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  1. Article ; Online: Perspectives in Oncology: a new article type for Medical Oncology.

    Pienta, Kenneth J

    Medical oncology (Northwood, London, England)

    2020  Volume 37, Issue 3, Page(s) 21

    MeSH term(s) Editorial Policies ; Humans ; Medical Oncology/trends ; Peer Review, Research ; Periodicals as Topic
    Language English
    Publishing date 2020-03-07
    Publishing country United States
    Document type Editorial
    ZDB-ID 1201189-7
    ISSN 1559-131X ; 0736-0118 ; 1357-0560
    ISSN (online) 1559-131X
    ISSN 0736-0118 ; 1357-0560
    DOI 10.1007/s12032-020-01349-x
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1899: 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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  2. Book: The conundrum of rising prostate-specific antigen

    Pienta, Kenneth J.

    prevention and treatment

    (Urology ; 62,6B = Suppl.)

    2003  

    Author's details guest ed.: Kenneth J. Pienta
    Series title Urology ; 62,6B = Suppl.
    Collection
    Language English
    Size 154 S. : Ill., graph. Darst.
    Publisher Elsevier Science
    Publishing place New York, NY
    Publishing country United States
    Document type Book
    HBZ-ID HT013914872
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Zs A 1142 -62,6B- not available for loan Zeitschriften-Lesesaal

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  3. Article ; Online: Dormant cancer cells: programmed quiescence, senescence, or both?

    Truskowski, Kevin / Amend, Sarah R / Pienta, Kenneth J

    Cancer metastasis reviews

    2023  Volume 42, Issue 1, Page(s) 37–47

    Abstract: Metastasis is the overwhelming driver of cancer mortality, accounting for the majority of cancer deaths. Many patients present with metastatic relapse years after eradication of the primary lesion. Disseminated cancer cells can undergo a durable ... ...

    Abstract Metastasis is the overwhelming driver of cancer mortality, accounting for the majority of cancer deaths. Many patients present with metastatic relapse years after eradication of the primary lesion. Disseminated cancer cells can undergo a durable proliferative arrest and lie dormant in secondary tissues before reentering the cell cycle to seed these lethal relapses. This process of cancer cell dormancy remains poorly understood, largely due to difficulties in studying these dormant cells. In the face of these challenges, the application of knowledge from the cellular senescence and quiescence fields may help to guide future thinking on the study of dormant cancer cells. Both senescence and quiescence are common programs of proliferative arrest that are integral to tissue development and homeostasis. Despite phenotypic differences, these two states also share common characteristics, and both likely play a role in cancer dormancy and delayed metastatic relapse. Understanding the cell biology behind these states, their overlaps and unique characteristics is critical to our future understanding of dormant cancer cells, as these cells likely employ some of the same molecular programs to promote survival and dissemination. In this review, we highlight the biology underlying these non-proliferative states, relate this knowledge to what we currently know about dormant cancer cells, and discuss implications for future work toward targeting these elusive metastatic seeds.
    MeSH term(s) Humans ; Neoplasms/pathology ; Cell Cycle ; Recurrence
    Language English
    Publishing date 2023-01-04
    Publishing country Netherlands
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 604857-2
    ISSN 1573-7233 ; 0167-7659
    ISSN (online) 1573-7233
    ISSN 0167-7659
    DOI 10.1007/s10555-022-10073-z
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1812: 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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  4. Article ; Online: An Enhancing Renal Mass in Metastatic Prostate Cancer.

    Rezaee, Michael E / Li, Huili / Pienta, Kenneth J

    Urology

    2023  Volume 175, Page(s) e15–e16

    MeSH term(s) Male ; Humans ; Prostatic Neoplasms/pathology ; Prostate-Specific Antigen ; Neoplasm Metastasis
    Chemical Substances Prostate-Specific Antigen (EC 3.4.21.77)
    Language English
    Publishing date 2023-03-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 192062-5
    ISSN 1527-9995 ; 0090-4295
    ISSN (online) 1527-9995
    ISSN 0090-4295
    DOI 10.1016/j.urology.2023.02.032
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1142: 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)
    Zs.MO 275: Show issues

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  5. Book: Hormone refractory prostate cancer

    Pienta, Kenneth J.

    (The urologic clinics of North America ; 26,2)

    1999  

    Author's details Kenneth J. Pienta, guest ed
    Series title The urologic clinics of North America ; 26,2
    Collection
    Keywords Bauchspeicheldrüsenkrebs
    Subject Pankreastumor ; Bauchspeicheldrüsentumor ; Pankreaskarzinom ; Pankreascarcinom ; Pankreasadenocarcinom ; Pankreasadenokarzinom
    Language English
    Size XI S., S. 263 - 434 : Ill., graph. Darst.
    Publisher Saunders
    Publishing place Philadelphia u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT010499802
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Se 269 -26,2- verfügbar in Königswinter Königswinter

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  6. Article ; Online: Peripheral androgen blockade in men with castrate-sensitive biochemical recurrent prostate cancer.

    Reyes, Diane K / Pienta, Kenneth J

    Medical oncology (Northwood, London, England)

    2021  Volume 38, Issue 7, Page(s) 80

    Abstract: The aim of the study was to evaluate the feasibility of utilizing peripheral androgen blockade in men with biochemical recurrent castrate-sensitive prostate cancer. A registration study to track outcomes of men with biochemical recurrent castrate- ... ...

    Abstract The aim of the study was to evaluate the feasibility of utilizing peripheral androgen blockade in men with biochemical recurrent castrate-sensitive prostate cancer. A registration study to track outcomes of men with biochemical recurrent castrate-sensitive prostate cancer treated with peripheral androgen blockade utilizing concomitant administration of finasteride and bicalutamide. Men were on intermittent peripheral blockade for a median 20.2 months, continuous peripheral blockade for a median 6.8 months, intermittent triple dose peripheral androgen blockade for a median 10.7 months, and continuous triple dose peripheral androgen blockade for 4.4 months before failing therapy. Six men (21%) had additional therapies during treatment that included metastasis-directed therapy (5/37, 14%), systemic Lu-177 (2/37, 5%), and salvage RT (1/37, 3%). The median time to progression, which includes time from initiation through all therapies to the initiation of ADT, was 37.6 months (IQR 20-74.7). From the start of PAB, median time to castrate resistance was 49.8 months (IQR 40.9-NR). After starting ADT, median time to castrate resistance was 8.8 months (IQR 4.6-17.7). Our data support the exploration of PAB as a treatment option in carefully selected patients who present with biochemical recurrence after failure of definitive local therapy for prostate cancer.
    MeSH term(s) Aged ; Androgen Antagonists/administration & dosage ; Androgens/metabolism ; Anilides/administration & dosage ; Antineoplastic Agents, Hormonal/administration & dosage ; Antineoplastic Combined Chemotherapy Protocols/administration & dosage ; Finasteride/administration & dosage ; Humans ; Male ; Middle Aged ; Neoplasm Recurrence, Local/diagnosis ; Neoplasm Recurrence, Local/drug therapy ; Neoplasm Recurrence, Local/metabolism ; Nitriles/administration & dosage ; Prostatic Neoplasms, Castration-Resistant/diagnosis ; Prostatic Neoplasms, Castration-Resistant/drug therapy ; Prostatic Neoplasms, Castration-Resistant/metabolism ; Tosyl Compounds/administration & dosage
    Chemical Substances Androgen Antagonists ; Androgens ; Anilides ; Antineoplastic Agents, Hormonal ; Nitriles ; Tosyl Compounds ; Finasteride (57GNO57U7G) ; bicalutamide (A0Z3NAU9DP)
    Language English
    Publishing date 2021-06-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1201189-7
    ISSN 1559-131X ; 0736-0118 ; 1357-0560
    ISSN (online) 1559-131X
    ISSN 0736-0118 ; 1357-0560
    DOI 10.1007/s12032-021-01506-w
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1899: 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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  7. Article: Punctuational evolution is pervasive in distal site metastatic colonization.

    Butler, George / Amend, Sarah R / Axelrod, Robert / Venditti, Chris / Pienta, Kenneth J

    bioRxiv : the preprint server for biology

    2024  

    Abstract: The evolution of metastasis represents a lethal stage of cancer progression. Yet, the evolutionary kinetics of metastatic disease remain unresolved. Here, using single cell CRISPR-Cas9 lineage tracing data, we show that in metastatic disease, gradual ... ...

    Abstract The evolution of metastasis represents a lethal stage of cancer progression. Yet, the evolutionary kinetics of metastatic disease remain unresolved. Here, using single cell CRISPR-Cas9 lineage tracing data, we show that in metastatic disease, gradual molecular evolution is punctuated by episodes of rapid evolutionary change associated with lineage divergence. By measuring punctuational effects across the metastatic cascade, we show that punctuational effects contribute more to the molecular diversity at distal site metastases compared to the paired primary tumor, suggesting qualitatively different modes of evolution may drive primary and metastatic tumor progression. This is the first empirical evidence for distinct patterns of molecular evolution at early and late stages of metastasis and demonstrates the complex interplay of cell intrinsic and extrinsic factors that shape lethal cancer.
    Language English
    Publishing date 2024-04-11
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.04.08.588529
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  8. Book: Diagnosis and treatment of genitourinary malignancies

    Pienta, Kenneth J.

    (Cancer treatment and research ; [88])

    1996  

    Author's details ed. by Kenneth J. Pienta
    Series title Cancer treatment and research ; [88]
    Collection
    Keywords Urogenital Neoplasms / diagnosis ; Urogenital Neoplasms / therapy ; Urogenitalkrebs ; Diagnose ; Therapie
    Subject Medizinische Behandlung ; Behandlung ; Krankenbehandlung ; Urogenitalkarzinom ; Ärztliche Diagnose
    Language English
    Size VI, 272 S. : Ill.
    Publisher Kluwer Acad. Publ
    Publishing place Dordrecht
    Publishing country Netherlands
    Document type Book
    HBZ-ID HT007805922
    ISBN 0-7923-4164-3 ; 978-0-7923-4164-2
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    1997 A 7390 order for loan Magazin

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  9. Article ; Online: Interplay between Cell Death and Cell Proliferation Reveals New Strategies for Cancer Therapy.

    Loftus, Luke V / Amend, Sarah R / Pienta, Kenneth J

    International journal of molecular sciences

    2022  Volume 23, Issue 9

    Abstract: Cell division and cell death are fundamental processes governing growth and development across the tree of life. This relationship represents an evolutionary link between cell cycle and cell death programs that is present in all cells. Cancer is ... ...

    Abstract Cell division and cell death are fundamental processes governing growth and development across the tree of life. This relationship represents an evolutionary link between cell cycle and cell death programs that is present in all cells. Cancer is characterized by aberrant regulation of both, leading to unchecked proliferation and replicative immortality. Conventional anti-cancer therapeutic strategies take advantage of the proliferative dependency of cancer yet, in doing so, are triggering apoptosis, a death pathway to which cancer is inherently resistant. A thorough understanding of how therapeutics kill cancer cells is needed to develop novel, more durable treatment strategies. While cancer evolves cell-intrinsic resistance to physiological cell death pathways, there are opportunities for cell cycle agnostic forms of cell death, for example, necroptosis or ferroptosis. Furthermore, cell cycle independent death programs are immunogenic, potentially licensing host immunity for additional antitumor activity. Identifying cell cycle independent vulnerabilities of cancer is critical for developing alternative strategies that can overcome therapeutic resistance.
    MeSH term(s) Apoptosis ; Cell Death ; Cell Proliferation ; Ferroptosis ; Humans ; Necroptosis ; Neoplasms/pathology
    Language English
    Publishing date 2022-04-25
    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/ijms23094723
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  10. Article: Escherichia coli

    Butler, George / Bos, Julia / Austin, Robert H / Amend, Sarah R / Pienta, Kenneth J

    Royal Society open science

    2023  Volume 10, Issue 8, Page(s) 230338

    Abstract: The evolution of antibiotic resistance is a fundamental problem in disease management but is rarely quantified on a single-cell level owing to challenges associated with capturing the spatial and temporal variation across a population. To evaluate cell ... ...

    Abstract The evolution of antibiotic resistance is a fundamental problem in disease management but is rarely quantified on a single-cell level owing to challenges associated with capturing the spatial and temporal variation across a population. To evaluate cell biological phenotypic responses, we tracked the single-cell dynamics of filamentous bacteria through time in response to ciprofloxacin antibiotic stress. We measured the degree of phenotypic variation in nucleoid length and the accumulation of protein damage under ciprofloxacin antibiotic and quantified the impact on bacterial survival. Increased survival was correlated with increased nucleoid length and the variation in this response was inversely correlated with antibiotic concentration. Survival time was also increased through clearance of misfolded proteins, an unexpected mechanism of stress relief deployed by the filamentous bacteria. Our results reveal a diverse range of survival tactics employed by bacteria in response to ciprofloxacin and suggest potential evolutionary routes to resistance.
    Language English
    Publishing date 2023-08-09
    Publishing country England
    Document type Journal Article
    ZDB-ID 2787755-3
    ISSN 2054-5703
    ISSN 2054-5703
    DOI 10.1098/rsos.230338
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