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  1. Article ; Online: Renal Cell Carcinoma of Variant Histology: Biology and Therapies.

    Msaouel, Pavlos / Genovese, Giannicola / Tannir, Nizar M

    Hematology/oncology clinics of North America

    2023  Volume 37, Issue 5, Page(s) 977–992

    Abstract: The term variant histology renal cell carcinomas (vhRCCs), also known as non-clear cell RCCs, refers to a diverse group of malignancies with distinct biologic and therapeutic considerations. The management of vhRCC subtypes is often based on ... ...

    Abstract The term variant histology renal cell carcinomas (vhRCCs), also known as non-clear cell RCCs, refers to a diverse group of malignancies with distinct biologic and therapeutic considerations. The management of vhRCC subtypes is often based on extrapolating results from the more common clear cell RCC studies or basket trials that are not specific to each histology. The unique management of each vhRCC subtype necessitates accurate pathologic diagnosis and dedicated research efforts. Herein, we discuss tailored recommendations for each vhRCC histology informed by ongoing research and clinical experience.
    MeSH term(s) Humans ; Carcinoma, Renal Cell/therapy ; Carcinoma, Renal Cell/diagnosis ; Carcinoma, Renal Cell/pathology ; Kidney Neoplasms/therapy ; Kidney Neoplasms/diagnosis ; Kidney Neoplasms/pathology ; Biology
    Language English
    Publishing date 2023-05-25
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 93115-9
    ISSN 1558-1977 ; 0889-8588
    ISSN (online) 1558-1977
    ISSN 0889-8588
    DOI 10.1016/j.hoc.2023.04.019
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  2. Article ; Online: KRAS-Dependency in Pancreatic Ductal Adenocarcinoma: Mechanisms of Escaping in Resistance to KRAS Inhibitors and Perspectives of Therapy.

    Gurreri, Enrico / Genovese, Giannicola / Perelli, Luigi / Agostini, Antonio / Piro, Geny / Carbone, Carmine / Tortora, Giampaolo

    International journal of molecular sciences

    2023  Volume 24, Issue 11

    Abstract: Pancreatic ductal adenocarcinoma (PDAC) is still one of the deadliest cancers in oncology because of its increasing incidence and poor survival rate. More than 90% of PDAC patients are KRAS mutated (KRASmu), with KRASG12D and KRASG12V being the most ... ...

    Abstract Pancreatic ductal adenocarcinoma (PDAC) is still one of the deadliest cancers in oncology because of its increasing incidence and poor survival rate. More than 90% of PDAC patients are KRAS mutated (KRASmu), with KRASG12D and KRASG12V being the most common mutations. Despite this critical role, its characteristics have made direct targeting of the RAS protein extremely difficult. KRAS regulates development, cell growth, epigenetically dysregulated differentiation, and survival in PDAC through activation of key downstream pathways, such as MAPK-ERK and PI3K-AKT-mammalian target of rapamycin (mTOR) signaling, in a KRAS-dependent manner. KRASmu induces the occurrence of acinar-to-ductal metaplasia (ADM) and pancreatic intraepithelial neoplasia (PanIN) and leads to an immunosuppressive tumor microenvironment (TME). In this context, the oncogenic mutation of KRAS induces an epigenetic program that leads to the initiation of PDAC. Several studies have identified multiple direct and indirect inhibitors of KRAS signaling. Therefore, KRAS dependency is so essential in KRASmu PDAC that cancer cells have secured several compensatory escape mechanisms to counteract the efficacy of KRAS inhibitors, such as activation of MEK/ERK signaling or YAP1 upregulation. This review will provide insights into KRAS dependency in PDAC and analyze recent data on inhibitors of KRAS signaling, focusing on how cancer cells establish compensatory escape mechanisms.
    MeSH term(s) Humans ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/metabolism ; Tumor Microenvironment ; Pancreatic Neoplasms
    Chemical Substances Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; KRAS protein, human
    Language English
    Publishing date 2023-05-26
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24119313
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  3. Article ; Online: The significance of sarcomatoid and rhabdoid dedifferentiation in renal cell carcinoma.

    Hahn, Andrew W / Lebenthal, Justin / Genovese, Giannicola / Sircar, Kanishka / Tannir, Nizar M / Msaouel, Pavlos

    Cancer treatment and research communications

    2022  Volume 33, Page(s) 100640

    Abstract: Dedifferentiation in renal cell carcinoma (RCC), either sarcomatoid or rhabdoid, is an infrequent event that may occur heterogeneously in the setting of any RCC histology and is associated with poor outcomes. Sarcomatoid dedifferentiation is associated ... ...

    Abstract Dedifferentiation in renal cell carcinoma (RCC), either sarcomatoid or rhabdoid, is an infrequent event that may occur heterogeneously in the setting of any RCC histology and is associated with poor outcomes. Sarcomatoid dedifferentiation is associated with inferior survival with angiogenesis targeted therapy and infrequent responses to cytotoxic chemotherapy. However, immune checkpoint therapy has significantly improved outcomes for patients with sarcomatoid dedifferentiation. Biologically, sarcomatoid dedifferentiation has increased programmed death-ligand 1 (PD-L1) expression and an inflamed tumor microenvironment, in addition to other distinct molecular alterations. Less is known about rhabdoid dedifferentiation from either a clinical, biological, or therapeutic perspective. In this focused review, we will discuss the prognostic implications, outcomes with systemic therapy, and underlying biology in RCC with either sarcomatoid or rhabdoid dedifferentiation present.
    Language English
    Publishing date 2022-09-22
    Publishing country England
    Document type Journal Article
    ISSN 2468-2942
    ISSN (online) 2468-2942
    DOI 10.1016/j.ctarc.2022.100640
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  4. Article ; Online: Renal Cell Carcinoma Unclassified with Medullary Phenotype in a Patient with Neurofibromatosis Type 2.

    Sarkar, Sanila / Throckmorton, Whitney / Bingham, Racheal / Msaouel, Pavlos / Genovese, Giannicola / Slopis, John / Rao, Priya / Sadighi, Zsila / Herzog, Cynthia E

    Current oncology (Toronto, Ont.)

    2023  Volume 30, Issue 3, Page(s) 3355–3365

    Abstract: We present, to our knowledge, the first reported case of germline neurofibromatosis Type 2 (NF2) associated with renal cell carcinoma unclassified with medullary phenotype (RCCU-MP) with somatic loss by immunohistochemistry of ... ...

    Abstract We present, to our knowledge, the first reported case of germline neurofibromatosis Type 2 (NF2) associated with renal cell carcinoma unclassified with medullary phenotype (RCCU-MP) with somatic loss by immunohistochemistry of the
    MeSH term(s) Female ; Humans ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/pathology ; Kidney Neoplasms/genetics ; Kidney Neoplasms/pathology ; Meningeal Neoplasms/genetics ; Meningioma/genetics ; Neurofibromatosis 2/complications ; Neurofibromatosis 2/genetics ; Phenotype
    Chemical Substances NF2 protein, human
    Language English
    Publishing date 2023-03-14
    Publishing country Switzerland
    Document type Case Reports ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1236972-x
    ISSN 1718-7729 ; 1198-0052
    ISSN (online) 1718-7729
    ISSN 1198-0052
    DOI 10.3390/curroncol30030255
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    Zs.A 4305: Show issues Location:
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  5. Article ; Online: Targeting proteostasis and autophagy in SMARCB1-deficient malignancies: where next?

    Msaouel, Pavlos / Carugo, Alessandro / Genovese, Giannicola

    Oncotarget

    2019  Volume 10, Issue 40, Page(s) 3979–3981

    Language English
    Publishing date 2019-06-18
    Publishing country United States
    Document type Editorial
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.26970
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  6. Article: Molecular hallmarks of renal medullary carcinoma: more to c-MYC than meets the eye.

    Msaouel, Pavlos / Walker, Cheryl L / Genovese, Giannicola / Tannir, Nizar M

    Molecular & cellular oncology

    2020  Volume 7, Issue 5, Page(s) 1777060

    Abstract: Renal medullary carcinoma (RMC) is a lethal disease that predominantly afflicts young individuals with sickle cell trait. Our recently reported molecular profiling of primary untreated RMC tissues elucidated distinct genomic and immune hallmarks of RMC, ... ...

    Abstract Renal medullary carcinoma (RMC) is a lethal disease that predominantly afflicts young individuals with sickle cell trait. Our recently reported molecular profiling of primary untreated RMC tissues elucidated distinct genomic and immune hallmarks of RMC, and identified MYC-induced replication stress as a targetable vulnerability for this disease.
    Language English
    Publishing date 2020-06-23
    Publishing country United States
    Document type Journal Article
    ISSN 2372-3556
    ISSN 2372-3556
    DOI 10.1080/23723556.2020.1777060
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  7. Article ; Online: Recent advancements in the treatment of metastatic clear cell renal cell carcinoma: A review of the evidence using second-generation p-values.

    Adashek, Jacob J / Genovese, Giannicola / Tannir, Nizar M / Msaouel, Pavlos

    Cancer treatment and research communications

    2020  Volume 23, Page(s) 100166

    Abstract: The therapeutic options for advanced or metastatic renal cell carcinoma (mRCC) have drastically evolved over the past 20 years. High-dose interleukin-2 (HD IL-2), which led to durable complete responses in a small fraction of patients by activating the ... ...

    Abstract The therapeutic options for advanced or metastatic renal cell carcinoma (mRCC) have drastically evolved over the past 20 years. High-dose interleukin-2 (HD IL-2), which led to durable complete responses in a small fraction of patients by activating the interleukin-2 (IL-2) pathway, faded in popularity with the advent of oral tyrosine kinase inhibitors directed against the VEGF pathway (VEGFR-TKI) showing better tolerability, wider applicability, higher objective response rates, and longer progression-free survival than HD IL-2. More recently, new insights on how to more efficiently harness the immune system led to the development of immune checkpoint inhibitor (ICI) therapies, which rapidly became an integral component of mRCC treatment. The recently approved regimen combining the PD-1 inhibitor, nivolumab, and the CTLA-4 inhibitor, ipilimumab, and the recently approved regimens combining the oral VEGFR-TKI, axitinib, with the PD-1 inhibitor, pembrolizumab, or the PD-L1 inhibitor, avelumab, were shown to yield improved outcomes compared with sunitinib, the VEGFR-TKI that was used as a comparator. The present review discusses the evidence behind the treatment approvals for mRCC and provides an overview of the current therapeutic landscape. We evaluated the results of randomized clinical trials for mRCC based on the effect size differences between treatments on relative scales and used second-generation p-values as a descriptive summary of the statistical evidence.
    Language English
    Publishing date 2020-01-03
    Publishing country England
    Document type Journal Article
    ISSN 2468-2942
    ISSN (online) 2468-2942
    DOI 10.1016/j.ctarc.2020.100166
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  8. Article ; Online: Systemic Therapies for the Management of Non-Clear Cell Renal Cell Carcinoma: What Works, What Doesn't, and What the Future Holds.

    Zoumpourlis, Panagiotis / Genovese, Giannicola / Tannir, Nizar M / Msaouel, Pavlos

    Clinical genitourinary cancer

    2020  Volume 19, Issue 2, Page(s) 103–116

    Abstract: Non-clear cell renal cell carcinoma (nccRCC) is a broad term that refers to a diverse group of tumors, each with its own distinct biologic and therapeutic profile. The management of nccRCCs is often based on extrapolating data from clinical trials in the ...

    Abstract Non-clear cell renal cell carcinoma (nccRCC) is a broad term that refers to a diverse group of tumors, each with its own distinct biologic and therapeutic profile. The management of nccRCCs is often based on extrapolating data from clinical trials in the more common clear cell renal cell carcinoma, but our emerging prospective and retrospective clinical experience in nccRCC allows us to make more precise recommendations tailored to each histology. The systemic therapy options for metastatic nccRCC include targeted therapies such as tyrosine kinase inhibitors, immune checkpoint inhibitors, and, for specific rare subtypes, cytotoxic chemotherapy. Each nccRCC histology may respond differently to these regimens, which makes accurate pathologic diagnosis imperative. In the present review, we discuss the available clinical and biological data that can help guide systemic therapy recommendations for specific nccRCC subtypes.
    MeSH term(s) Carcinoma, Renal Cell/drug therapy ; Humans ; Kidney Neoplasms/drug therapy ; Prospective Studies ; Retrospective Studies
    Language English
    Publishing date 2020-12-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 2225121-2
    ISSN 1938-0682 ; 1558-7673
    ISSN (online) 1938-0682
    ISSN 1558-7673
    DOI 10.1016/j.clgc.2020.11.005
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  9. Article ; Online: Role of Epithelial-to-Mesenchymal Transition in Inflammatory Bowel Disease.

    Lovisa, Sara / Genovese, Giannicola / Danese, Silvio

    Journal of Crohn's & colitis

    2018  Volume 13, Issue 5, Page(s) 659–668

    Abstract: Intestinal fibrosis is an inevitable complication in patients with inflammatory bowel disease [IBD], occurring in its two major clinical manifestations: ulcerative colitis and Crohn's disease. Fibrosis represents the final outcome of the host reaction to ...

    Abstract Intestinal fibrosis is an inevitable complication in patients with inflammatory bowel disease [IBD], occurring in its two major clinical manifestations: ulcerative colitis and Crohn's disease. Fibrosis represents the final outcome of the host reaction to persistent inflammation, which triggers a prolonged wound healing response resulting in the excessive deposition of extracellular matrix, eventually leading to intestinal dysfunction. The process of epithelial-to-mesenchymal transition [EMT] represents an embryonic program relaunched during wound healing, fibrosis and cancer. Here we discuss the initial observations and the most recent findings highlighting the role of EMT in IBD-associated intestinal fibrosis and fistulae formation. In addition, we briefly review knowledge on the cognate process of endothelial-to-mesenchymal transition [EndMT]. Understanding EMT functionality and the molecular mechanisms underlying the activation of this mesenchymal programme will permit designing new therapeutic strategies to halt the fibrogenic response in the intestine.
    MeSH term(s) Animals ; Colitis, Ulcerative/pathology ; Crohn Disease/pathology ; Disease Models, Animal ; Epithelial-Mesenchymal Transition ; Fibrosis ; Humans ; Inflammatory Bowel Diseases/pathology ; Intestinal Fistula/etiology ; Intestinal Fistula/pathology ; Intestines/pathology ; Mice
    Language English
    Publishing date 2018-12-05
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2390120-2
    ISSN 1876-4479 ; 1873-9946
    ISSN (online) 1876-4479
    ISSN 1873-9946
    DOI 10.1093/ecco-jcc/jjy201
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    Zs.A 6634: Show issues Location:
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  10. Article ; Online: TAM kinase inhibition and immune checkpoint blockade- a winning combination in cancer treatment?

    Msaouel, Pavlos / Genovese, Giannicola / Gao, Jianjun / Sen, Suvajit / Tannir, Nizar M

    Expert opinion on therapeutic targets

    2020  Volume 25, Issue 2, Page(s) 141–151

    Abstract: ... ...

    Abstract Introduction
    MeSH term(s) Animals ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/adverse effects ; Antineoplastic Agents/pharmacology ; Clinical Trials as Topic/methods ; Drug Synergism ; Humans ; Immune Checkpoint Inhibitors/administration & dosage ; Immune Checkpoint Inhibitors/adverse effects ; Immune Checkpoint Inhibitors/pharmacology ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Neoplasms/immunology ; Protein Kinase Inhibitors/administration & dosage ; Protein Kinase Inhibitors/adverse effects ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins/antagonists & inhibitors ; Proto-Oncogene Proteins/metabolism ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors ; Receptor Protein-Tyrosine Kinases/metabolism ; c-Mer Tyrosine Kinase/antagonists & inhibitors ; c-Mer Tyrosine Kinase/metabolism
    Chemical Substances Antineoplastic Agents ; Immune Checkpoint Inhibitors ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; TYRO3 protein, human (EC 2.7.10.1) ; axl receptor tyrosine kinase (EC 2.7.10.1) ; c-Mer Tyrosine Kinase (EC 2.7.10.1)
    Language English
    Publishing date 2020-12-31
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2055208-7
    ISSN 1744-7631 ; 1472-8222
    ISSN (online) 1744-7631
    ISSN 1472-8222
    DOI 10.1080/14728222.2021.1869212
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