Nursing 2050 Written Assignment: Nov 7, 2014 “Bladder Cancer drug BCG in short supply (Mellor, C. (2014, September 11)” read the headline of the Nova Scotia Chronicle Herald on Thursday, September 11, 2014. A manufacturing issue at Merck Canada Inc. in its North Carolina plant put a short supply to BCG (Bacillus Calmette-Guerin strain tice) sold under the name OncoTICE. “BCG is considered “gold standard” and mainstay for treating bladder cancer that has not invaded muscle tissue" as well as functioning as a tuberculosis vaccine. “BCG is an attenuated mycobacterium developed from the Mycobacterium bovis strain. The precise mechanism of action has not been clearly determined; however, the pronounced infiltration of the bladder wall by
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BCG makes initial contact with tumor cells by means of a fibronectin attachment protein, followed by internalization of the BCG in the cells directing a cell-mediated immunologic response. It has been found in recent studies to be a predominantly T-helper/inducer cell-mediated response with persistence of inflammatory cytokines (Th1-type) for a long time within the BCG- induced granulomas, which maybe be key factor in the recurrence-free state of the patient. The prolonged inflammation results in a continuous level of activating cytokines such as the Interleukin-2, Interferon-gamma and Interleukin-12. In laboratory, the two cellular cytotoxic effector mechanisms that have been determined are the commonly implicated leukocyte-activated killer (LAK) cell cytotoxicity and a newly distinguished cytotoxic phenomenon known as the ‘BCG-activated killer (BAK) cell phenomenon.’ The involved effector cells are the activated natural killer cells (NK cells), in which selectively kill malignant targets (Kapoor, R., Vijjan, V. & Singh, P. (2008))”. Research has also proven that the BCG not only has a local immune activation but “…some degree of a systemic response as well, determined by the multiple cytokines that may be
BCG makes initial contact with tumor cells by means of a fibronectin attachment protein, followed by internalization of the BCG in the cells directing a cell-mediated immunologic response. It has been found in recent studies to be a predominantly T-helper/inducer cell-mediated response with persistence of inflammatory cytokines (Th1-type) for a long time within the BCG- induced granulomas, which maybe be key factor in the recurrence-free state of the patient. The prolonged inflammation results in a continuous level of activating cytokines such as the Interleukin-2, Interferon-gamma and Interleukin-12. In laboratory, the two cellular cytotoxic effector mechanisms that have been determined are the commonly implicated leukocyte-activated killer (LAK) cell cytotoxicity and a newly distinguished cytotoxic phenomenon known as the ‘BCG-activated killer (BAK) cell phenomenon.’ The involved effector cells are the activated natural killer cells (NK cells), in which selectively kill malignant targets (Kapoor, R., Vijjan, V. & Singh, P. (2008))”. Research has also proven that the BCG not only has a local immune activation but “…some degree of a systemic response as well, determined by the multiple cytokines that may be