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  1. AU="Chauhan, Gaurav B"
  2. AU=Hanjaya-Putra Donny
  3. AU=Powell James
  4. AU="Russell, Todd"
  5. AU=Forth Scott
  6. AU="Kreutzer, Susanne" AU="Kreutzer, Susanne"
  7. AU="St John, Maie"
  8. AU=Gerhardy A
  9. AU="Qi, Huixin"
  10. AU="Dobosiewicz, May"
  11. AU="Srivastava, Rakesh"
  12. AU="Grevtsov K.I."

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  1. Artikel ; Online: Correction: Maternal Embryonic Leucine Zipper Kinase Is Associated with Metastasis in Triple-negative Breast Cancer.

    Xie, Xuemei / Chauhan, Gaurav B / Edupuganti, Ramakrishna / Kogawa, Takahiro / Park, Jihyun / Tacam, Moises / Tan, Alex W / Mughees, Mohd / Vidhu, Fnu / Liu, Diane D / Taliaferro, Juliana M / Pitner, Mary Kathryn / Browning, Luke S / Lee, Ju-Hyeon / Bertucci, François / Shen, Yu / Wang, Jian / Ueno, Naoto T / Krishnamurthy, Savitri /
    Hortobagyi, Gabriel N / Tripathy, Debu / Van Laere, Steven J / Bartholomeusz, Geoffrey / Dalby, Kevin N / Bartholomeusz, Chandra

    Cancer research communications

    2024  Band 4, Heft 1, Seite(n) 236

    Sprache Englisch
    Erscheinungsdatum 2024-01-28
    Erscheinungsland United States
    Dokumenttyp Published Erratum
    ISSN 2767-9764
    ISSN (online) 2767-9764
    DOI 10.1158/2767-9764.CRC-24-0046
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Maternal Embryonic Leucine Zipper Kinase is Associated with Metastasis in Triple-negative Breast Cancer.

    Xie, Xuemei / Chauhan, Gaurav B / Edupuganti, Ramakrishna / Kogawa, Takahiro / Park, Jihyun / Tacam, Moises / Tan, Alex W / Mughees, Mohd / Vidhu, Fnu / Liu, Diane D / Taliaferro, Juliana M / Pitner, Mary Kathryn / Browning, Luke S / Lee, Ju-Hyeon / Shen, Yu / Wang, Jian / Ueno, Naoto T / Krishnamurthy, Savitri / Hortobagyi, Gabriel N /
    Tripathy, Debu / Van Laere, Steven J / Bartholomeusz, Geoffrey / Dalby, Kevin N / Bartholomeusz, Chandra

    Cancer research communications

    2023  Band 3, Heft 6, Seite(n) 1078–1092

    Abstract: Triple-negative breast cancer (TNBC) has high relapse and metastasis rates and a high proportion of cancer stem-like cells (CSC), which possess self-renewal and tumor initiation capacity. MELK (maternal embryonic leucine zipper kinase), a protein kinase ... ...

    Abstract Triple-negative breast cancer (TNBC) has high relapse and metastasis rates and a high proportion of cancer stem-like cells (CSC), which possess self-renewal and tumor initiation capacity. MELK (maternal embryonic leucine zipper kinase), a protein kinase of the Snf1/AMPK kinase family, is known to promote CSC maintenance and malignant transformation. However, the role of MELK in TNBC metastasis is unknown; we sought to address this in the current study. We found that
    Significance: These findings indicate that MELK is a driver of aggressiveness and metastasis in TNBC.
    Mesh-Begriff(e) Humans ; Animals ; Mice ; Triple Negative Breast Neoplasms/genetics ; Mice, Nude ; Leucine Zippers ; Cell Proliferation/physiology ; Neoplasm Recurrence, Local ; Protein Serine-Threonine Kinases/genetics
    Chemische Substanzen MELK protein, human (EC 2.7.1.-) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2023-06-20
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ISSN 2767-9764
    ISSN (online) 2767-9764
    DOI 10.1158/2767-9764.CRC-22-0330
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: CD44 expression contributes to trastuzumab resistance in HER2-positive breast cancer cells.

    Boulbes, Delphine R / Chauhan, Gaurav B / Jin, Quanri / Bartholomeusz, Chandra / Esteva, Francisco J

    Breast cancer research and treatment

    2015  Band 151, Heft 3, Seite(n) 501–513

    Abstract: Resistance to HER2-targeted therapies remains a major obstacle in the treatment of HER2-overexpressing breast cancer. CD44, a putative breast cancer stem cell (CSC) marker, is overexpressed in trastuzumab-resistant breast cancer cells. While CSC-related ... ...

    Abstract Resistance to HER2-targeted therapies remains a major obstacle in the treatment of HER2-overexpressing breast cancer. CD44, a putative breast cancer stem cell (CSC) marker, is overexpressed in trastuzumab-resistant breast cancer cells. While CSC-related genes may play a role in the development of trastuzumab resistance, conflicting results have been published about CSC response to trastuzumab. We hypothesized that CD44 contributes to trastuzumab resistance independently of its role as a CSC marker. We used trastuzumab-sensitive breast cancer cell lines and their trastuzumab-resistant isogenic counterparts to evaluate the role of CD44 in response to trastuzumab. miRNA and mRNA expression were analyzed using microarray chips. A gene set enrichment analysis was created and matched with response to trastuzumab in cells and patient samples. The proportions of CSC in trastuzumab-resistant cells were similar to or lower than in the trastuzumab-sensitive cells. However, CD44 expression levels were significantly higher in both trastuzumab-resistant cell lines and its knockdown led to an increased response to trastuzumab. The invasiveness and anchorage-independent growth of trastuzumab-resistant cells were higher and blocked by downregulation of CD44. Results also showed that CD44-related resistance to trastuzumab is regulated by miRNAs. We identified a CD44-related gene expression profile that correlated with response to trastuzumab in cell lines and breast cancer patients. CD44 mediates trastuzumab resistance in HER2-positive breast cancer cells independently of its role as a CSC marker and that this role of CD44 is partly regulated by miRNA.
    Mesh-Begriff(e) Antineoplastic Agents/pharmacology ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Cell Line, Tumor ; Drug Resistance, Neoplasm/genetics ; Female ; Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks ; Humans ; Hyaluronan Receptors/genetics ; MicroRNAs/genetics ; RNA, Small Interfering/genetics ; Receptor, ErbB-2/metabolism ; Trastuzumab/pharmacology
    Chemische Substanzen Antineoplastic Agents ; Hyaluronan Receptors ; MicroRNAs ; RNA, Small Interfering ; Receptor, ErbB-2 (EC 2.7.10.1) ; Trastuzumab (P188ANX8CK)
    Sprache Englisch
    Erscheinungsdatum 2015-05-14
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 604563-7
    ISSN 1573-7217 ; 0167-6806
    ISSN (online) 1573-7217
    ISSN 0167-6806
    DOI 10.1007/s10549-015-3414-3
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

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  4. Artikel ; Online: HER family kinase domain mutations promote tumor progression and can predict response to treatment in human breast cancer.

    Boulbes, Delphine R / Arold, Stefan T / Chauhan, Gaurav B / Blachno, Korina V / Deng, Nanfu / Chang, Wei-Chao / Jin, Quanri / Huang, Tzu-Hsuan / Hsu, Jung-Mao / Brady, Samuel W / Bartholomeusz, Chandra / Ladbury, John E / Stone, Steve / Yu, Dihua / Hung, Mien-Chie / Esteva, Francisco J

    Molecular oncology

    2014  Band 9, Heft 3, Seite(n) 586–600

    Abstract: Resistance to HER2-targeted therapies remains a major obstacle in the treatment of HER2-overexpressing breast cancer. Understanding the molecular pathways that contribute to the development of drug resistance is needed to improve the clinical utility of ... ...

    Abstract Resistance to HER2-targeted therapies remains a major obstacle in the treatment of HER2-overexpressing breast cancer. Understanding the molecular pathways that contribute to the development of drug resistance is needed to improve the clinical utility of novel agents, and to predict the success of targeted personalized therapy based on tumor-specific mutations. Little is known about the clinical significance of HER family mutations in breast cancer. Because mutations within HER1/EGFR are predictive of response to tyrosine kinase inhibitors (TKI) in lung cancer, we investigated whether mutations in HER family kinase domains are predictive of response to targeted therapy in HER2-overexpressing breast cancer. We sequenced the HER family kinase domains from 76 HER2-overexpressing invasive carcinomas and identified 12 missense variants. Patients whose tumors carried any of these mutations did not respond to HER2 directed therapy in the metastatic setting. We developed mutant cell lines and used structural analyses to determine whether changes in protein conformation could explain the lack of response to therapy. We also functionally studied all HER2 mutants and showed that they conferred an aggressive phenotype and altered effects of the TKI lapatinib. Our data demonstrate that mutations in the finely tuned HER kinase domains play a critical function in breast cancer progression and may serve as prognostic and predictive markers.
    Mesh-Begriff(e) Animals ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Computational Biology ; Disease Progression ; ErbB Receptors/chemistry ; ErbB Receptors/genetics ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Humans ; Lapatinib ; Mice, Nude ; Mutant Proteins/chemistry ; Mutation/genetics ; Phenotype ; Phosphorylation/drug effects ; Prognosis ; Protein Structure, Tertiary ; Quinazolines/pharmacology ; Treatment Outcome
    Chemische Substanzen Mutant Proteins ; Quinazolines ; Lapatinib (0VUA21238F) ; ErbB Receptors (EC 2.7.10.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
    Sprache Englisch
    Erscheinungsdatum 2014-11-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2415106-3
    ISSN 1878-0261 ; 1574-7891
    ISSN (online) 1878-0261
    ISSN 1574-7891
    DOI 10.1016/j.molonc.2014.10.011
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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