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Article ; Online: Endocrine Therapy for Leptomeningeal Metastases from ER-Positive Breast Cancer: Case Report and a Review of the Literature.

Zoghi, Behyar / Elledge, Richard

2016 Volume 22, Issue 2, Page(s) 218–223

Abstract: Leptomeningeal disease is an uncommon complication of estrogen receptor positive breast cancer. While there is little consensus on the standard of care, recommendations from current clinical practice guidelines are to treat with intrathecal chemotherapy, ...

Abstract	Leptomeningeal disease is an uncommon complication of estrogen receptor positive breast cancer. While there is little consensus on the standard of care, recommendations from current clinical practice guidelines are to treat with intrathecal chemotherapy, necessitating invasive procedures and potentially resulting in a substantial incidence of serious complications and side effects. Here, we review all published evidence of the effectiveness of systemic hormonal therapy alone in treating this condition, with the advantage of requiring no invasive procedures and having virtually no serious complications or side effects. Evidence indicates that most hormonal therapies can penetrate the central nervous system and can be an effective treatment of endocrine sensitive breast cancer that is widely metastatic to the leptomeninges.
MeSH term(s)	Antineoplastic Agents, Hormonal/therapeutic use ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Female ; Humans ; Meningeal Neoplasms/drug therapy ; Meningeal Neoplasms/secondary ; Middle Aged ; Receptors, Estrogen/metabolism
Chemical Substances	Antineoplastic Agents, Hormonal ; Receptors, Estrogen
Language	English
Publishing date	2016-03
Publishing country	United States
Document type	Case Reports ; Journal Article ; Review
ZDB-ID	1289960-4
ISSN	1524-4741 ; 1075-122X
ISSN (online)	1524-4741
ISSN	1075-122X
DOI	10.1111/tbj.12554
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Article ; Online: Tales from a targeted therapy.

Elledge, Richard M

Journal of clinical oncology : official journal of the American Society of Clinical Oncology

2006 Volume 24, Issue 9, Page(s) 1323–1325

MeSH term(s)	Antineoplastic Agents, Hormonal/pharmacology ; Antineoplastic Agents, Hormonal/therapeutic use ; Breast Neoplasms/drug therapy ; Breast Neoplasms/physiopathology ; Clinical Trials as Topic ; Female ; Humans ; Medical Oncology/trends ; Receptors, Estrogen/drug effects ; Receptors, Estrogen/physiology ; Research Design ; Tamoxifen/pharmacology ; Tamoxifen/therapeutic use
Chemical Substances	Antineoplastic Agents, Hormonal ; Receptors, Estrogen ; Tamoxifen (094ZI81Y45)
Language	English
Publishing date	2006-03-20
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	604914-x
ISSN	1527-7755 ; 0732-183X
ISSN (online)	1527-7755
ISSN	0732-183X
DOI	10.1200/JCO.2005.04.6672
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Zs.A 1847: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: BRCA1 deficiency in mature CD8

Wu, Bogang / Qi, Leilei / Chiang, Huai-Chin / Pan, Haihui / Zhang, Xiaowen / Greenbaum, Alexandra / Stark, Elizabeth / Wang, Li-Ju / Chen, Yidong / Haddad, Bassem R / Clagett, Dionyssia / Isaacs, Claudine / Elledge, Richard / Horvath, Anelia / Hu, Yanfen / Li, Rong

Journal for immunotherapy of cancer

2023 Volume 11, Issue 2

Abstract: ... Women ... ...

Abstract	Women with
MeSH term(s)	Female ; Mice ; Animals ; CD8-Positive T-Lymphocytes ; Antineoplastic Agents ; Neoplasms ; Immunity ; Mice, Knockout ; Carcinogenesis
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2023-01-31
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2719863-7
ISSN	2051-1426 ; 2051-1426
ISSN (online)	2051-1426
ISSN	2051-1426
DOI	10.1136/jitc-2022-005852
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Article: Effects of Radiation Therapy on Breast Epithelial Cells in BRCA1/2 Mutation Carriers.

Chiang, Huai-Chin / Elledge, Richard / Larson, Paula / Jatoi, Ismail / Li, Rong / Hu, Yanfen

Breast cancer : basic and clinical research

2015 Volume 9, Page(s) 25–29

Abstract: Women carrying BRCA1 and BRCA2 mutations have significantly elevated risk of developing breast and ovarian cancers. BRCA1-associated breast cancer likely originates from progenitors of the luminal epithelial lineage. Recent studies indicate that ... ...

Abstract	Women carrying BRCA1 and BRCA2 mutations have significantly elevated risk of developing breast and ovarian cancers. BRCA1-associated breast cancer likely originates from progenitors of the luminal epithelial lineage. Recent studies indicate that radiation therapy (RT) for BRCA1 cancer patients is associated with lower incidence of developing subsequent ipsilateral breast cancer. In the current study, we analyzed tumor-free breast tissue procured via prophylactic bilateral mastectomy from three BRCA1 and one BRCA2 mutation carriers, who had been previously treated with RT for unilateral breast cancers. Freshly isolated breast cells from the irradiated and nonirradiated breast tissue of the same individuals were subjected to flow cytometry, using established cell-surface markers. Two out of the three BRCA1 carriers and one BRCA2 carrier exhibited significantly diminished luminal cell population in the irradiated breast versus the nonirradiated side. There was also RT-associated reduction in the colony-forming ability of the breast epithelial cells. Our finding suggests that prior RT could result in the depletion of the luminal epithelial compartment and thus reduced incidence of BRCA1/2-associated breast cancer.
Language	English
Publishing date	2015-06-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	2423804-1
ISSN	1178-2234
ISSN	1178-2234
DOI	10.4137/BCBCR.S26774
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Article ; Online: ERα-related chromothripsis enhances concordant gene transcription on chromosome 17q11.1-q24.1 in luminal breast cancer.

Lin, Chun-Lin / Tan, Xi / Chen, Meizhen / Kusi, Meena / Hung, Chia-Nung / Chou, Chih-Wei / Hsu, Ya-Ting / Wang, Chiou-Miin / Kirma, Nameer / Chen, Chun-Liang / Lin, Ching-Hung / Lathrop, Kate I / Elledge, Richard / Kaklamani, Virginia G / Mitsuya, Kohzoh / Huang, Tim H-M

BMC medical genomics

2020 Volume 13, Issue 1, Page(s) 69

Abstract: Background: Chromothripsis is an event of genomic instability leading to complex chromosomal alterations in cancer. Frequent long-range chromatin interactions between transcription factors (TFs) and targets may promote extensive translocations and copy- ... ...

Abstract	Background: Chromothripsis is an event of genomic instability leading to complex chromosomal alterations in cancer. Frequent long-range chromatin interactions between transcription factors (TFs) and targets may promote extensive translocations and copy-number alterations in proximal contact regions through inappropriate DNA stitching. Although studies have proposed models to explain the initiation of chromothripsis, few discussed how TFs influence this process for tumor progression. Methods: This study focused on genomic alterations in amplification associated regions within chromosome 17. Inter-/intra-chromosomal rearrangements were analyzed using whole genome sequencing data of breast tumors in the Cancer Genome Atlas (TCGA) cohort. Common ERα binding sites were defined based on MCF-7, T47D, and MDA-MB-134 breast cancer cell lines using univariate K-means clustering methods. Nanopore sequencing technology was applied to validate frequent rearrangements detected between ATC loci on 17q23 and an ERα hub on 20q13. The efficacy of pharmacological inhibition of a potentially druggable target gene on 17q23 was evaluated using breast cancer cell lines and patient-derived circulating breast tumor cells. Results: There are five adjoining regions from 17q11.1 to 17q24.1 being hotspots of chromothripsis. Inter-/intra-chromosomal rearrangements of these regions occurred more frequently in ERα-positive tumors than in ERα-negative tumors. In addition, the locations of the rearrangements were often mapped within or close to dense ERα binding sites localized on these five 17q regions or other chromosomes. This chromothriptic event was linked to concordant upregulation of 96 loci that predominantly regulate cell-cycle machineries in advanced luminal tumors. Genome-editing analysis confirmed that an ERα hub localized on 20q13 coordinately regulates a subset of these loci localized on 17q23 through long-range chromosome interactions. One of these loci, Tousled Like Kinase 2 (TLK2) known to participate in DNA damage checkpoint control, is an actionable target using phenothiazine antipsychotics (PTZs). The antiproliferative effect of PTZs was prominent in high TLK2-expressing cells, compared to low expressing cells. Conclusion: This study demonstrates a new approach for identifying tumorigenic drivers from genomic regions highly susceptible to ERα-related chromothripsis. We found a group of luminal breast tumors displaying 17q-related chromothripsis for which antipsychotics can be repurposed as treatment adjuncts.
MeSH term(s)	Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Cycle ; Cell Proliferation ; Chromosomes, Human, Pair 17/genetics ; Chromothripsis ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Prognosis ; Survival Rate ; Transcription, Genetic ; Tumor Cells, Cultured ; Whole Exome Sequencing ; Whole Genome Sequencing
Chemical Substances	Biomarkers, Tumor ; ESR1 protein, human ; Estrogen Receptor alpha
Language	English
Publishing date	2020-05-14
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1755-8794
ISSN (online)	1755-8794
DOI	10.1186/s12920-020-0729-7
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Article ; Online: Intrinsic apoptotic pathway activation increases response to anti-estrogens in luminal breast cancers.

Williams, Michelle M / Lee, Linus / Werfel, Thomas / Joly, Meghan M Morrison / Hicks, Donna J / Rahman, Bushra / Elion, David / McKernan, Courtney / Sanchez, Violeta / Estrada, Monica V / Massarweh, Suleiman / Elledge, Richard / Duvall, Craig / Cook, Rebecca S

Cell death & disease

2018 Volume 9, Issue 2, Page(s) 21

Abstract: Estrogen receptor-α positive (ERα+) breast cancer accounts for approximately 70-80% of the nearly 25,0000 new cases of breast cancer diagnosed in the US each year. Endocrine-targeted therapies (those that block ERα activity) serve as the first line of ... ...

Abstract	Estrogen receptor-α positive (ERα+) breast cancer accounts for approximately 70-80% of the nearly 25,0000 new cases of breast cancer diagnosed in the US each year. Endocrine-targeted therapies (those that block ERα activity) serve as the first line of treatment in most cases. Despite the proven benefit of endocrine therapies, however, ERα+ breast tumors can develop resistance to endocrine therapy, causing disease progression or relapse, particularly in the metastatic setting. Anti-apoptotic Bcl-2 family proteins enhance breast tumor cell survival, often promoting resistance to targeted therapies, including endocrine therapies. Herein, we investigated whether blockade of anti-apoptotic Bcl-2 family proteins could sensitize luminal breast cancers to anti-estrogen treatment. We used long-term estrogen deprivation (LTED) of human ERα+ breast cancer cell lines, an established model of sustained treatment with and acquired resistance to aromatase inhibitors (AIs), in combination with Bcl-2/Bcl-xL inhibition (ABT-263), finding that ABT-263 induced only limited tumor cell killing in LTED-selected cells in culture and in vivo. Interestingly, expression and activity of the Bcl-2-related factor Mcl-1 was increased in LTED cells. Genetic Mcl-1 ablation induced apoptosis in LTED-selected cells, and potently increased their sensitivity to ABT-263. Increased expression and activity of Mcl-1 was similarly seen in clinical breast tumor specimens treated with AI + the selective estrogen receptor downregulator fulvestrant. Delivery of Mcl-1 siRNA loaded into polymeric nanoparticles (MCL1 si-NPs) decreased Mcl-1 expression in LTED-selected and fulvestrant-treated cells, increasing tumor cell death and blocking tumor cell growth. These findings suggest that Mcl-1 upregulation in response to anti-estrogen treatment enhances tumor cell survival, decreasing response to therapeutic treatments. Therefore, strategies blocking Mcl-1 expression or activity used in combination with endocrine therapies would enhance tumor cell death.
MeSH term(s)	Aniline Compounds/pharmacology ; Animals ; Apoptosis/drug effects ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Down-Regulation/drug effects ; Estrogen Antagonists/pharmacology ; Female ; Fulvestrant/pharmacology ; Gene Targeting ; Humans ; Mice ; Myeloid Cell Leukemia Sequence 1 Protein/metabolism ; Receptors, Estrogen/metabolism ; Signal Transduction/drug effects ; Sulfonamides/pharmacology ; Up-Regulation/drug effects ; bcl-X Protein/metabolism
Chemical Substances	Aniline Compounds ; Estrogen Antagonists ; MCL1 protein, human ; Myeloid Cell Leukemia Sequence 1 Protein ; Receptors, Estrogen ; Sulfonamides ; bcl-X Protein ; Fulvestrant (22X328QOC4) ; navitoclax (XKJ5VVK2WD)
Language	English
Publishing date	2018-01-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-017-0072-x
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Article ; Online: Erratum to: A phase II study of combined fulvestrant and everolimus in patients with metastatic estrogen receptor (ER)-positive breast cancer after aromatase inhibitor (AI) failure.

Massarweh, Suleiman / Romond, Edward / Black, Esther P / Van Meter, Emily / Shelton, Brent / Kadamyan-Melkumian, Vera / Stevens, Mark / Elledge, Richard

Breast cancer research and treatment

2015 Volume 149, Issue 2, Page(s) 565

Language	English
Publishing date	2015-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	604563-7
ISSN	1573-7217 ; 0167-6806
ISSN (online)	1573-7217
ISSN	0167-6806
DOI	10.1007/s10549-015-3263-0
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Zs.A 1655: Show issues

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Article ; Online: A phase II trial of capecitabine concomitantly with whole-brain radiotherapy followed by capecitabine and sunitinib for brain metastases from breast cancer.

Niravath, Polly / Tham, Yee Lu / Wang, Tao / Rodriguez, Angel / Foreman, Claudette / Hilsenbeck, Susan G / Elledge, Richard / Rimawi, Mothaffar

The oncologist

2015 Volume 20, Issue 1, Page(s) 13

Abstract: Background: Brain metastasis from breast cancer presents a significant threat to women's health and quality of life. Capecitabine and sunitinib have shown some activity in this setting; therefore, we conducted a single-arm phase II trial with these ... ...

Abstract	Background: Brain metastasis from breast cancer presents a significant threat to women's health and quality of life. Capecitabine and sunitinib have shown some activity in this setting; therefore, we conducted a single-arm phase II trial with these agents. Methods: Patients with breast cancer and central nervous system (CNS) metastases received whole-brain radiotherapy concurrently with capecitabine (1,000 mg/m(2) per day for 14 consecutive days), followed by concomitant capecitabine (2,000 mg/m(2) per day for 2 weeks followed by a 1-week break) and sunitinib (37.5 mg daily, continuously). The primary endpoint was progression-free survival (PFS). Results: Of 25 planned patients that would be required to detect a 4-month improvement (from 5 to 9 months) in median PFS with 80% power, 12 were enrolled, and the study was then closed for slow accrual. Median PFS was 4.7 months, and median overall survival was 10 months. In the CNS, 25% had progressive disease, and 83% experienced extra-CNS progression. The most common side effects were fatigue and nausea. Conclusion: In 12 evaluable patients studied, concurrent capecitabine and whole-brain radiation followed by capecitabine and sunitinib did not extend PFS over historical rates and was associated with significant toxicity. Our study was small and closed due to slow accrual.
MeSH term(s)	Brain Neoplasms/drug therapy ; Brain Neoplasms/pathology ; Brain Neoplasms/radiotherapy ; Brain Neoplasms/secondary ; Breast Neoplasms/drug therapy ; Breast Neoplasms/pathology ; Breast Neoplasms/radiotherapy ; Capecitabine ; Combined Modality Therapy ; Deoxycytidine/administration & dosage ; Deoxycytidine/analogs & derivatives ; Disease-Free Survival ; Female ; Fluorouracil/administration & dosage ; Fluorouracil/analogs & derivatives ; Humans ; Indoles/administration & dosage ; Pyrroles/administration & dosage
Chemical Substances	Indoles ; Pyrroles ; Deoxycytidine (0W860991D6) ; Capecitabine (6804DJ8Z9U) ; Fluorouracil (U3P01618RT) ; sunitinib (V99T50803M)
Language	English
Publishing date	2015-01
Publishing country	United States
Document type	Clinical Trial, Phase II ; Journal Article
ZDB-ID	1409038-7
ISSN	1549-490X ; 1083-7159
ISSN (online)	1549-490X
ISSN	1083-7159
DOI	10.1634/theoncologist.2014-0278
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Zs.A 4845: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Pathologic changes in breast cancer after anti-estrogen therapy.

Samarnthai, Norasate / Elledge, Richard / Prihoda, Thomas J / Huang, Jian / Massarweh, Suleiman / Yeh, I-Tien

The breast journal

2012 Volume 18, Issue 4, Page(s) 362–366

Abstract: Breast cancer patients do not commonly receive anti-estrogens prior to surgical excision. We reviewed a cohort of patients who received preoperative anti-estrogen therapy after baseline biopsy and then had a repeat biopsy after several weeks on treatment. ...

Abstract	Breast cancer patients do not commonly receive anti-estrogens prior to surgical excision. We reviewed a cohort of patients who received preoperative anti-estrogen therapy after baseline biopsy and then had a repeat biopsy after several weeks on treatment. Patients with estrogen receptor positive tumors received anastrozole and fulvestrant in combination with gefitinib. Core needle biopsies were performed at day 1 and 21, and tumors were completely excised if operable at day 112. All patients were postmenopausal. Following treatment, tumors had degenerative changes including smudged nuclei, decreased nuclear size, intranuclear vacuoles, vacuolated cytoplasm, and increased cellular discohesion. In addition, increased tubule formation and intracytoplasmic lumina were seen in 6/9 cases (66.7%) and decreased mitotic rate was demonstrated in 7/9 cases (77.8%). These findings indicate increased differentiation of the tumor cells in response to anti-estrogen therapy and that may correlate with clinical response.
MeSH term(s)	Aged ; Aged, 80 and over ; Biopsy, Large-Core Needle ; Breast Neoplasms/drug therapy ; Breast Neoplasms/pathology ; Breast Neoplasms/surgery ; Cell Differentiation/drug effects ; Cytoplasm/drug effects ; Estradiol/analogs & derivatives ; Estradiol/therapeutic use ; Estrogen Antagonists/therapeutic use ; Female ; Humans ; Middle Aged ; Nitriles/therapeutic use ; Postmenopause ; Receptors, Estrogen/metabolism ; Treatment Outcome ; Triazoles/therapeutic use
Chemical Substances	Estrogen Antagonists ; Nitriles ; Receptors, Estrogen ; Triazoles ; fulvestrant (22X328QOC4) ; anastrozole (2Z07MYW1AZ) ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2012-07
Publishing country	United States
Document type	Journal Article ; Randomized Controlled Trial ; Research Support, N.I.H., Extramural
ZDB-ID	1289960-4
ISSN	1524-4741 ; 1075-122X
ISSN (online)	1524-4741
ISSN	1075-122X
DOI	10.1111/j.1524-4741.2012.01251.x
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Article ; Online: Association of radiotherapy with preferential depletion of luminal epithelial cells in a BRCA1 mutation carrier

Chiang Huai-Chin / Nair Sreejith J / Yeh I-Tien / Santillan Alfredo A / Hu Yanfen / Elledge Richard / Li Rong

Experimental Hematology & Oncology, Vol 1, Iss 1, p

2012 Volume 31

Abstract: Abstract Radiation therapy (RT) after breast conservation therapy has recently been linked with significant reduction in risk of ipsilateral breast cancer among BRCA1 mutation carriers. However, the exact mechanism by which RT reduces incidence of BRCA1 - ...

Abstract	Abstract Radiation therapy (RT) after breast conservation therapy has recently been linked with significant reduction in risk of ipsilateral breast cancer among BRCA1 mutation carriers. However, the exact mechanism by which RT reduces incidence of BRCA1 -associated cancer remains unclear. Here we studied fresh breast tissue from a BRCA1 mutation carrier who was initially treated with a lumpectomy and RT for a unilateral cancer and two years later chose a prophylactic bilateral mastectomy while remaining cancer-free. Flow cytometry analysis demonstrated a strikingly lower luminal cell population in the irradiated breast as compared to the non-irradiated breast, which was confirmed by immunohistochemistry. Furthermore, the irradiated breast tissue exhibited very low progenitor cell activity in vitro . Given the emerging evidence that BRCA1 tumors originate from luminal progenitor cells, our observations suggest that preferential and long-lasting elimination of luminal ductal epithelium may partly underlie the mechanism of RT-associated reduction in recurrence of BRCA1 -associated cancer.
Keywords	Radiation ; Luminal progenitor cells ; Cell of origin ; BRCA1 ; Diseases of the blood and blood-forming organs ; RC633-647.5 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Internal medicine ; DOAJ:Medicine (General) ; DOAJ:Health Sciences ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; DOAJ:Oncology
Subject code	610 ; 616
Language	English
Publishing date	2012-10-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
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