receptor (PR +).
Researchers at the Icahn School of Medicine at Mount Sinai have identified a protein that can be targeted to suppress growth of a common type of breast cancer known as «estrogen receptor positive» (ER +), including ER + cancers that are resistant to standard treatments.
According to Dr. Irie, the research is especially important because it supports the potential therapeutic value of targeting PTK6 in ER + breast cancers, which constitute the most common subtype of breast cancer.
Standard treatments for ER + breast cancer are endocrine therapies such as tamoxifen and aromatase inhibitors.
«We are excited and gratified by these remarkable results, which could lead to a new way to treat these drug resistant metastases of ER + breast cancers and / or prevent their metastases in the first place.»
«However, some breast cancer patients still develop metastatic ER + disease despite these common endocrine therapies, so newer treatments are very important and necessary to kill endocrine therapy - resistant cancers.»
It can promote cancer cell survival and growth of ER + breast cancer cells.
The team has studied the most common kind of breast tumour — estrogen - positive (ER +) and accounting for 80 % of breast cancer tumour cases — that is characterised by a long period of latency with no symptoms.
In the second study, researchers examined whether aspirin is associated with breast density, which is a widely accepted risk factor for both estrogen receptor minus (ER --RRB- and estrogen receptor positive (ER +) breast cancers, and can be a key factor in detecting tumors during routine mammograms.
The drug was approved by the FDA as a combination first - line therapy for postmenopausal women with ER + / HER2 - breast cancer, as initial endocrine - based treatment for their metastatic disease.
About 75 percent of breast cancers are ER + and grow in response to the hormone estrogen.
In this study published in Cell Reports, Alexandra Van Keymeulen and colleagues generated a new transgenic line - allowing lineage tracing of ER + luminal cells to investigate luminal cell heterogeneity and identify the origin of ER + luminal cells and the mechanisms regulating their pubertal expansion and adult maintenance.

Not exact matches

You can post easily to Google + (and I did, for a while), but few of us have time to manage Facebook posts, LinkedIn updates, our Twitter activity, and then jump over to see who has liked (er, plus one'd) a message, let alone track followers (er, circles).
I am a registered nurse with 25 + years of in hospital experience, in the ICU / ER.
Because frozen banana + 1 other fruit + super foods + water = lunch... er, smoothie.
We don't need another 30 + er.
In a nutshell, I wanted super hearty sprouted grain breads + lots of beans + high (er) fiber baby food pouches + chia - seed laced fruit smoothies and tons of water.
In those mice, inositol triphosphate receptor type - 3 (IP3R3), a MAM - enriched calcium ion (Ca2 +) channel on ER, was disappeared from the MAM.
A novel CISD2 mutation associated with a classical Wolfram syndrome phenotype alters Ca2 + homeostasis and ER - mitochondria interactions.
Patients whose tumors were ER - negative and / or lymph - node - positive had received systematic chemotherapy, ER - positive or LN - negative patients had not, and none of the patients with Her2 + tumors received Herceptin (trastuzumab).
Effects of palmitate on ER and cytosolic Ca2 + homeostasis in β - cells.
Hon et al created a low - passage cancer cell line using a Her2 + ER - / PR - tumor from an East Indian female.
Abbreviations: Aβ, amyloid β - peptide; AD, Alzheimer's disease; ALS, amyotrophic lateral sclerosis; Ambra1, activating molecule in Beclin -1-regulated autophagy; AMPK, AMP - activated protein kinase; APP, amyloid precursor protein; AR, androgen receptor; Atg, autophagy - related; AV, autophagic vacuole; Bcl, B - cell lymphoma; BH3, Bcl - 2 homology 3; CaMKKβ, Ca2 + - dependent protein kinase kinase β; CHMP2B, charged multivesicular body protein 2B; CMA, chaperone - mediated autophagy; 2 ′ 5 ′ ddA, 2 ′, 5 ′ - dideoxyadenosine; deptor, DEP - domain containing mTOR - interacting protein; DRPLA, dentatorubral pallidoluysian atrophy; 4E - BP1, translation initiation factor 4E - binding protein - 1; Epac, exchange protein directly activated by cAMP; ER, endoplasmic reticulum; ERK1 / 2, extracellular - signal - regulated kinase 1/2; ESCRT, endosomal sorting complex required for transport; FAD, familial AD; FDA, U.S. Food and Drug Administration; FIP200, focal adhesion kinase family - interacting protein of 200 kDa; FoxO3, forkhead box O3; FTD, frontotemporal dementia; FTD3, FTD linked to chromosome 3; GAP, GTPase - activating protein; GR, guanidine retinoid; GSK3, glycogen synthase kinase 3; HD, Huntington's disease; hiPSC, human induced pluripotent stem cell; hVps, mammalian vacuolar protein sorting homologue; IKK, inhibitor of nuclear factor κB kinase; IMPase, inositol monophosphatase; IP3R, Ins (1,4,5) P3 receptor; I1R, imidazoline - 1 receptor; JNK1, c - Jun N - terminal kinase 1; LC3, light chain 3; LD, Lafora disease; L - NAME, NG - nitro - L - arginine methyl ester; LRRK2, leucine - rich repeat kinase 2; MIPS, myo - inositol -1-phosphate synthase; mLST8, mammalian lethal with SEC13 protein 8; MND, motor neuron disease; mTOR, mammalian target of rapamycin; mTORC, mTOR complex; MVB, multivesicular body; NAC, N - acetylcysteine; NBR1, neighbour of BRCA1 gene 1; NOS, nitric oxide synthase; p70S6K, ribosomal protein S6 kinase - 1; PD, Parkinson's disease; PDK1, phosphoinositide - dependent kinase 1; PE, phosphatidylethanolamine; PI3K, phosphoinositide 3 - kinase; PI3KC1a, class Ia PI3K; PI3KC3, class III PI3K; PI3KK, PI3K - related protein kinase; PINK1, PTEN - induced kinase 1; PKA, protein kinase A; PLC, phospholipase C; polyQ, polyglutamine; PS, presenilin; PTEN, phosphatase and tensin homologue deleted from chromosome 10; Rag, Ras - related GTP - binding protein; raptor, regulatory - associated protein of mTOR; Rheb, Ras homologue enriched in brain; rictor, rapamycin - insensitive companion of mTOR; SBMA, spinobulbar muscular atrophy; SCA, spinocerebellar ataxia; SLC, solute carrier; SMER, small - molecule enhancer of rapamycin; SMIR, small - molecule inhibitor of rapamycin; SNARE, N - ethylmaleimide - sensitive factor - attachment protein receptor; SOD1, copper / zinc superoxide dismutase 1; TFEB, transcription factor EB; TOR, target of rapamycin; TSC, tuberous sclerosis complex; ULK1, UNC -51-like kinase 1; UVRAG, UV irradiation resistance - associated gene; VAMP, vesicle - associated membrane protein; v - ATPase, vacuolar H + - ATPase; Vps, vacuolar protein sorting
Again, within the HER2 + sub-group, ER / PR − tumors have much higher MELK expression than ER / PR + ones (Figure 2I).
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