Expression of bcl‐2 in testicular carcinoma

Eid, Hanna; Gulyás, Miklós; Gergely, Lajos; Bodrogi, I.; Institoris, Etel; Bak, M.

doi:10.1002/(sici)1097-0142(19980715)83:2<331::aid-cncr17>3.3.co;2-3

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“…[6][7][8][9][10][11][12][13][14] By contrast, decreased expression of MT-1 and MT-2 is related to poor prognosis in patients with prostate, testicular, and liver tumors. [15][16][17][18] In nonpathological tissue, MT-1 and MT-2 are mainly present in the cytoplasm. In rapidly proliferating cells, however, MT-1 and MT-2 are translocated to the nucleus from the cytoplasm.…”

Section: Introductionmentioning

confidence: 99%

Expression of metallothionein‐1 and metallothionein‐2 as a prognostic marker in hepatocellular carcinoma

Park

2013

J of Gastro and Hepatol

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Section: Introductionmentioning

confidence: 99%

Expression of metallothionein‐1 and metallothionein‐2 as a prognostic marker in hepatocellular carcinoma

Park

2013

J of Gastro and Hepatol

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“…Burger and colleagues compared parental NT2 teratocarcinoma cells with NT2 cells expressing human papilloma virus E6 protein and found no di erences in chemosensitivity (Burger et al, 1999). However parental NT2 cells express low basal levels of p53 relative to most other teratocarcinoma cell lines (Burger et al, 1999) and clinical studies of germ cell tumors have demonstrated a positive correlation between degree of nuclear p53 immunoreactivity and response to treatment (Eid et al, 1997). Therefore studies utilizing NT2 cells do not address the potentially important role of high level wild-type p53 expression for the sensitivity of teratocarcinoma cells to DNA damage.…”

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confidence: 99%

A p53 dose-response relationship for sensitivity to DNA damage in isogenic teratocarcinoma cells

2001

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Teratocarcinomas are tumors that arise from primordial germ cells and are readily curable with DNA-damaging chemotherapeutic drugs. Teratocarcinoma cells ex vivo in tissue culture are also relatively chemosensitive and undergo apoptotic death in response to DNA damage. We have previously hypothesized that the observed sensitivity of this tumor type to DNA damage is related to high basal expression of wild-type p53 protein. We have now addressed this issue by characterizing the DNA damage response of isogenic teratocarcinoma cells that di er only in their level of expression of wild-type p53 protein. We ®nd a clear p53 dose-response relationship in these cells for rapid apoptosis following DNA damage that correlates with diminished colony formation in clonogenic survival assays. These results suggest that strategies to increase basal wild-type p53 protein expression prior to treatment with DNA-damaging drugs may improve curability in other tumor types. Oncogene (2001) 20, 2982 ± 2986.

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“…Chemostatic drugs are supposed to cause an inhibition or dysregulation of apoptosis [39]. Other mechanisms that have been implicated in the development of chemoresistance in cancers cells are modulation of enzymes involved in DNA repair [65][66][67], intracellular sequestration with metallothioneins [68], exocytosis in which proteins such as kinesins and dynines may be involved and modification of protein kinase C activity. These mechanisms are summarized in Fig.…”

Section: The Development Of Chemoresistancementioning

confidence: 99%

Proteomics for studying cancer cells and the development of chemoresistance

Hütter¹,

Sinha

2001

Proteomics

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Extensive studies during the last decades have identified several mechanisms through which cells escape the cytotoxic effects of a variety of chemotherapeutic drugs. One type of drug resistance is called multidrug resistance (MDR), because selection with one anticancer drug leads to cross-resistance with a wide range of other drugs. These MDR cells express frequently plasma transport proteins like p-glycoprotein. But cellular resistance to chemotherapy is multifactorial and may be affected by the cell cycle stage and proliferation status, biochemical mechanisms such as detoxification, cellular drug transport, or DNA replication and repair mechanisms. Several laboratory techniques, such as polymerase chain reaction, immunocytochemistry, flow cytometry, blotting, and fluorescent microscopy have been used for the identification of MDR markers and mechanisms. We review the possibilities in studying cancer biology and development of chemoresistance in cancer treatment using the proteomic approach.

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Expression of bcl‐2 in testicular carcinoma

Abstract: These findings revealed that bcl-2 expression occurs in GCTTs. Furthermore, they suggest that bcl-2 is associated with a more advanced malignant phenotype of this tumor.

Cited by 3 publications

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Expression of metallothionein‐1 and metallothionein‐2 as a prognostic marker in hepatocellular carcinoma

Expression of metallothionein‐1 and metallothionein‐2 as a prognostic marker in hepatocellular carcinoma

A p53 dose-response relationship for sensitivity to DNA damage in isogenic teratocarcinoma cells

Proteomics for studying cancer cells and the development of chemoresistance

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