Fwd: Resection of a locally advanced hilar tumor and the hepatic artery after stepwise hepatic arterial embolization: A case report.

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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Sat, Jun 21, 2008 at 6:01 PM
Subject: Resection of a locally advanced hilar tumor and the hepatic artery after stepwise hepatic arterial embolization: A case report.
To: mesothelioma77@gmail.com


[1]World J Gastroenterol. 2008 Jun 14; 14(22): 3587-90
Miura T, Hakamada K, Ohata T, Narumi S, Toyoki Y, Nara M, Ishido K, Ohashi M, Akasaka H, Jin H, Kubo N, Ono S, Kijima H, Sasaki M

We herein report a case of a hilar tumor with extensive invasion to the proper hepatic artery, which was successfully treated with a radical resection in a 57-year-old female patient after a stepwise hepatic arterial embolization. She underwent right colectomy and partial hepatectomy for advanced colon cancer two years ago and radiofrequency ablation therapy for a liver metastasis one year ago, respectively. A recurrent tumor was noted around the proper hepatic artery with invasion to the left hepatic duct and right hepatic artery 7 mo previously. We planned a radical resection for the patient 5 mo after the absence of tumor progression was confirmed while he was undergoing chemotherapy. To avoid surgery-related liver failure, we tried to promote the formation of collateral hepatic arteries after stepwise arterial embolization of the posterior and anterior hepatic arteries two weeks apart. Finally, the proper hepatic artery was occluded after formation of collateral flow from the inferior phrenic and superior mesenteric arteries was confirmed. One month later, a left hepatectomy with hepatic arterial resection was successfully performed without any major complications.



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Source: http://www.hubmed.org/display.cgi?uids=18567092
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Fwd: Man saved by new cancer treatment

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From: Search for lung cancer <rssfwd@rssfwd.com>
Date: Sat, Jun 21, 2008 at 6:01 PM
Subject: Man saved by new cancer treatment
To: mesothelioma77@gmail.com

An Oregon man, given less than a year to live, had a complete remission of advanced deadly skin cancer after an experimental treatment that revved up his immune system to fight the tumours.

Sat, 21 Jun 2008 07:00:00 GMT

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Source: http://timestranscript.canadaeast.com/rss/article/331771
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Fwd: Enzymatic metabolites of lycopene induce Nrf2-mediated expression of phase II detoxifying/antioxidant enzymes in human bronchial epithelial cells.

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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Sat, Jun 21, 2008 at 6:01 PM
Subject: Enzymatic metabolites of lycopene induce Nrf2-mediated expression of phase II detoxifying/antioxidant enzymes in human bronchial epithelial cells.
To: mesothelioma77@gmail.com


[1]Int J Cancer. 2008 Jun 19;
Lian F, Wang XD

Lycopene can be cleaved by carotene 9',10'-oxygenase at its 9',10' double bond to form apo-10'-lycopenoids, including apo-10'-lycopenal, -lycopenol and -lycopenoic acid. The latter has been recently shown to inhibit lung carcinogenesis both in vivo and in vitro, however, the mechanism(s) underlying this protection is not well defined. In the present study, we report that treatment with apo-10'-lycopenoic acid, in a time- and dose-dependent manner, results in the nuclear accumulation of transcription factor Nrf2 (nuclear factor E(2)-related factor 2) protein in BEAS-2B human bronchial epithelial cells. The activation of Nrf2 by apo-10'-lycopenoic acid is associated with the induction of phase II detoxifying/antioxidant enzymes including heme oxygenase-1, NAD(P)H:quinone oxidoreductase 1, glutathione S-transferases, and glutamate-cysteine ligases in BEAS-2B cells. Furthermore, apo-10'-lycopenoic acid treatment increased total intracellular glutathione levels and suppressed both endogenous reactive oxygen species generation and H(2)O(2)-induced oxidative damage in BEAS-2B cells. In addition, both apo-10'-lycopenol and apo-10'-lycopenal induced heme oxygenase-1 gene expression in BEAS-2B cells. These data strongly suggest that the anti-carcinogenic and antioxidant functions of lycopene may be mediated by apo-10'-lycopenoids via activating Nrf2 and inducing phase II detoxifying/antioxidant enzymes. (c) 2008 Wiley-Liss, Inc.



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Source: http://www.hubmed.org/display.cgi?uids=18566994
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Fwd: Significant antitumor activity in vivo following treatment with the microtubule agent ENMD-1198.

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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Sat, Jun 21, 2008 at 6:02 PM
Subject: Significant antitumor activity in vivo following treatment with the microtubule agent ENMD-1198.
To: mesothelioma77@gmail.com


[1]Mol Cancer Ther. 2008 Jun; 7(6): 1472-82
Lavallee TM, Burke PA, Swartz GM, Hamel E, Agoston GE, Shah J, Suwandi L, Hanson AD, Fogler WE, Sidor CF, Treston AM

Clinical studies using the microtubule-targeting agent 2-methoxyestradiol (2ME2; Panzem) in cancer patients show that treatment is associated with clinical benefit, including prolonged stable disease, complete and partial responses, and an excellent safety profile. Studies have shown that 2ME2 is metabolized by conjugation at positions 3 and 17 and oxidation at position 17. To define structure-activity relationships for these positions of 2ME2 and to generate metabolically stable analogues with improved anti-tubulin properties, a series of analogues was generated and three lead analogues were selected, ENMD-1198, ENMD-1200, and ENMD-1237. These molecules showed improved metabolic stability with >65% remaining after 2-h incubation with hepatocytes. Pharmacokinetic studies showed that oral administration of the compounds resulted in increased plasma levels compared with 2ME2. All three analogues bind the colchicine binding site of tubulin, induce G(2)-M cell cycle arrest and apoptosis, and reduce hypoxia-inducible factor-1alpha levels. ENMD-1198 and ENMD-1200 showed improved in vitro antiproliferative activities. Significant reductions in tumor volumes compared with vehicle-treated mice were observed in an orthotopic breast carcinoma (MDA-MB-231) xenograft model following daily oral treatment with all compounds (ANOVA, P

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Source: http://www.hubmed.org/display.cgi?uids=18566218
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Fwd: Finding early invasive breast cancers: a practical approach.

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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Sat, Jun 21, 2008 at 6:02 PM
Subject: Finding early invasive breast cancers: a practical approach.
To: mesothelioma77@gmail.com


[1]Radiology. 2008 Jul; 248(1): 61-76
Harvey JA, Nicholson BT, Cohen MA

Detection of early invasive breast cancer is important, as patient survival is high when the cancer is 2 cm or smaller. Invasive breast cancers typically manifest mammographically as focal asymmetries or masses. Strategies for detecting focal asymmetries and masses on screening mammograms include side-by-side comparison, looking for parenchymal contour deformity, close inspection of the retromammary fat, identifying the presence of associated findings, and comparison with prior mammograms. Focal asymmetries are often normal but are concerning when there is distortion of the normal breast architecture. Masses and focal asymmetries are best evaluated in the diagnostic setting by using spot compression and true lateral views and, frequently, ultrasonography. Management of a lesion depends on the worst imaging feature. Indications for an assessment of probably benign findings are very specific but are often misapplied. This review for residents provides a practical approach to the detection and management of breast masses and focal asymmetries.



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Source: http://www.hubmed.org/display.cgi?uids=18566169
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Fwd: ISG15 as a novel tumor biomarker for drug sensitivity.

---------- Forwarded message ----------
From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Sat, Jun 21, 2008 at 6:02 PM
Subject: ISG15 as a novel tumor biomarker for drug sensitivity.
To: mesothelioma77@gmail.com


[1]Mol Cancer Ther. 2008 Jun; 7(6): 1430-9
Desai SD, Wood LM, Tsai YC, Hsieh TS, Marks JR, Scott GL, Giovanella BC, Liu LF

Tumor cells are known to exhibit highly varied sensitivity to camptothecins (CPT; e.g., irinotecan and topotecan). However, the factors that determine CPT sensitivity/resistance are largely unknown. Recent studies have shown that the ubiquitin-like protein, IFN-stimulated gene 15 (ISG15), which is highly elevated in many human cancers and tumor cell lines, antagonizes the ubiquitin/proteasome pathway. In the present study, we show that ISG15 is a determinant for CPT sensitivity/resistance possibly through its effect on proteasome-mediated repair of topoisomerase I (TOP1)-DNA covalent complexes. First, short hairpin RNA-mediated knockdown of either ISG15 or UbcH8 (major E2 for ISG15) in breast cancer ZR-75-1 cells decreased CPT sensitivity, suggesting that ISG15 overexpression in tumors could be a factor affecting intrinsic CPT sensitivity in tumor cells. Second, the level of ISG15 was found to be significantly reduced in several tumor cells selected for resistance to CPT, suggesting that altered ISG15 regulation could be a significant determinant for acquired CPT resistance. Parallel to reduced CPT sensitivity, short hairpin RNA-mediated knockdown of either ISG15 or UbcH8 in ZR-75-1 cells resulted in increased proteasomal degradation of CPT-induced TOP1-DNA covalent complexes. Taken together, these results suggest that ISG15, which interferes with proteasome-mediated repair of TOP1-DNA covalent complexes, is a potential tumor biomarker for CPT sensitivity. [Mol Cancer Ther 2008;7(6):1430-9].



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Source: http://www.hubmed.org/display.cgi?uids=18566215
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