The use of an in vitro adenosine triphosphate-based chemotherapy response assay to predict chemotherapeutic response in breast cancer

Kim, Hyun Ah; Yom, Cha Kyong; Moon, Byung In; Choe, Kuk Jin; Sung, Sun Hee; Han, Woon Sup; Choi, Hye Young; Kim, Hye‐Kyoung; Park, Heung Kyu; Choi, Sung Ho; Yoon, Eun Jin; Oh, Seung Jin

doi:10.1016/j.breast.2007.06.001

Cited by 29 publications

(26 citation statements)

References 38 publications

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“…If the T/C ratio is low, we expect good therapeutic efficacy. The usefulness of chemosensitivity testing has been reported for various cancers, for example those of the gastrointestinal tract, lung, ovary, and breast, and malignant melanoma [5][6][7][8][9][10]. For gastric cancer, especially, the reported sensitivity, specificity, and accuracy of chemosensitivity testing are, respectively, 82.7, 70.7, and 73.6% [11].…”

Section: Introductionmentioning

confidence: 98%

ATP assay-guided chemosensitivity testing for gemcitabine with biopsy specimens obtained from unresectable pancreatic cancer using endoscopic ultrasonography-guided fine-needle aspiration

et al. 2011

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Section: Introductionmentioning

confidence: 98%

ATP assay-guided chemosensitivity testing for gemcitabine with biopsy specimens obtained from unresectable pancreatic cancer using endoscopic ultrasonography-guided fine-needle aspiration

et al. 2011

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“…It also has been demonstrated that downregulation of Bcl-2 in several breast cancer cells enhances their drug sensitivity to doxorubicin and taxanes [9]. However, in breast cancer tissues, Bcl-xL expression was not significantly associated with response to chemotherapy [10,11], whereas decreased Bax expression promotes drugs resistance [12] and it has been linked to poor clinical outcome in breast cancer [13]. Moreover, Bak downregulation suppressed taxol-induced apoptosis in MDA-MB-231 cells [1].…”

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confidence: 97%

Paclitaxel sensitivity of breast cancer cells requires efficient mitotic arrest and disruption of Bcl-xL/Bak interaction

Flores

Castilla

Ávila

et al. 2011

Breast Cancer Res Treat

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Taxanes are being used for the treatment of breast cancer. However, cancer cells frequently develop resistance to these drugs with the subsequent recurrence of the tumor. MDA-MB-231 and T-47D breast cancer cell lines were used to assess the effect of paclitaxel treatment on apoptosis and cell cycle, the possible mechanisms of paclitaxel resistance as well as the enhancement of paclitaxel-induced apoptosis based on its combination with phenylethyl isothiocyanate (PEITC). T-47D cells undergo apoptosis in response to paclitaxel treatment. The induction of apoptosis was associated with a robust mitotic arrest and the disruption of Bcl-xL/Bak interaction. By contrary, MDA-MB-231 cells were insensitive to paclitaxel-induced apoptosis and this was associated with a high percentage of cells that slip out of paclitaxel-imposed mitotic arrest and also with the maintenance of Bcl-xL/Bak interaction. The sequential treatment of MDA-MB-231 cells with PEITC followed by paclitaxel inhibited the slippage induced by paclitaxel and increased the apoptosis induction achieved with any of the drugs alone. In breast cancer tissues, high Bcl-xL expression was correlated with a shorter time of disease-free survival in patients treated with a chemotherapeutic regimen that contains paclitaxel, in a statistically significant way. Thus, resistance to paclitaxel in MDA-MB-231 cells is related to the inability to disrupt the Bcl-xL/Bak interaction and increased slippage. In this context, the combination of a drug that induces a strong mitotic arrest, such as paclitaxel, with another that inhibits slippage, such as PEITC, translates into increased apoptotic induction.

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“…Several approaches aim at giving the chemosensitivity status as quickly as possible before initiating systemic treatment: pharmacogenomic predictors [40] address the patient, while tumor-based tests either use in vitro response assays [41,42] or molecular profiling.…”

Section: Tp53 Status and Response To Chemotherapy In Breast Cancermentioning

confidence: 99%

<i>TP53</i> Status and Response to Chemotherapy in Breast Cancer

et al. 2008

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Despite its central role in the control of apoptosis, senescence and cell cycle arrest, the tumor suppressor protein p53 remains an enigma for its possible role in predicting response to chemotherapy in cancer patients. Many studies remained inconclusive, others showed a better response for tumors with normal p53, and some recent studies showed adverse effects of normal p53 for response to treatment. p53 is not only a powerful pro-apoptotic factor in response to drug-induced DNA damages but also a potential inducer of cell cycle arrest, protecting tumor cells from further cytotoxic damages. Our review describes the classical as well as the more recent concepts. In order to draw definite conclusions, future works should use more reliable methods to assess the TP53 status and should address more homogeneous tumor subpopulations treated with homogeneous chemotherapy regimens.

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The use of an in vitro adenosine triphosphate-based chemotherapy response assay to predict chemotherapeutic response in breast cancer

Cited by 29 publications

References 38 publications

ATP assay-guided chemosensitivity testing for gemcitabine with biopsy specimens obtained from unresectable pancreatic cancer using endoscopic ultrasonography-guided fine-needle aspiration

ATP assay-guided chemosensitivity testing for gemcitabine with biopsy specimens obtained from unresectable pancreatic cancer using endoscopic ultrasonography-guided fine-needle aspiration

Paclitaxel sensitivity of breast cancer cells requires efficient mitotic arrest and disruption of Bcl-xL/Bak interaction

<i>TP53</i> Status and Response to Chemotherapy in Breast Cancer

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