Log in

Relevant bibliographies by topics / Mammary gland involution

Contents

Journal articles
Dissertations / Theses
Books
Book chapters
Conference papers
Reports

Academic literature on the topic 'Mammary gland involution'

Author: Grafiati

Published: 10 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Mammary gland involution.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Mammary gland involution"

1

Dickson, S. R., and M. J. Warburton. "Enhanced synthesis of gelatinase and stromelysin by myoepithelial cells during involution of the rat mammary gland." Journal of Histochemistry & Cytochemistry 40, no. 5 (May 1992): 697–703. http://dx.doi.org/10.1177/40.5.1315355.

Full text

Abstract:

During the involution of the mammary gland there is destruction of the basement membrane as the secretory alveolar structures degenerate. Immunofluorescence staining of sections of rat mammary gland with antibodies to 72 KD gelatinase (MMP-2) and stromelysin (MMP-3) revealed increased production of these two proteinases during involution. This increased expression was mostly restricted to myoepithelial cells. Increased expression during involution was also demonstrated by immunoblotting techniques. Gelatin zymography indicated that the predominant metalloproteinase present in involuting rat mammary glands was a 66 KD gelatinase.

APA, Harvard, Vancouver, ISO, and other styles

2

Lund, L. R., S. F. Bjorn, M. D. Sternlicht, B. S. Nielsen, H. Solberg, P. A. Usher, R. Osterby, et al. "Lactational competence and involution of the mouse mammary gland require plasminogen." Development 127, no. 20 (October 15, 2000): 4481–92. http://dx.doi.org/10.1242/dev.127.20.4481.

Full text

Abstract:

Urokinase-type plasminogen activator expression is induced in the mouse mammary gland during development and post-lactational involution. We now show that primiparous plasminogen-deficient (Plg(−/−)) mice have seriously compromised mammary gland development and involution. All mammary glands were underdeveloped and one-quarter of the mice failed to lactate. Although the glands from lactating Plg(−/−) mice were initially smaller, they failed to involute after weaning, and in most cases they failed to support a second litter. Alveolar regression was markedly reduced and a fibrotic stroma accumulated in Plg(−/−) mice. Nevertheless, urokinase and matrix metalloproteinases (MMPs) were upregulated normally in involuting glands of Plg(−/−) mice, and fibrin did not accumulate in the glands. Heterozygous Plg(+/−) mice exhibited haploinsufficiency, with a definite, but less severe mammary phenotype. These data demonstrate a critical, dose-dependent requirement for Plg in lactational differentiation and mammary gland remodeling during involution.

APA, Harvard, Vancouver, ISO, and other styles

3

Talhouk, R. S., M. J. Bissell, and Z. Werb. "Coordinated expression of extracellular matrix-degrading proteinases and their inhibitors regulates mammary epithelial function during involution." Journal of Cell Biology 118, no. 5 (September 1, 1992): 1271–82. http://dx.doi.org/10.1083/jcb.118.5.1271.

Full text

Abstract:

Extracellular matrix (ECM) plays an important role in the maintenance of mammary epithelial differentiation in culture. We asked whether changes in mouse mammary specific function in vivo correlate with changes in the ECM. We showed, using expression of beta-casein as a marker, that the temporal expression of ECM-degrading proteinases and their inhibitors during lactation and involution are inversely related to functional differentiation. After a lactation period of 9 d, mammary epithelial cells maintained beta-casein expression up to 5 d of involution. Two metalloproteinases, 72-kD gelatinase (and its 62-kD active form), and stromelysin, and a serine proteinase tissue plasminogen activator were detected by day four of involution, and maintained expression until at least day 10. The expression of their inhibitors, the tissue inhibitor of metalloproteinases (TIMP) and plasminogen activator inhibitor-1, preceded the onset of ECM-degrading proteinase expression and was detected by day two of involution, and showed a sharp peak of expression centered on days 4-6 of involution. When involution was accelerated by decreasing lactation to 2 d, there was an accelerated loss of beta-casein expression evident by day four and a shift in expression of ECM-remodeling proteinases and inhibitors to a focus at 2-4 d of involution. To further extend the correlation between mammary-specific function and ECM remodeling we initiated involution by sealing just one gland in an otherwise hormonally sufficient lactating animal. Alveoli in the sealed gland contained casein for at least 7 d after sealing, and closely resembled those in a lactating gland. The relative expression of TIMP in the sealed gland increased, whereas the expression of stromelysin was much lower than that of a hormone-depleted involuting gland, indicating that the higher the ratio of TIMP to ECM-degrading proteinases the slower the process of involution. To test directly the functional role of ECM-degrading proteinases in the loss of tissue-specific function we artificially perturbed the ECM-degrading proteinase-inhibitor ratio in a normally involuting gland by maintaining high concentrations of TIMP protein with the use of surgically implanted slow-release pellets. In a concentration-dependent fashion, involuting mammary glands that received TIMP implants maintained high levels of casein and delayed alveolar regression. These data suggest that the balance of ECM-degrading proteinases and their inhibitors regulates the organization of the basement membrane and the tissue-specific function of the mammary gland.(ABSTRACT TRUNCATED AT 400 WORDS)

APA, Harvard, Vancouver, ISO, and other styles

4

Schwertfeger, Kathryn L., Monica M. Richert, and Steven M. Anderson. "Mammary Gland Involution Is Delayed by Activated Akt in Transgenic Mice." Molecular Endocrinology 15, no. 6 (June 1, 2001): 867–81. http://dx.doi.org/10.1210/mend.15.6.0663.

Full text

Abstract:

Abstract Activation of the antiapoptotic protein kinase Akt is induced by a number of growth factors that regulate mammary gland development. Akt is expressed during mammary gland development, and expression decreases at the onset of involution. To address Akt actions in mammary gland development, transgenic mice were generated expressing constitutively active Akt in the mammary gland under the control of the mouse mammary tumor virus (MMTV) promoter. Analysis of mammary glands from these mice reveals a delay in both involution and the onset of apoptosis. Expression of tissue inhibitor of metalloproteinase-1 (TIMP-1), an inhibitor of matrix metalloproteinases (MMPs), is prolonged and increased in the transgenic mice, suggesting that disruption of the MMP:TIMP ratio may contribute to the delayed mammary gland involution observed in the transgenic mice.

APA, Harvard, Vancouver, ISO, and other styles

5

Bernhardt, Sarah M., and Pepper Schedin. "Abstract B011: The anti-cancer effects of vitamin D are blocked postpartum, due to suppression of vitamin D metabolism in the involuting liver." Cancer Prevention Research 15, no. 12_Supplement_1 (December 1, 2022): B011. http://dx.doi.org/10.1158/1940-6215.dcis22-b011.

Full text

Abstract:

Abstract Postpartum mammary gland involution is a physiologic window of increased breast cancer risk. It has been proposed that the poor prognosis associated with postpartum breast cancer is due to the involuting mammary microenvironment promoting progression of indolent lesions to invasive disease. As such, the involuting gland has been implicated as a target for preventive strategies. Vitamin D has anti-cancer properties, and there are data demonstrating that vitamin D supplementation protects against breast cancer progression in mouse models. Moreover, vitamin D deficiency is prevalent in postpartum women, suggesting that vitamin D supplementation during the vitamin D-deficient, at-risk window of involution may be an approach for preventing the progression of indolent lesions. Here, we characterized how vitamin D deficiency and supplementation affect tumor growth in a mouse model of postpartum breast cancer. Vitamin D deficiency and sufficiency were established in BALB/c mice through feeding diets containing low or high levels of vitamin D. Quantification of serum 25(OH)D verified that diets resulted in vitamin D deficiency (25.8±4.3nmol/L;mean±stdev) or sufficiency (66.4±11.7nmol/L) at levels comparable to humans. Murine mammary cancer cells (D2A1, 2×104 cells, 20µL) were injected into mammary fatpads of involuting (2 days post wean), or age-matched nulliparous mice (n=5-12 mice/group), and tumor growth tracked for 4 weeks. Independent of vitamin D status, tumors exposed to the involuting mammary gland grew 1.8-fold larger than tumors exposed to the nulliparous gland (p<0.001); consistent with prior data showing that the microenvironment of the involuting gland is tumor promotional. Interestingly, while vitamin D supplementation of nulliparous mice associated with a 3.4-fold reduction in tumor growth (p=0.03), vitamin D supplementation of involution mice did not reduce tumor growth. Dietary vitamin D is metabolized to its active form in the liver. Our group has previously shown that the liver also undergoes weaning-induced involution. Thus, we tested if involution of the liver impairs metabolism of vitamin D to its active form, potentially contributing to the null effects of vitamin D supplementation in involution mice. We collected serum from mice on vitamin D deficient and supplemented diets across reproductive time points (nulliparous, lactation, involution days 2, 4, 6), and found that vitamin D supplementation during involution was insufficient to restore serum vitamin D to levels of sufficiency. Further, gene expression analysis of livers show that expression of Cyp2r1 and Cyp27a1—genes involved in vitamin D activation—were reduced during involution. Together, these findings suggest that impaired metabolism of vitamin D during involution may reduce the availability of active vitamin D, and contribute to the null effect observed in involution mice. Understanding the mechanisms by which mammary gland involution influences the anti-cancer effects of vitamin D is required to optimize cancer prevention strategies that target this window. Citation Format: Sarah M Bernhardt, Pepper Schedin. The anti-cancer effects of vitamin D are blocked postpartum, due to suppression of vitamin D metabolism in the involuting liver [abstract]. In: Proceedings of the AACR Special Conference on Rethinking DCIS: An Opportunity for Prevention?; 2022 Sep 8-11; Philadelphia, PA. Philadelphia (PA): AACR; Can Prev Res 2022;15(12 Suppl_1): Abstract nr B011.

APA, Harvard, Vancouver, ISO, and other styles

6

Jena, Manoj Kumar, and Ashok Kumar Mohanty. "NEW INSIGHTS OF MAMMARY GLAND DURING DIFFERENT STAGES OF DEVELOPMENT." Asian Journal of Pharmaceutical and Clinical Research 10, no. 11 (November 1, 2017): 35. http://dx.doi.org/10.22159/ajpcr.2017.v10i11.20801.

Full text

Abstract:

Mammary gland is a unique organ with its function of milk synthesis, secretion, and involution to prepare the gland for subsequent lactation. The mammary epithelial cells proliferate, differentiate, undergo apoptosis, and tissue remodeling following a cyclic pathway in lactation – involution – lactation cycle, thus fine tuning the molecular events through hormones, and regulatory molecules. Several studies are performed on the mammary gland development, lactogenesis, and involution process in molecular details. The developmental stages of mammary gland are embryonic, pre-pubertal, pubertal, pregnancy, lactation, and involution. Major developmental processes occur after puberty with hormones and growth factors playing crucial role. The two major pathways such as Janus kinases-signal transducer and activator of transcription pathway and PI3K-Akt pathway play a major role in maintaining the lactation. The involution process is a well-orchestrated event involving several signaling molecules and making the gland ready for subsequent lactation. The review focuses on findings with molecular details of different stages of the mammary gland development and signaling pathways involved in lactation–involution cycle. Deep insight into the developmental stages of mammary gland will pave the way to understand mammary gland biology, apoptosis, oncogenesis, and it will help the researchers to use mammary gland as a model for research on various aspects.

APA, Harvard, Vancouver, ISO, and other styles

7

Atabai, Kamran, Rafael Fernandez, Xiaozhu Huang, Iris Ueki, Ahnika Kline, Yong Li, Sepid Sadatmansoori, et al. "Mfge8 Is Critical for Mammary Gland Remodeling during Involution." Molecular Biology of the Cell 16, no. 12 (December 2005): 5528–37. http://dx.doi.org/10.1091/mbc.e05-02-0128.

Full text

Abstract:

Apoptosis is a critical process in normal mammary gland development and the rapid clearance of apoptotic cells prevents tissue injury associated with the release of intracellular antigens from dying cells. Milk fat globule-EGF-factor 8 (Mfge8) is a milk glycoprotein that is abundantly expressed in the mammary gland epithelium and has been shown to facilitate the clearance of apoptotic lymphocytes by splenic macrophages. We report that mice with disruption of Mfge8 had normal mammary gland development until involution. However, abnormal mammary gland remodeling was observed postlactation in Mfge8 mutant mice. During early involution, Mfge8 mutant mice had increased numbers of apoptotic cells within the mammary gland associated with a delay in alveolar collapse and fat cell repopulation. As involution progressed, Mfge8 mutants developed inflammation as assessed by CD45 and CD11b staining of mammary gland tissue sections. With additional pregnancies, Mfge8 mutant mice developed progressive dilatation of the mammary gland ductal network. These data demonstrate that Mfge8 regulates the clearance of apoptotic epithelial cells during mammary gland involution and that the absence of Mfge8 leads to inflammation and abnormal mammary gland remodeling.

APA, Harvard, Vancouver, ISO, and other styles

8

Rivera, Olivia C., Stephen R. Hennigar, and Shannon L. Kelleher. "ZnT2 is critical for lysosome acidification and biogenesis during mammary gland involution." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 315, no. 2 (August 1, 2018): R323—R335. http://dx.doi.org/10.1152/ajpregu.00444.2017.

Full text

Abstract:

Mammary gland involution, a tightly regulated process of tissue remodeling by which a lactating mammary gland reverts to the prepregnant state, is characterized by the most profound example of regulated epithelial cell death in normal tissue. Defects in the execution of involution are associated with lactation failure and breast cancer. Initiation of mammary gland involution requires upregulation of lysosome biogenesis and acidification to activate lysosome-mediated cell death; however, specific mediators of this initial phase of involution are not well described. Zinc transporter 2 [ZnT2 ( SLC30A2)] has been implicated in lysosome biogenesis and lysosome-mediated cell death during involution; however, the direct role of ZnT2 in this process has not been elucidated. Here we showed that ZnT2-null mice had impaired alveolar regression and reduced activation of the involution marker phosphorylated Stat3, indicating insufficient initiation of mammary gland remodeling during involution. Moreover, we found that the loss of ZnT2 inhibited assembly of the proton transporter vacuolar ATPase on lysosomes, thereby decreasing lysosome abundance and size. Studies in cultured mammary epithelial cells revealed that while the involution signal TNFα promoted lysosome biogenesis and acidification, attenuation of ZnT2 impaired the lysosome response to this involution signal, which was not a consequence of cytoplasmic Zn accumulation. Our findings establish ZnT2 as a novel regulator of vacuolar ATPase assembly, driving lysosome biogenesis, acidification, and tissue remodeling during the initiation of mammary gland involution.

APA, Harvard, Vancouver, ISO, and other styles

9

Alexander, Caroline M., Sushma Selvarajan, John Mudgett, and Zena Werb. "Stromelysin-1 Regulates Adipogenesis during Mammary Gland Involution." Journal of Cell Biology 152, no. 4 (February 12, 2001): 693–703. http://dx.doi.org/10.1083/jcb.152.4.693.

Full text

Abstract:

The matrix metalloproteinase MMP-3/stromelysin-1 (Str1) is highly expressed during mammary gland involution induced by weaning. During involution, programmed cell death of the secretory epithelium takes place concomitant with the repopulation of the mammary fat pad with adipocytes. In this study, we have used a genetic approach to determine the role of Str1 during mammary involution. Although Str1 has been shown to induce unscheduled apoptosis when expressed ectopically during late pregnancy (Alexander, C.M., E.W. Howard, M.J. Bissell, and Z. Werb. 1996. J. Cell Biol. 135:1669–1677), we found that during post-lactational involution, mammary glands from transgenic mice that overexpress the tissue inhibitor of metalloproteinases, TIMP-1 (TO), or mice carrying a targeted mutation in Str1 showed accelerated differentiation and hypertrophy of adipocytes, while epithelial apoptosis was unaffected. These data suggest that matrix metalloproteinases (MMPs) do not induce unscheduled epithelial cell death after weaning, but instead alter the stromal microenvironment. We used adipogenic 3T3-L1 cells as a cell culture model to test the function of MMPs during adipocyte differentiation. Fibroblastic 3T3-L1 progenitor cells expressed very low levels of MMPs or TIMPs. The transcription of a number of MMP and TIMP mRNAs [Str1, MT1-MMP, (MMP-14) collagenase-3 (MMP-13), gelatinase A (MMP-2), and TIMP-1, -2 and -3] was induced in committed preadipocytes, but only differentiated adipocytes expressed an activated MMP, gelatinase A. The addition of MMP inhibitors (GM 6001 and TIMP-1) dramatically accelerated the accumulation of lipid during differentiation. We conclude that MMPs, especially Str1, determine the rate of adipocyte differentiation during involutive mammary gland remodeling.

APA, Harvard, Vancouver, ISO, and other styles

10

Feng, Z., A. Marti, B. Jehn, H. J. Altermatt, G. Chicaiza, and R. Jaggi. "Glucocorticoid and progesterone inhibit involution and programmed cell death in the mouse mammary gland." Journal of Cell Biology 131, no. 4 (November 15, 1995): 1095–103. http://dx.doi.org/10.1083/jcb.131.4.1095.

Full text

Abstract:

Milk production during lactation is a consequence of the suckling stimulus and the presence of glucocorticoids, prolactin, and insulin. After weaning the glucocorticoid hormone level drops, secretory mammary epithelial cells die by programmed cell death and the gland is prepared for a new pregnancy. We studied the role of steroid hormones and prolactin on the mammary gland structure, milk protein synthesis, and on programmed cell death. Slow-release plastic pellets containing individual hormones were implanted into a single mammary gland at lactation. At the same time the pups were removed and the consequences of the release of hormones were investigated histologically and biochemically. We found a local inhibition of involution in the vicinity of deoxycorticosterone- and progesterone-release pellets while prolactin-release pellets were ineffective. Dexamethasone, a very stable and potent glucocorticoid hormone analogue, inhibited involution and programmed cell death in all the mammary glands. It led to an accumulation of milk in the glands and was accompanied by an induction of protein kinase A, AP-1 DNA binding activity and elevated c-fos, junB, and junD mRNA levels. Several potential target genes of AP-1 such as stromelysin-1, c-jun, and SGP-2 that are induced during normal involution were strongly inhibited in dexamethasone-treated animals. Our results suggest that the cross-talk between steroid hormone receptors and AP-1 previously described in cells in culture leads to an impairment of AP-1 activity and to an inhibition of involution in the mammary gland implying that programmed cell death in the postlactational mammary gland depends on functional AP-1.

APA, Harvard, Vancouver, ISO, and other styles

More sources

Dissertations / Theses on the topic "Mammary gland involution"

1

Hughes, Katherine. "Inflammation and remodelling in mammary gland involution." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607688.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Kreuzaler, Peter Anton. "Cell death modalities in mammary gland involution." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609378.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Treisman, Loren Lee. "The role of the PARbZips in mammary gland involution." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614361.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Staniszewska, Anna Dominika. "Roles of Stat3 in mammary gland development, involution and breast cancer." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610277.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Anderson, Torri R. "Determination of expression of Fliz1 during involution of the mouse mammary gland." Thesis, Villanova University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=1565164.

Full text

Abstract:

Remodeling of the mouse mammary gland is a highly coordinated process that occurs after the removal of suckling pups from the mother. Involution, or shrinking of the mammary gland, after removal of the pups has been linked to apoptotic events within the mouse mammary tissue during forced weaning. Several transcription factors are hypothesized to be involved in this process. A transcription factor known as GATA-3, which was first identified in the thymus, is also important for maintenance of various tissue types within the mouse mammary gland; its loss leads to epithelial cell detachment and eventual death. Another transcription factor known as fetal zinc liver finger protein 1, or Fliz1, has been found to regulate GATA-3 in T-cells. This interaction had not been elucidated during involution in mouse mammary tissue. I hypothesized that Fliz1 is expressed at heightened levels during mouse mammary gland involution following forced weaning of pups, and that this expression correlates with a decrease in GATA-3 levels, with increased expression of the pro-apoptotic protein BAD. Using qRT-PCR, immunoblotting and immunohistochemistry I have shown that Fliz1 is indeed expressed in involuting mouse mammary gland tissue as well as several other tissue types. However, levels of Fliz1 remain fairly constant during involution. The findings also show that Cathepsin L, a known apoptotic marker for mammary gland involution, is substantially up-regulated during the process of mammary gland involution in the mouse. The study also revealed that GATA-3 levels as hypothesized decrease substantially during the process of mouse mammary gland involution, indicating that GATA-3 is required for maintenance of the mouse mammary gland.

APA, Harvard, Vancouver, ISO, and other styles

6

Marshall, Aaron. "The Biology of Mammary Gland Serotonin Synthesis and Transport." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1251229830.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Pai, Vaibhav Prakash. "Serotonin Regulation of Mammary Gland Involution and its Role in Breast Cancer Progression." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1237565289.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Patel, Amita. "Transcriptional regulation of cathepsin L during mouse mammary gland involution a test of STAT3 involvement /." Click here for download, 2006. http://wwwlib.umi.com/cr/villanova/fullcit?p1432835.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Stairiker, Patricia A. "The role of L in involution and the termination of lactation in the mouse mammary gland." Click here for download, 2007. http://proquest.umi.com/pqdweb?did=1075710531&sid=3&Fmt=2&clientId=3260&RQT=309&VName=PQD.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Stairiker, Patricia A. "The role of cathepsin L in involution and the termination of lactation in the mouse mammary gland." Click here for download, 2006. http://wwwlib.umi.com/cr/villanova/fullcit?p1432836.

Full text

APA, Harvard, Vancouver, ISO, and other styles

More sources

Books on the topic "Mammary gland involution"

1

Hojilla, Carlo Vincent. The role of TIMP3 in mammary gland morphogenesis, involution, inflammation, and tumourigenesis. 2006.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Mammary gland involution"

1

Marti, Andreas, Hans Graber, Hedvika Lazar, Philipp M. Ritter, Anna Baltzer, Rolf Jaggi, and Anu Srinivasan. "Caspases: Decoders of Apoptotic Signals During Mammary Involution." In Biology of the Mammary Gland, 195–201. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/0-306-46832-8_24.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Bielke, Wolfgang, Guo Ke, Robert Strange, and Robert Friis. "Apoptosis in Mammary Gland Involution: Isolation and Characterization of Apoptosis-Specific Genes." In Intercellular Signalling in the Mammary Gland, 45–55. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Monaghan, Paul, Nina Perusinghe, and W. Howard Evans. "Dramatic Changes in Gap Junction Expression in the Mammary Gland During Pregnancy, Lactation and Involution." In Intercellular Signalling in the Mammary Gland, 181–82. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_37.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Fetherston, Catherine M., Chee Seong Lee, and Peter E. Hartmann. "Mammary Gland Defense: The Role of Colostrum, Milk and Involution Secretion." In Advances in Nutritional Research Volume 10, 167–98. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0661-4_8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Tonner, Elizabeth, James Beattie, and David J. Flint. "Production of an Insulin-Like Growth Factor Binding Protein by the Involuting Rat Mammary Gland." In Intercellular Signalling in the Mammary Gland, 103–4. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_25.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Lloyd-Lewis, Bethan, Timothy J. Sargeant, Peter A. Kreuzaler, Henrike K. Resemann, Sara Pensa, and Christine J. Watson. "Analysis of the Involuting Mouse Mammary Gland: An In Vivo Model for Cell Death." In Methods in Molecular Biology, 165–86. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6475-8_7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Hurley, W. L. "MAMMARY GLAND | Growth, Development, Involution." In Encyclopedia of Dairy Sciences, 1689–97. Elsevier, 2002. http://dx.doi.org/10.1016/b0-12-227235-8/00278-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Hurley, W. L., and J. J. Loor. "Mammary Gland | Growth, Development and Involution." In Encyclopedia of Dairy Sciences, 338–45. Elsevier, 2011. http://dx.doi.org/10.1016/b978-0-12-374407-4.00291-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Loor, J. J., F. Batistel, M. Bionaz, W. L. Hurley, and E. Vargas-Bello-Pérez. "Mammary Gland: Gene Networks Controlling Development and Involution." In Reference Module in Food Science. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-818766-1.00001-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Loor, J. J., F. Batistel, M. Bionaz, and W. L. Hurley. "Mammary Gland: Gene Networks Controlling Development and Involution." In Reference Module in Food Science. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-08-100596-5.00883-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Mammary gland involution"

1

Garofalo, Jennifer-Marie, Dawn Bowers, Richard Browne, Brian MacQueen, Terry Mashtare, and Patricia A. Masso-Welch. "Abstract 5460: Effects of ethanol exposure during involution on mouse mammary gland." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5460.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Ramachandran, Sabarish, Selvakumar Elangovan, Puttur D. Prasad, Vadivel Ganapathy, and Muthusamy Thangaraju. "Abstract LB-236: Differential regulation of STAT3 in mammary gland involution as well as in mammary tumorigeneis." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-236.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Martinson, Holly, Sonail Jindal, Virginia Borges, and Pepper Schedin. "Abstract A31: Immune cell influx during postpartum mammary gland involution reveals immunosuppression and tumor promotion." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-a31.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Lyons, Traci R., Virginia F. Borges, Courtney B. Betts, Puja Kapoor, Holly A. Martinson, Sonali Jindal, and Pepper Schedin. "Abstract B099: Postpartum mammary gland involution promotes COX-2 dependent tumor cell invasion of lymphatics." In Abstracts: AACR Special Conference on Advances in Breast Cancer Research: Genetics, Biology, and Clinical Applications - October 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1557-3125.advbc-b099.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Ramachandran, Sabarish, Selvakumar Elangovan, Rajneesh Pathania, Puttur Devi Prasad, Vadivel Ganapathy, and Muthusamy Thangaraju. "Abstract 18: Slc5a8 inactivation is associated with mammary gland involution delay, early onset of mammary tumorigenesis and accelerated lung metastasis." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-18.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Guo, Qiuchen, and Pepper J. Schedin. "Abstract LB-009: Collagen regulation in postpartum mammary gland involution, a novel breast cancer prevention target." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-lb-009.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Cook, Katherine L., Anni Warri, Rong Hu, Lu Jin, Alan Zwart, David R. Soto Pantoja, Jie Liu, Toren Finkel, and Robert Clarke. "Abstract 1667: Autophagy and unfolded protein response (UPR) signaling regulates progression of apoptosis in mammary gland involution." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1667.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Vallone, Sabrina A., Martín García Solá, Robert D. Cardiff, Roberto P. Meiss, Lewis A. Chodosh, Carolina Shere-Levy, Edith C. C. Kordon, Nancy E. Hynes, and Albana Gattelli. "Abstract 3685: Sustained Ret expression during mammary gland post-lactation induces premature involution and enhances cancer potential." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3685.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Shinde, Neelam, Kirti Kaul, Allen Zhang, Saba Mehra, Resham Mawalkar, Hee Kyung Kim, Ramesh Ganju, Sarmila Majumder, and Bhuvaneswari Ramaswamy. "Abstract PS17-28: Abrupt involution of lactating mammary gland induces metabolic reprogramming conducive to pro-tumorigenic changes." In Abstracts: 2020 San Antonio Breast Cancer Virtual Symposium; December 8-11, 2020; San Antonio, Texas. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.sabcs20-ps17-28.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Lyons, Traci R., Jenean O'Brien, Matthew Conklin, Patricia Keely, Virginia Borges, and Pepper Schedin. "Abstract B61: Postpartum mammary gland involution drives DCIS progression through collagen and COX-2, identifying a target for intervention." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Oct 22-25, 2011; Boston, MA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1940-6207.prev-11-b61.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Mammary gland involution"

1

Cowin, Pamela. Targeting the Prometastatic Microenvironment of the Involuting Mammary Gland. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada612509.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!