Just when we thought we knew all there was to know and love about breastfeeding, the Internet goes and captures the most relatable and hilarious parts of nursing our little ones. From expressing exactly what we know babies are thinking to capturing the highs and lows of weaning, extended nursing , and breastfeeding in public, these hysterical memes just get it so, so right. And they prove that no matter what we're going through, nursing mamas are truly never alone. From the painful beginnings to those marathon nursing sessions that last half the night, the breastfeeding journey can be one heck of a rollercoaster ride for everyone involved. In fact, sometimes breastfeeding moms are left wondering where their own bodies end and their little babies' hungry mouths begin.
For the Unpredictable Breastfeeding Moments
BRCA1-associated breast cancer exhibits significantly higher levels of chromosomal abnormalities than sporadic breast cancers. However, the molecular mechanisms regarding the roles of BRCA1 in maintaining genome integrity remain elusive. These data reveal a role of BRCA1 in maintaining genome integrity by interplaying with p53 and genes that are involved in the spindle checkpoint and apoptosis. The spindle checkpoint ensures the astonishing accuracy of chromosome segregation by preventing cells with unaligned chromosomes from exiting mitosis. The molecular components of the spindle checkpoint include at least two evolutionarily conserved protein families, Mad and Bub 1 , 2. It was shown that Mad2 binds selectively to unattached kinetochores and is capable of inhibiting anaphase-promoting complex together with BubR1 3 , 4. Consistently, microinjection of Mad2 antibodies yields premature anaphase onset and chromosome missegregation 5. Despite the essential role of Mad2 in the spindle checkpoint, it is unclear how the expression of Mad2 is regulated. Ample experimental evidence indicates that BRCA1 plays essential roles in maintaining genome integrity 8 — It has been shown that mouse embryos carrying targeted disruptions of Brca1 died at early embryonic developmental stages because of pmediated apoptosis triggered by genetic instability 11 ,
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Antiproliferative effects of 1,dihydroxyvitamin D 3 on breast cells - A mini review. The hormone 1,dihydroxyvitamin D 3 1, OH 2 D 3 , the active form of vitamin D 3 , is an important regulator of calcium homeostasis, exerts antiproliferative effects on various cell systems and can induce differentiation in some kinds of hematopoietic cells. These effects are triggered by its receptor, vitamin D receptor VDR , a phosphoprotein member of the nuclear receptor superfamily, which functions as a transcriptional factor. Many factors such as glucocorticoids, estrogens, retinoids, proliferation rate and cell transformation can modulate VDR levels. VDR is expressed in mammary tissue and breast cancer cells, which are potential targets to hormone action. Besides having antiproliferative properties, vitamin D might also reduce the invasiveness of cancer cells and act as an anti-angiogenesis agent. All of these antitumoral features suggest that the properties of vitamin D could be explored for chemopreventive and therapeutic purposes in cancer. However, hypercalcemia is an undesirable side effect associated with pharmacological doses of 1, OH 2 D 3. Some promising 1, OH 2 D 3 analogs have been developed, which are less hypercalcemic in spite of being potent antiproliferative agents. They represent a new field of investigation.
We have previously demonstrated that fibroblast growth factor receptor 2 FGFR2 activates ribosomal s6 kinase 2 RSK2 in mammary epithelial cells and that this pathway promotes in vitro cell growth and migration. The online version of this article doi Fibroblast growth factor receptors FGFRs and their ligands FGFs play an important role in mammalian ontogenesis, angiogenesis and wound healing. FGFR family consists of four tyrosine kinase receptors FGFR1—4 that are expressed in multiple alternatively spliced variants, which define ligand specificity and downstream signalling pathways [ 1 ]. In BCa patients, increased both nuclear and cytoplasmic FGFR2 expression correlated with lower overall and disease-free survival [ 3 ]. Preclinical studies of FGFR-specific small molecule inhibitors provide evidence to suggest that FGFR2 amplification might serve as a new therapeutic target, especially in TNBC, notoriously resistant to currently available therapies [ 5 ]. In accordance with that, a number of experimental studies in various BCa models demonstrated high efficiency of FGFR inhibitors in the induction of tumour growth arrest [ 6 — 8 ].