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  1. Article: Terminal differentiation and anti-tumorigenic effects of prolactin in breast cancer.

    Ali, Suhad / Hamam, Dana / Liu, Xueqing / Lebrun, Jean-Jacques

    Frontiers in endocrinology

    2022  Volume 13, Page(s) 993570

    Abstract: Breast cancer is a major disease affecting women worldwide. A woman has 1 in 8 lifetime risk of developing breast cancer, and morbidity and mortality due to this disease are expected to continue to rise globally. Breast cancer remains a challenging ... ...

    Abstract Breast cancer is a major disease affecting women worldwide. A woman has 1 in 8 lifetime risk of developing breast cancer, and morbidity and mortality due to this disease are expected to continue to rise globally. Breast cancer remains a challenging disease due to its heterogeneity, propensity for recurrence and metastasis to distant vital organs including bones, lungs, liver and brain ultimately leading to patient death. Despite the development of various therapeutic strategies to treat breast cancer, still there are no effective treatments once metastasis has occurred. Loss of differentiation and increased cellular plasticity and stemness are being recognized molecularly and clinically as major derivers of heterogeneity, tumor evolution, relapse, metastasis, and therapeutic failure. In solid tumors, breast cancer is one of the leading cancer types in which tumor differentiation state has long been known to influence cancer behavior. Reprograming and/or restoring differentiation of cancer cells has been proposed to provide a viable approach to reverse the cancer through differentiation and terminal maturation. The hormone prolactin (PRL) is known to play a critical role in mammary gland lobuloalveolar development/remodeling and the terminal differentiation of the mammary epithelial cells promoting milk proteins gene expression and lactation. Here, we will highlight recent discoveries supporting an anti-tumorigenic role for PRL in breast cancer as a "pro/forward-differentiation" pathway restricting plasticity, stemness and tumorigenesis.
    MeSH term(s) Breast Neoplasms/metabolism ; Carcinogenesis ; Female ; Humans ; Milk Proteins ; Neoplasm Recurrence, Local ; Prolactin/metabolism ; Prolactin/pharmacology
    Chemical Substances Milk Proteins ; Prolactin (9002-62-4)
    Language English
    Publishing date 2022-09-08
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2022.993570
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Prolactin receptor-driven combined luminal and epithelial differentiation in breast cancer restricts plasticity, stemness, tumorigenesis and metastasis.

    Shams, Anwar / Binothman, Najat / Boudreault, Julien / Wang, Ni / Shams, Fuad / Hamam, Dana / Tian, Jun / Moamer, Alaa / Dai, Meiou / Lebrun, Jean-Jacques / Ali, Suhad

    Oncogenesis

    2021  Volume 10, Issue 1, Page(s) 10

    Abstract: Dedifferentiation increased cellular plasticity and stemness are established derivers of tumor heterogeneity, metastasis and therapeutic failure resulting in incurable cancers. Therefore, it is essential to decipher pro/forward-differentiation mechanisms ...

    Abstract Dedifferentiation increased cellular plasticity and stemness are established derivers of tumor heterogeneity, metastasis and therapeutic failure resulting in incurable cancers. Therefore, it is essential to decipher pro/forward-differentiation mechanisms in cancer that may serve as therapeutic targets. We found that interfering with expression of the receptor for the lactogenic hormone prolactin (PRLR) in breast cancer cells representative of the luminal and epithelial breast cancer subtypes (hormone receptor positive (HR+) and HER2-enriched (HER2-E) resulted in loss of their differentiation state, enriched for stem-like cell subpopulations, and increased their tumorigenic capacity in a subtype-specific manner. Loss of PRLR expression in HR+ breast cancer cells caused their dedifferentiation generating a mesenchymal-basal-like phenotype enriched in CD44+ breast cancer stem-like cells (BCSCs) showing high tumorigenic and metastatic capacities and resistance to anti-hormonal therapy. Whereas loss of PRLR expression in HER2-E breast cancer cells resulted in loss of their luminal differentiation yet enriched for epithelial ALDH+ BCSC population showing elevated HER2-driven tumorigenic, multi-organ metastatic spread, and resistance to anti-HER2 therapy. Collectively, this study defines PRLR as a driver of precise luminal and epithelial differentiation limiting cellular plasticity, stemness, and tumorigenesis and emphasizing the function of pro/forward-differentiation pathways as a foundation for the discovery of anti-cancer therapeutic targets.
    Language English
    Publishing date 2021-01-14
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2674437-5
    ISSN 2157-9024
    ISSN 2157-9024
    DOI 10.1038/s41389-020-00297-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Circulating microRNAs in breast cancer: novel diagnostic and prognostic biomarkers.

    Hamam, Rimi / Hamam, Dana / Alsaleh, Khalid A / Kassem, Moustapha / Zaher, Waleed / Alfayez, Musaad / Aldahmash, Abdullah / Alajez, Nehad M

    Cell death & disease

    2017  Volume 8, Issue 9, Page(s) e3045

    Abstract: Effective management of breast cancer depends on early diagnosis and proper monitoring of patients' response to therapy. However, these goals are difficult to achieve because of the lack of sensitive and specific biomarkers for early detection and for ... ...

    Abstract Effective management of breast cancer depends on early diagnosis and proper monitoring of patients' response to therapy. However, these goals are difficult to achieve because of the lack of sensitive and specific biomarkers for early detection and for disease monitoring. Accumulating evidence in the past several years has highlighted the potential use of peripheral blood circulating nucleic acids such as DNA, mRNA and micro (mi)RNA in breast cancer diagnosis, prognosis and for monitoring response to anticancer therapy. Among these, circulating miRNA is increasingly recognized as a promising biomarker, given the ease with which miRNAs can be isolated and their structural stability under different conditions of sample processing and isolation. In this review, we provide current state-of-the-art of miRNA biogenesis, function and discuss the advantages, limitations, as well as pitfalls of using circulating miRNAs as diagnostic, prognostic or predictive biomarkers in breast cancer management.
    MeSH term(s) Antineoplastic Agents/therapeutic use ; Biomarkers, Tumor/blood ; Biomarkers, Tumor/genetics ; Breast Neoplasms/diagnosis ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Circulating MicroRNA/blood ; Circulating MicroRNA/genetics ; Early Diagnosis ; Female ; Gene Expression Regulation, Neoplastic ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Microarray Analysis/methods ; Neoplasm Proteins/blood ; Neoplasm Proteins/genetics ; Prognosis ; RNA, Neoplasm/blood ; RNA, Neoplasm/genetics ; Real-Time Polymerase Chain Reaction/methods
    Chemical Substances Antineoplastic Agents ; Biomarkers, Tumor ; Circulating MicroRNA ; Neoplasm Proteins ; RNA, Neoplasm
    Language English
    Publishing date 2017-09-07
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/cddis.2017.440
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: MicroRNA-3148 acts as molecular switch promoting malignant transformation and adipocytic differentiation of immortalized human bone marrow stromal cells via direct targeting of the SMAD2/TGFβ pathway.

    Vishnubalaji, Radhakrishnan / Elango, Ramesh / Manikandan, Muthurangan / Siyal, Abdul-Aziz / Ali, Dalia / Al-Rikabi, Ammar / Hamam, Dana / Hamam, Rimi / Benabdelkamel, Hicham / Masood, Afshan / Alanazi, Ibrahim O / Alfadda, Assim A / Alfayez, Musaad / Aldahmash, Abdullah / Kassem, Moustapha / Alajez, Nehad M

    Cell death discovery

    2020  Volume 6, Page(s) 79

    Abstract: MicroRNAs (miRs/miRNAs) play a key role in posttranscriptional regulation of gene expression and are implicated in a number of physiological and pathological conditions, including cellular malignant transformation. In the current study, we investigated ... ...

    Abstract MicroRNAs (miRs/miRNAs) play a key role in posttranscriptional regulation of gene expression and are implicated in a number of physiological and pathological conditions, including cellular malignant transformation. In the current study, we investigated the role of miR-3148 in regulating human stromal (mesenchymal) stem cell (hMSC) differentiation and transformation. Stable expression of miR-3148 in telomerized hMSC (hMSC-miR-3148) led to significant increase in in vitro adipocytic differentiation and suppression of osteoblastic differentiation. Concordantly, global gene expression profiling revealed significant enrichment in cholesterol biosynthesis pathway, and pathways related to enhanced cell movement and survival, whereas processes related to bone and connective tissue developments, cell death, apoptosis, and necrosis were downregulated. Global proteomic analysis using 2D-DIGE followed by mass spectrometry (MS) revealed significant changes in protein expression in hMSC-miR-3148 and enrichment in protein networks associated with carcinogenesis. Functional studies revealed that hMSC-miR-3148 exhibited enhanced in vitro cell proliferation, colony formation, migration, invasion, sphere formation, doxorubicin resistance, and increased active number of cells in S and G2/M cell cycle phases and formed sarcoma-like tumors with adipocyte infiltration when implanted into immunocompromised mice. SMAD2 was identified as bone fide gene target for miR-3148 using qRT-PCR, Western blotting, and UTR-based reporter assay. In agreement with our data, SMAD2 expression was downregulated in 47% of patients with soft tissue sarcoma. Bioinformatics analysis revealed that elevated miR-3148 expression correlates with poor prognosis in several human cancer types, including sarcoma. Our study identified miR-3148 as factor regulating hMSC differentiation and is involved in promoting malignant transformation of telomerized hMSC.
    Language English
    Publishing date 2020-09-01
    Publishing country United States
    Document type Journal Article
    ISSN 2058-7716
    ISSN 2058-7716
    DOI 10.1038/s41420-020-00312-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Exosomes isolated from cancer patients' sera transfer malignant traits and confer the same phenotype of primary tumors to oncosuppressor-mutated cells.

    Abdouh, Mohamed / Hamam, Dana / Gao, Zu-Hua / Arena, Vincenzo / Arena, Manuel / Arena, Goffredo Orazio

    Journal of experimental & clinical cancer research : CR

    2017  Volume 36, Issue 1, Page(s) 113

    Abstract: Background: Horizontal transfer of malignant traits from the primary tumor to distant organs, through blood circulating factors, has recently become a thoroughly studied metastatic pathway to explain cancer dissemination. Recently, we reported that ... ...

    Abstract Background: Horizontal transfer of malignant traits from the primary tumor to distant organs, through blood circulating factors, has recently become a thoroughly studied metastatic pathway to explain cancer dissemination. Recently, we reported that oncosuppressor gene-mutated human cells undergo malignant transformation when exposed to cancer patients' sera. We also observed that oncosuppressor mutated cells would show an increased uptake of cancer-derived exosomes and we suggested that oncosuppressor genes might protect the integrity of the cell genome by blocking integration of cancer-derived exosomes. In the present study, we tested the hypothesis that cancer patients' sera-derived exosomes might be responsible for the malignant transformation of target cells and that oncosuppressor mutation would promote their increased uptake. We also sought to unveil the mechanisms behind the hypothesized phenomena.
    Methods: We used human BRCA1 knockout (BRCA1-KO) fibroblasts as target cells. Cells were treated in vitro with cancer patients' sera or cancer patients' sera-derived exosomes. Treated cells were injected into NOD-SCID mice. Immunohistochemical analyses were performed to determine the differentiation state of the xenotransplants. Mass spectrometry analyses of proteins from cancer exosomes and the BRCA1-KO fibroblasts' membrane were performed to investigate possible de novo expression of molecules involved in vesicles uptake. Blocking of the identified molecules in vitro was performed and in vivo experiments were conducted to confirm the role of these molecules in the malignant transformation carried out by cancer-derived exosomes.
    Results: Cells treated with exosomes isolated from cancer patients' sera underwent malignant transformation and formed tumors when transplanted into immunodeficient mice. Histological analyses showed that the tumors were carcinomas that differentiated into the same lineage of the primary tumors of blood donors. Oncosuppressor mutation promoted the de novo expression, on the plasma membrane of target cells, of receptors, responsible for the increased uptake of cancer-derived exosomes. The selective blocking of these receptors inhibited the horizontal transfer of malignant traits.
    Conclusion: These findings strengthen the hypothesis that oncogenic factors transferred via circulating cancer exosomes, induce malignant transformation of target cells even at distance. Oncosuppressor genes might protect the integrity of the cell genome by inhibiting the uptake of cancer-derived exosomes.
    MeSH term(s) Animals ; BRCA1 Protein/genetics ; Cell Line, Tumor ; Cell Proliferation/genetics ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/pathology ; Exosomes/genetics ; Exosomes/pathology ; Gene Knockout Techniques ; Humans ; Mice ; Neoplasms/blood ; Neoplasms/pathology ; Phenotype ; Xenograft Model Antitumor Assays
    Chemical Substances BRCA1 Protein ; BRCA1 protein, human
    Language English
    Publishing date 2017-08-30
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 803138-1
    ISSN 1756-9966 ; 0392-9078
    ISSN (online) 1756-9966
    ISSN 0392-9078
    DOI 10.1186/s13046-017-0587-0
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  6. Article: Novel blood test to predict neoplastic activity in healthy patients and metastatic recurrence after primary tumor resection.

    Abdouh, Mohamed / Hamam, Dana / Arena, Vincenzo / Arena, Manuel / Alamri, Hussam / Arena, Goffredo Orazio

    Journal of circulating biomarkers

    2016  Volume 5, Page(s) 1849454416663661

    Abstract: We reported that single oncosuppressor-mutated (SOM) cells turn malignant when exposed to cancer patients' sera. We tested the possibility to incorporate this discovery into a biological platform able to detect cancer in healthy individuals and to ... ...

    Abstract We reported that single oncosuppressor-mutated (SOM) cells turn malignant when exposed to cancer patients' sera. We tested the possibility to incorporate this discovery into a biological platform able to detect cancer in healthy individuals and to predict metastases after tumor resection. Blood was drawn prior to tumor resection and within a year after surgery. Blood samples from healthy individuals or metastatic patients were used as negative and positive controls, respectively. Patients at risk for cancer were included in the screening cohort. Once treated, cells were injected into nonobese diabetic/severe combined immunodeficiency mice to monitor tumor growth. All samples of sera coming from metastatic patients transformed SOM cells into malignant cells. Four samples from screened patients transformed SOM cells. Further clinical tests done on these patients showed the presence of early cancerous lesions despite normal tumor markers. Based on the xenotransplants size, we were able to predict metastasis in three patients before diagnostic tests confirmed the presence of the metastatic lesions. These data show that this serum-based platform has potentials to be used for cancer screening and for identification of patients at risks to develop metastases regardless of the Tumor Node Metastasis (TNM) stage or tumor markers level.
    Language English
    Publishing date 2016-11-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2802655-X
    ISSN 1849-4544 ; 1849-4544
    ISSN (online) 1849-4544
    ISSN 1849-4544
    DOI 10.1177/1849454416663661
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  7. Article ; Online: Transfer of malignant trait to BRCA1 deficient human fibroblasts following exposure to serum of cancer patients.

    Hamam, Dana / Abdouh, Mohamed / Gao, Zu-Hua / Arena, Vincenzo / Arena, Manuel / Arena, Goffredo Orazio

    Journal of experimental & clinical cancer research : CR

    2016  Volume 35, Page(s) 80

    Abstract: Background: It was reported that metastases might occur via transfer of biologically active blood circulating molecules from the primary tumor to distant organs rather than only migration of cancer cells. We showed in an earlier study that exposure of ... ...

    Abstract Background: It was reported that metastases might occur via transfer of biologically active blood circulating molecules from the primary tumor to distant organs rather than only migration of cancer cells. We showed in an earlier study that exposure of immortalized human embryonic kidney cells (HEK 293) to cancer patient sera, induce their transformation into undifferentiated cancers due to a horizontal transfer of malignant traits. In the present work, we tested the hypothesis that even other human cells as long as they are deficient for a single oncosuppressor gene might undergo malignant transformation when exposed to human cancer serum.
    Methods: We used the CRISPR/Cas9 system to establish a stable BRCA1 knockout (KO) in human fibroblasts. The BRCA1-KO fibroblasts were exposed to cancer patients' sera or healthy patients' sera for 2 weeks. Treated cells were analyzed for cell proliferation and transformation to study their susceptibility to the oncogenic potential of cancer patients' sera and to determine the possible mechanisms underlying their hypothesized transformation.
    Results: BRCA1-KO fibroblasts treated with cancer patients' sera displayed higher proliferation and underwent malignant transformation as opposed to wild type control fibroblasts, which were not affected by exposure to cancer patients' sera. The malignant transformation was not seen when BRCA1-KO fibroblasts were treated with healthy human sera. Histological analysis of tumors generated by BRCA1-KO fibroblasts showed that they were carcinomas with phenotypical characteristics related to the cancers of the blood donor patients. Interestingly, BRCA1-KO fibroblasts were significantly more prone to internalize serum-derived exosomes, when compared to wild type fibroblasts. This suggests that oncosuppressor genes might protect the integrity of the cell genome also by blocking integration of cancer-derived exosomes.
    Conclusion: These data support the hypothesis that any human cells carrying a single oncosuppressor mutation is capable of integrating cancer factors carried in the blood and undergo complete malignant transformation. Oncosuppressor genes might protect the cell genome by impeding the integration inside the cells of these mutating factors.
    MeSH term(s) Adult ; Aged ; Animals ; BRCA1 Protein/genetics ; Cell Proliferation ; Cell Transformation, Neoplastic/genetics ; Culture Media, Conditioned/pharmacology ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Fibroblasts/pathology ; Gene Knockout Techniques ; HEK293 Cells ; Humans ; Mice ; Middle Aged ; Neoplasm Transplantation ; Neoplasms/blood ; Serum/chemistry
    Chemical Substances BRCA1 Protein ; BRCA1 protein, human ; Culture Media, Conditioned
    Language English
    Publishing date 2016-05-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 803138-1
    ISSN 1756-9966 ; 0392-9078
    ISSN (online) 1756-9966
    ISSN 0392-9078
    DOI 10.1186/s13046-016-0360-9
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2065: Show issues Location:
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  8. Article ; Online: microRNAs as regulators of adipogenic differentiation of mesenchymal stem cells.

    Hamam, Dana / Ali, Dalia / Kassem, Moustapha / Aldahmash, Abdullah / Alajez, Nehad M

    Stem cells and development

    2015  Volume 24, Issue 4, Page(s) 417–425

    Abstract: microRNAs (miRNAs) constitute complex regulatory network, fine tuning the expression of a myriad of genes involved in different biological and physiological processes, including stem cell differentiation. Mesenchymal stem cells (MSCs) are multipotent ... ...

    Abstract microRNAs (miRNAs) constitute complex regulatory network, fine tuning the expression of a myriad of genes involved in different biological and physiological processes, including stem cell differentiation. Mesenchymal stem cells (MSCs) are multipotent stem cells present in the bone marrow stroma, and the stroma of many other tissues, and can give rise to a number of mesoderm-type cells including adipocytes and osteoblasts, which form medullary fat and bone tissues, respectively. The role of bone marrow fat in bone mass homeostasis is an area of intensive investigation with the aim of developing novel approaches for enhancing osteoblastic bone formation through inhibition of bone marrow fat formation. A number of recent studies have reported several miRNAs that enhance or inhibit adipogenic differentiation of MSCs and with potential use in microRNA-based therapy to regulate adipogenesis in the context of treating bone diseases and metabolic disorders. The current review focuses on miRNAs and their role in regulating adipogenic differentiation of MSCs.
    MeSH term(s) Adipocytes/cytology ; Adipocytes/metabolism ; Adipogenesis ; Animals ; Humans ; Mesenchymal Stromal Cells/cytology ; Mesenchymal Stromal Cells/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2015-02-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2142214-X
    ISSN 1557-8534 ; 1547-3287
    ISSN (online) 1557-8534
    ISSN 1547-3287
    DOI 10.1089/scd.2014.0331
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