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  1. Article ; Online: First Case of Covid-19 in the United States.

    Tsung, Kangla

    The New England journal of medicine

    2020  Volume 382, Issue 21, Page(s) e53

    MeSH term(s) Betacoronavirus ; COVID-19 ; Coronavirus ; Coronavirus Infections ; Humans ; Pandemics ; Pneumonia, Viral ; SARS-CoV-2 ; United States
    Keywords covid19
    Language English
    Publishing date 2020-04-22
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMc2004794
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    Ua VI Zs.34: Show issues Location:
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  3. Article ; Online: Tumor reductive therapies and antitumor immunity.

    Guo, Huiqin / Tsung, Kangla

    Oncotarget

    2017  Volume 8, Issue 33, Page(s) 55736–55749

    Abstract: Tumor reductive therapy is to reduce tumor burden through direct killing of tumor cells. So far, there is no report on the connection between antitumor immunity and tumor reductive therapies. In the last few years, a new category of cancer treatment, ... ...

    Abstract Tumor reductive therapy is to reduce tumor burden through direct killing of tumor cells. So far, there is no report on the connection between antitumor immunity and tumor reductive therapies. In the last few years, a new category of cancer treatment, immunotherapy, emerged and they are categorized separately from classic cytotoxic treatments (chemo and radiation therapy). The most prominent examples include cellular therapies (LAK and CAR-T) and immune checkpoint inhibitors (anti-PD-1 and CTLA-4). Recent advances in clinical immunotherapy and our understanding of the mechanism behind them revealed that these therapies have a closer relationship with classic cancer treatments than we thought. In many cases, the effectiveness of classic therapies is heavily influenced by the status of the underlying antitumor-immunity. On the other hand, immunotherapies have shown better outcome when combined with tumor reductive therapies, not only due to the combined effects of tumor killing by each therapy but also because of a synergy between the two. Many clinical observations can be explained once we start to look at these classic therapies from an immunity standpoint. We have seen their direct effect on tumor antigen
    Language English
    Publishing date 2017-08-15
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.18469
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: An immunological view of chemotherapy.

    Tsung, Kangla / Norton, Jeffrey A

    Immunotherapy

    2015  Volume 7, Issue 9, Page(s) 941–943

    MeSH term(s) Animals ; Combined Modality Therapy ; Drug Therapy ; Humans ; Immunity/drug effects ; Immunotherapy ; Interleukin-12/immunology ; Interleukin-12/therapeutic use ; Neoplasms/immunology ; Neoplasms/therapy ; Receptors, Pattern Recognition/immunology ; T-Lymphocytes/immunology
    Chemical Substances Receptors, Pattern Recognition ; Interleukin-12 (187348-17-0)
    Language English
    Publishing date 2015
    Publishing country England
    Document type Editorial
    ISSN 1750-7448
    ISSN (online) 1750-7448
    DOI 10.2217/imt.15.62
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  5. Article ; Online: In situ vaccine, immunological memory and cancer cure.

    Tsung, Kangla / Norton, Jeffrey A

    Human vaccines & immunotherapeutics

    2016  Volume 12, Issue 1, Page(s) 117–119

    Abstract: As surgery is able to remove primary tumors and limit metastases, the major challenge in cancer management is the prevention of post-resection recurrence and metastases. From the immune point of view, tumor resection removes the supply of tumor antigens ... ...

    Abstract As surgery is able to remove primary tumors and limit metastases, the major challenge in cancer management is the prevention of post-resection recurrence and metastases. From the immune point of view, tumor resection removes the supply of tumor antigens that maintain an active concomitant antitumor immunity elicited by the primary tumor, and may also signal for deposition of immunological memory against future metastases. However, the natural course of this antitumor immunity in many cancer patients following complete tumor resection may not be favorable because protection is often lost after 1-3 years. Recent studies suggest that chemotherapy is able to activate this pre-existing antitumor immunity, and tumor resection following immune activation may lead to higher levels of immunological memory against future tumor antigens (in the form of metastases). Interleukin-12 added to chemotherapy mimics the function of a vaccine adjuvant in that it helps to enhance the antitumor immunity activated by chemotherapy and leaves a much stronger antitumor immune memory. This finding, when applied to cancer management, may help to maintain a strong and long lasting antitumor immunity following complete tumor resection, thus eliminating post-surgery recurrence and metastases.
    MeSH term(s) Adjuvants, Immunologic/administration & dosage ; Drug Therapy/methods ; Humans ; Immunologic Memory ; Interleukin-12/administration & dosage ; Neoplasm Metastasis/prevention & control ; Neoplasms/drug therapy ; Recurrence ; Treatment Outcome
    Chemical Substances Adjuvants, Immunologic ; Interleukin-12 (187348-17-0)
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2664176-8
    ISSN 2164-554X ; 2164-5515
    ISSN (online) 2164-554X
    ISSN 2164-5515
    DOI 10.1080/21645515.2015.1073427
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6967: Show issues Location:
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  6. Article: Lessons from Coley's Toxin.

    Tsung, Kangla / Norton, Jeffrey A

    Surgical oncology

    2006  Volume 15, Issue 1, Page(s) 25–28

    Abstract: The active molecule in Coley's Toxin is not tumor necrosis factor (TNF) or endotoxin (LPS), but interleukin-12 (IL-12). IL-12 holds the key to improved anti-tumor immuns response. ...

    Abstract The active molecule in Coley's Toxin is not tumor necrosis factor (TNF) or endotoxin (LPS), but interleukin-12 (IL-12). IL-12 holds the key to improved anti-tumor immuns response.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Clinical Trials as Topic ; Cytokines/metabolism ; Endotoxins/metabolism ; Humans ; Immunotherapy/methods ; Interleukin-12/chemistry ; Lymphocytes/metabolism ; Mice ; Neoplasms/immunology ; Neoplasms/therapy ; Tumor Necrosis Factors/chemistry
    Chemical Substances Antineoplastic Agents ; Cytokines ; Endotoxins ; Tumor Necrosis Factors ; Interleukin-12 (187348-17-0)
    Language English
    Publishing date 2006-07
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 1107810-8
    ISSN 1879-3320 ; 0960-7404
    ISSN (online) 1879-3320
    ISSN 0960-7404
    DOI 10.1016/j.suronc.2006.05.002
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    Zs.A 3409: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: IL-12 augments antitumor responses to cycled chemotherapy.

    Zhang, Lingbing / Feng, Dongdong / Hu, Yingbin / Tsung, Kangla / Norton, Jeffrey A

    Journal of immunotherapy (Hagerstown, Md. : 1997)

    2015  Volume 38, Issue 4, Page(s) 137–144

    Abstract: Loss of antitumor response to repeated chemotherapy is a major cause of treatment failure in cancer patients. The development of acquired drug resistance is thought to come primarily from changes in tumor cells, and not host response to the tumor. Our ... ...

    Abstract Loss of antitumor response to repeated chemotherapy is a major cause of treatment failure in cancer patients. The development of acquired drug resistance is thought to come primarily from changes in tumor cells, and not host response to the tumor. Our recent study shows that antitumor immunity is activated and contributes significantly to the efficacy of chemotherapy. In this study of mouse tumor models, we demonstrate that loss of antitumor response during multiple cycles of chemotherapy is associated with a lack of immune activation, and not intrinsic tumor cell drug resistance. More importantly, we show that adding interleukin-12 (IL-12) to cycled chemotherapy maintains and even increases antitumor immune response in both immunogenic and nonimmunogenic murine tumors and significantly prolongs survival. In some instances, larger tumor burdens that relapse following an initial cycle of cyclophosphamide and IL-12 are eradicated by subsequent cycles of the same treatment at the same doses. Further analysis demonstrates that the initial cycle of the combined therapy increases antitumor immunity of the host. In other mice when tumors are not eradicated by the current cycle of therapy, it serves as a starting point for the subsequent cycles of treatment to generate higher levels of antitumor immunity and greater antitumor response. These results show that the status of host antitumor immunity is a critical factor affecting antitumor efficacy during repeated administration of chemotherapy. Further, IL-12 augments the antitumor immune response under such conditions.
    MeSH term(s) Adjuvants, Immunologic/administration & dosage ; Animals ; Cell Line, Tumor ; Cyclophosphamide/administration & dosage ; Cytotoxicity, Immunologic/drug effects ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/immunology ; Female ; Humans ; Immunity, Cellular/drug effects ; Interferon-gamma/metabolism ; Interleukin-12/administration & dosage ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neoplasm Transplantation ; Neoplasms/drug therapy ; Neoplasms/immunology ; Recurrence
    Chemical Substances Adjuvants, Immunologic ; Interleukin-12 (187348-17-0) ; Interferon-gamma (82115-62-6) ; Cyclophosphamide (8N3DW7272P)
    Language English
    Publishing date 2015-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1064067-8
    ISSN 1537-4513 ; 1053-8550 ; 1524-9557
    ISSN (online) 1537-4513
    ISSN 1053-8550 ; 1524-9557
    DOI 10.1097/CJI.0000000000000074
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    Zs.A 1778: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  8. Article ; Online: Preexisting antitumor immunity augments the antitumor effects of chemotherapy.

    Zhang, Lingbing / Feng, Dongdong / Yu, Lynda X / Tsung, Kangla / Norton, Jeffrey A

    Cancer immunology, immunotherapy : CII

    2013  Volume 62, Issue 6, Page(s) 1061–1071

    Abstract: Efficacy of cancer chemotherapy is generally believed to be the result of direct drug killing of tumor cells. However, increased tumor cell killing does not always lead to improved efficacy. Herein, we demonstrate that the status of antitumor immunity at ...

    Abstract Efficacy of cancer chemotherapy is generally believed to be the result of direct drug killing of tumor cells. However, increased tumor cell killing does not always lead to improved efficacy. Herein, we demonstrate that the status of antitumor immunity at the time of chemotherapy treatment is a critical factor affecting the therapeutic outcome in that tumor-bearing mice that possess preexisting antitumor immunity respond to chemotherapy much better than those that do not. Enhancing antitumor immunity before or at the time of chemotherapy-induced antigen release increases subsequent response to chemotherapy significantly. By in vitro and in vivo measurements of antitumor immunity, we found a close correlation between the intensity of antitumor immunity activated by chemotherapy and the efficacy of treatment. Immune intervention with interleukin-12 during the early phase of chemotherapy-induced immune activation greatly amplifies the antitumor response, often resulting in complete tumor eradication not only at the chemo-treated local site, but also systemically. These findings provide additional evidence for an immune-mediated antitumor response to chemotherapy. Further, our results show that timely immune modification of chemotherapy-activated antitumor immunity can result in enhanced antitumor-immune response and complete tumor eradication.
    MeSH term(s) Animals ; Antigens, Neoplasm/immunology ; Antigens, Neoplasm/metabolism ; Antineoplastic Agents/administration & dosage ; Cell Line, Tumor ; Disease Models, Animal ; Female ; Humans ; Immunity/drug effects ; Mice ; Mice, Knockout ; Neoplasms/drug therapy ; Neoplasms/immunology ; Neoplasms/mortality ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Treatment Outcome
    Chemical Substances Antigens, Neoplasm ; Antineoplastic Agents
    Language English
    Publishing date 2013-04-18
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 195342-4
    ISSN 1432-0851 ; 0340-7004
    ISSN (online) 1432-0851
    ISSN 0340-7004
    DOI 10.1007/s00262-013-1417-7
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    Zs.A 1237: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  9. Article: Inhibition of host signal transducer and activator of transcription factor 6 results in cure with cyclophosphamide and interleukin 12 immunotherapy.

    Norton, Jeffrey A / Li, Michelle / Lee, Natalie C / Tsung, Kangla

    Annals of surgical oncology

    2006  Volume 13, Issue 1, Page(s) 118–124

    Abstract: Background: Interleukin (IL)-12 immunotherapy is highly effective against established immunogenic tumors. However, nonimmunogenic tumors fail to respond to IL-12 therapy. Analysis of tumor rejection of the immunogenic tumors shows that a preexisting ... ...

    Abstract Background: Interleukin (IL)-12 immunotherapy is highly effective against established immunogenic tumors. However, nonimmunogenic tumors fail to respond to IL-12 therapy. Analysis of tumor rejection of the immunogenic tumors shows that a preexisting antitumor immune response is required for an effective IL-12 response. It is not known whether this lack of a preexisting host antitumor immune response is a limiting factor for the lack of response to IL-12 therapy by nonimmunogenic tumors.
    Methods: Experiments were done using the spontaneously arising nonimmunogenic metastatic murine breast 4T1 carcinoma in normal and STAT6 knockout BALB/c mice.
    Results: 4T1 is nonimmunogenic in normal mice, and established subcutaneous tumors are resistant to immunotherapy with cyclophosphamide (Cy) plus IL-12. However, in STAT6 knockout mice, 4T1 becomes immunogenic, and established 4T1 tumors are eradicated by Cy plus IL-12. Adoptive transfer of spleen cells from normal mice into STAT6 knockout mice before tumor inoculation reduces both the immunogenicity and response to Cy plus IL-12 immunotherapy of 4T1 in the recipient mice.
    Conclusions: Cy plus IL-12 immunotherapy can eradicate nonimmunogenic tumors as long as a preexisting immunity is established in the tumor-bearing host. Furthermore, the STAT6 pathway is likely involved in the suppression of the development of host antitumor immunity.
    MeSH term(s) Animals ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Breast Neoplasms/drug therapy ; Cyclophosphamide/pharmacology ; Immunohistochemistry ; Immunotherapy, Adoptive ; Interleukin-12/pharmacology ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Neoplasms, Experimental/drug therapy ; Signal Transduction ; Transcription Factors/drug effects
    Chemical Substances Transcription Factors ; Interleukin-12 (187348-17-0) ; Cyclophosphamide (8N3DW7272P)
    Language English
    Publishing date 2006-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1200469-8
    ISSN 1534-4681 ; 1068-9265
    ISSN (online) 1534-4681
    ISSN 1068-9265
    DOI 10.1245/ASO.2006.03.514
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    Zs.A 4042: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  10. Article: Cure of an established nonimmunogenic tumor, SCC VII, with a novel interleukin 12-based immunotherapy regimen in C3H mice.

    Mandpe, Aditi H / Tsung, Kangla / Norton, Jeffrey A

    Archives of otolaryngology--head & neck surgery

    2003  Volume 129, Issue 7, Page(s) 786–792

    Abstract: Objective: To develop a murine model of effective treatment with immunotherapy for established head and neck squamous cell carcinoma.: Design: Prospective animal study. Subjects Female C3H mice, 8 to 12 weeks old.: Interventions: A subcutaneous ... ...

    Abstract Objective: To develop a murine model of effective treatment with immunotherapy for established head and neck squamous cell carcinoma.
    Design: Prospective animal study. Subjects Female C3H mice, 8 to 12 weeks old.
    Interventions: A subcutaneous inoculation of 2 x 10(5) SCC VII cells in C3H mice was established for 7 to 12 days. Tests for concomitant immunity were performed, with and without interleukin 12 modification. Tumors were also tested for responsiveness to interleukin 12 (5 mice) and to cyclophosphamide followed by interleukin 12 (5 mice). SCC VII tumors in 24 mice were treated with interleukin 12 followed by cyclophosphamide and interleukin 12. Five mice with tumors treated with isotonic sodium chloride solution served as controls. Tumors were measured 3 to 4 times weekly, and cure was defined as complete regression of the tumor for at least 60 days. Cured mice were rechallenged with 2 x 10(5) SCC VII cells to verify antitumor immunity. Immunohistochemistry of regressing tumors was performed for CD4+ and CD8+ T cells.
    Results: Tumor-bearing mice easily developed second tumors when challenged with 2 x 10(5) tumor cells in the opposite flank. However, interleukin 12 treatment provided immunity to second tumors in 8 (100%) of 8 mice when started at day 4 and in 2 (40%) of 5 when treated from day 7. SCC VII did not respond to standard interleukin 12 or cyclophosphamide plus interleukin 12 therapy. Seventy-five percent of animals (18/24) treated with interleukin 12 followed by cyclophosphamide plus interleukin 12 were successfully cured, and all cured mice resisted subsequent challenge with SCC VII. Immunohistochemistry of regressed tumors showed an intense CD4+ and CD8+ infiltrate that was absent in the untreated and nonresponding tumors.
    Conclusions: Nonimmunogenic SCC VII is a nonimmunogenic tumor that can be converted into an immunogenic tumor with interleukin 12 treatment. Additional treatment with cyclophosphamide plus interleukin 12 leads to complete regression in 75% of mice.
    MeSH term(s) Adjuvants, Immunologic/therapeutic use ; Animals ; CD4 Antigens/metabolism ; CD8 Antigens/metabolism ; Carcinoma, Squamous Cell/drug therapy ; Carcinoma, Squamous Cell/immunology ; Carcinoma, Squamous Cell/metabolism ; Female ; Immunohistochemistry ; Immunotherapy ; Interleukin-12/therapeutic use ; Mice ; Mice, Inbred C3H ; Models, Animal ; Prospective Studies
    Chemical Substances Adjuvants, Immunologic ; CD4 Antigens ; CD8 Antigens ; Interleukin-12 (187348-17-0)
    Language English
    Publishing date 2003-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 632721-7
    ISSN 1538-361X ; 0886-4470 ; 2168-6181
    ISSN (online) 1538-361X
    ISSN 0886-4470 ; 2168-6181
    DOI 10.1001/archotol.129.7.786
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