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[1.] Iam/Fragment 012 01 - Diskussion
Zuletzt bearbeitet: 2014-04-06 12:14:05 Guckar
Fragment, Gesichtet, Hawkins and Dawson 2006, Iam, KomplettPlagiat, SMWFragment, Schutzlevel sysop

Typus
KomplettPlagiat
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 12, Zeilen: 1-14
Quelle: Hawkins and Dawson 2006
Seite(n): 1654, Zeilen: r.col: 20-48
Systemic chemotherapy has had limited impact in HCC (Leung et al. 2002;Mathurin et al. 1998). Historically, radiation therapy (RT) has played a minor role in the management of patients with unresectable liver cancer, primarily because of the low tolerance of the whole liver to RT and challenges associated with delivering highly conformal, high-dose RT to liver tumors while sparing dose to the uninvolved liver. There is a below 5% risk of radiation-induced liver injury after uniform whole-liver RT of 28 to 35 Gy delivered over 3 weeks, (Emami et al. 1991;Leung et al. 2002) doses that are far less than those required to eradicate tumor. The most common liver toxicity observed in North America is radiation-induced liver disease (RILD), which is a clinical syndrome of anicteric hepatomegaly, ascites and elevated liver enzymes (particularly serum alkaline phosphatase) that occurs from 2 weeks to 3 months after external beam RT (Leung et al. 2002). Treatment for RILD consists of supportive measures and in the minority of patients, it can result in liver failure. Reactivation of viral hepatitis and precipitation of underlying liver disease also can occur after RT for HCC (Cheng et al. 2004b).

Cheng JC, Wu JK, Lee PC, Liu HS, Jian JJ, Lin YM, Sung JL, Jan GJ (2004b) Biologic susceptibility of hepatocellular carcinoma patients treated with radiotherapy to radiation-induced liver disease. Int J Radiat Oncol Biol Phys 60:1502-1509

Emami B, Lyman J, Brown A, Coia L, Goitein M, Munzenrider JE, Shank B, Solin LJ, Wesson M (1991) Tolerance of normal tissue to therapeutic irradiation. Int J Radiat Oncol Biol Phys 21:109-122

Leung TW, Tang AM, Zee B, Yu SC, Lai PB, Lau WY, Johnson PJ (2002) Factors predicting response and survival in 149 patients with unresectable hepatocellular carcinoma treated by combination cisplatin, interferon-alpha, doxorubicin and 5-fluorouracil chemotherapy. Cancer 94:421-427

Mathurin P, Rixe O, Carbonell N, Bernard B, Cluzel P, Bellin MF, Khayat D, Opolon P, Poynard T (1998) Review article: Overview of medical treatments in unresectable hepatocellular carcinoma--an impossible meta-analysis? Aliment Pharmacol Ther 12:111-126

Systemic chemotherapy has had limited impact in

HCC.31–33 [...]

Historically, radiation therapy (RT) has played a minor role in the management of patients with unresectable liver cancer, primarily because of the low tolerance of the whole liver to RT and challenges associated with delivering highly conformal, high-dose RT to liver tumors while sparing dose to the uninvolved liver. There is a >5% risk of radiation-induced liver injury after uniform whole-liver RT of 28 gray (Gy) to 35 Gy delivered over 3 weeks,34,35 doses that are far less than those required to eradicate tumor. The most common liver toxicity observed in North America is radiation-induced liver disease (RILD), which is a clinical syndrome of anicteric hepatomegaly, ascites, and elevated liver enzymes (particularly serum alkaline phosphatase) that occurs from 2 weeks to 3 months after external beam RT.35 Treatment for RILD consists of supportive measures, and, in the minority of patients, it can result in liver failure. Reactivation of viral hepatitis and precipitation of underlying liver disease also can occur after RT for HCC.36


31. Mathurin P, Rixe O, Carbonell N, et al. Review article: overview of medical treatments in unresectable hepatocellular carcinoma—an impossible metaanalysis? Aliment Pharmacol Ther. 1998;12:111-126.

32. Burroughs A, Hochhauser D, Meyer T. Systemic treatment and liver transplantation for hepatocellular carcinoma: two ends of the therapeutic spectrum. Lancet Oncol. 2004;5:409-418.

33. Leung TW, Tang AM, Zee B, et al. Factors predicting response and survival in 149 patients with unresectable hepatocellular carcinoma treated by combination cisplatin, interferon-alpha, doxorubicin and 5-fluorouracil chemotherapy. Cancer. 2002;94:421-427.

34. Emami B, Lyman J, Brown A, et al. Tolerance of normal tissue to therapeutic irradiation. Int J Radiat Oncol Biol Phys. 1991;21:109-122.

35. Lawrence TS, Robertson JM, Anscher MS, Jirtle RL, Ensminger WD, Fajardo LF. Hepatic toxicity resulting from cancer treatment. Int J Radiat Oncol Biol Phys. 1995;31:1237-1248.

36. Cheng JC, Wu JK, Lee PC, et al. Biologic susceptibility of hepatocellular carcinoma patients treated with radiotherapy to radiation-induced liver disease. Int J Radiat Oncol Biol Phys. 2004;60:1502-1509.

Anmerkungen

The copied text starts on the previous page: Iam/Fragment 011 30

Note that the copied material is not always correctly reproduced: ">5% risk" --> "below 5% risk".

Sichter
(Hindemith) Schumann

[2.] Iam/Fragment 012 16 - Diskussion
Zuletzt bearbeitet: 2014-03-12 19:32:39 Graf Isolan
BauernOpfer, Fragment, Gesichtet, Iam, Matsumura et al 2008, SMWFragment, Schutzlevel sysop

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Seite: 12, Zeilen: 16-17
Quelle: Matsumura et al 2008
Seite(n): 3099, Zeilen: right col. 28-33
[Induction of chemokines in tumors after irradiation has already been reported (Matsumura et al. 2008).] Evidence is accumulating that ionizing radiation (IR) therapy, a treatment modality routinely used to kill cancer cells, can modulate the expression of several [receptors and cytokines by cancer cells and tumor stroma, resulting in modifications of the tumor microenvironment that can be exploited to enhance the effects of immunotherapy (Demaria and Formenti 2007).]

Demaria S, Formenti SC (2007) Sensors of ionizing radiation effects on the immunological microenvironment of cancer. Int J Radiat Biol 83:819-825

Evidence is accumulating that ionizing radiation (IR) therapy, a treatment modality routinely employed to kill cancer cells, can modulate the expression of several receptors and cytokines by cancer cells and tumor stroma, resulting in modifications of the tumor microenvironment that can be exploited to enhance the effects of IT (reviewed in references 20 and 21).

20. Demaria S, Bhardwaj N, McBride WH, Formenti SC. Combining radiotherapy and immunotherapy: a revived partnership. Int J Radiat Oncol Biol Phys 2005;63:655–666. [PubMed: 16199306]

21. Demaria S, Formenti SC. Sensors of ionizing radiation effects on the immunological microenvironment of cancer. Int J Radiat Biol 2007;83:1–7. [PubMed: 17357435]

Anmerkungen

The source is mentioned right before the passage starts. Nothing has been marked as a citation though the wording (and one of the references) are identical. The take-over is continued on the next page.

Sichter
(Graf Isolan) Schumann

[3.] Iam/Fragment 012 18 - Diskussion
Zuletzt bearbeitet: 2014-03-12 19:43:41 Graf Isolan
BauernOpfer, Fragment, Gesichtet, Iam, Kamrava et al 2009, SMWFragment, Schutzlevel sysop

Typus
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Untersuchte Arbeit:
Seite: 12, Zeilen: 18-18
Quelle: Kamrava et al 2009
Seite(n): 1268, Zeilen: 1ff
12a diss Iam.png

Figure 6: The combined use of radiation, immunotherapy and angiogenesis inhibitors-by normalizing blood flow and lowering intratumoral pressure, angiogenesis inhibitors enable T cells to gain efficient access to the tumor, while increasing the necessary components for effective T-cell function at the tumor site. Furthermore, by reducing hypoxia, antiangiogenic agents allow for optimization of radiotherapy, thereby providing the immune system with a rich supply of tumor antigens while modulating tumor-cell phenotype for enhanced T-cell killing (adapted by Kamrava et al. 2009)


Kamrava M, Bernstein MB, Camphausen K, Hodge JW (2009) Combining radiation, immunotherapy, and antiangiogenesis agents in the management of cancer: the Three Musketeers or just another quixotic combination? Mol Biosyst 5:1262-1270

12a source Iam.png

Fig. 4 The combined use of radiation, immunotherapy, and angiogenesis inhibitors-by normalizing blood flow and lowering intratumoral pressure, angiogenesis inhibitors enable T cells to gain efficient access to the tumor, while increasing the necessary components for effective T-cell function at the tumor site. Furthermore, by reducing hypoxia, antiangiogenic agents allow for optimization of radiotherapy, thereby providing the immune system with a rich supply of tumor antigens while modulating tumor-cell phenotype for enhanced T-cell killing.

Anmerkungen

The source is given, but it is not clear to the reader that the image as well as the extensive caption have both been taken from it.

"adapted by Kamrava et al. 2009" should probably be "adopted from Kamrava et al. 2009"

Sichter
(Hindemith) Schumann


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