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First regarding the references, we believe that one reference by Takeuchi et al1 was omitted due to formatting of the paper and was overlooked on our part. The references cited as 37-39 regard the Bcl2 knockout mice and are discussed and referred to later in the paper. Second, our paper dealt with mitomycin C MMC ; hypersensitivity of the Fancc mouse model we generated. We believe that our discussion is in fact an overview of the possible in vivo effects of MMC, and we did not dismiss oxygen radical formation as a possible effect during the metabolism of MMC. Nonetheless, one still does not know if reactive oxygen species ROS ; formation is responsible for the hypersensitivity of the Fancc mice treated with MMC, although we believe that the effect we observed may result from a defect in DNA repair. In fact, more information is now becoming available regarding a DNA repair defect in FA. 1. FA cells were shown to be specifically sensitive to interstrand crosslinks and not intrastrand crosslinks confirming the specificity of the defect in crosslink repair.2 2. FA cells were shown to lack a repair complex that specifically binds DNA crosslinks.3 3. The increased ROS-induced lesion 8OHdG, in FA patients cells also supports the idea of a lack of a repair mechanism; without repair, the lesions remain in the DNA. 4. FANCA and FANCC have been shown to interact in a complex and translocate to the nucleus; this implies a more direct role of FANCC in repair.4 5. FA cells have been shown to be defective in double-strand break repair.5 Oxidative DNA damage is repaired by the BER pathway, which may share steps with the crosslink repair pathway. Thus, increased sensitivity of FA cells to MMC caused by either oxidative damage or crosslinks, or both, support the notion of an altered repair mechanism. We did, however, discuss the possible effect of ROS formation in the toxicity of MMC. Although MMC is known to induce a wide variety of lesions in the DNA, several papers have described the inability of FA cells to repair crosslinked DNA as the principal cause of MMC sensitivity. Again, we do not dismiss ROS formation as a possible mechanism in the toxicity of MMC in the Fancc mice, and we would be more than willing to provide Dr Pagano with the Fancc mice if he wishes to test his hypothesis. Until we find the true function of the FA proteins, one can only speculate on the defects present in FA cells. Madeleine Carreau Manuel Buchwald Program in Genetics and Genomic Biology Research Institute Hospital for Sick Children Toronto, Ontario, Canada REFERENCES 1. Takeuchi T, Morimoto K: Increased formation of 8-hydroxydeoxyguanosine, an oxidative DNA damage, in lymphoblasts from Fanconi's anemia patients due to possible catalase deficiency. Carcinogenesis 14: 1115, 1993 Fujiwara Y, Nakamura M, Yokoo S: A new anticancer platinum compound, ; - R ; -2-aminomethyl-pyrrolidine 1, 1-cyclobutanedicar.

Studies in mice have shown enhanced mRNA expression for both IL-12R subunits in activated T cells in the presence of B7 accessory cells 45, 46 ; . Furthermore, it has been demonstrated in mice that CD28 costimulation, acting through IL-2, is necessary for both the normal expression of IL-12R 2 and subsequent differentiation of autoreactive effector cells 26 ; . This requirement for CD28 signaling may impact not only the level of IL-12R surface expression, but also the receptors ability to signal as well 47 ; . In human PBMC, IL-12R is not present on the surface of unstimulated cells, but can be induced by exogenous IL-2 alone. By contrast, induction of the IL-12R on PHA blasts appears to be largely IL-2-independent 48, 49 ; . In OKT3-stimulated PBMC, antiCD28 Ab has been reported to augment IL-12R 1 surface expression and IL-12 binding; however, these authors did not determine if this enhancement was IL-2-dependent 49 ; . Our studies demonstrate that IL-12R levels are undiminished on HAT-treated PBMC and thus cannot account for the deficit in IFN- production from these cultures. The results indicate that the.

Experiments with different concentrations of mitomycin C revealed that LDH activity was considerably increased at concentrations of 0.005% and higher P 0.01 ; . No significant differences in activity were noted at concentrations of 0.005%, 0.01%, 0.02%, and 0.06% Fig. 1A ; . LDH activity after treatment with 0.01% mitomycin C was time dependent and continued to increase until 24 hours Fig. 1B ; . In the group treated with mitomycin C, Hoechst 33342 staining clearly revealed apoptotic characteristics, such as nuclear condensation and shrinkage of cytoplasm Fig. 2 ; . In flow cytometric analyses of apoptotic cells using annexin V-FITC, untreated cells Fig. 3A ; were primarily annexin V-FITC and PI negative, indicating viability and no apoptosis. After treatment with 0.01% mitomycin C, a significant number of cells were annexin V-FITC positive and PI negative Figs. 3B, 3C ; , signifying that cells were in the early stages of apoptosis, but still viable. After 24 hours, the cells progressed to a later stage of apoptosis and stained positively for both PI and annexin V, indicating nonviability Fig. 3D ; . The CPP32-like inhibitor Z-VAD-FMK did not affect LDH activity triggered by 0.01% mitomycin C P 0.05; Fig. 4 ; . However, LDH activity was significantly decreased by the caspase-8 inhibitor, IETD-CHO, and the caspase-9 inhibitor, Z-LEHD-FMK P 0.03, 0.05, respectively; Figs. 5 and 6 ; . On immunostaining with cytochrome c, positive findings, such as a punctate appearance around the cytosol, were clearly noted in keratocytes Figs. 7B, 7C ; photographed and modicon.
TACE procedures TACE was performed with the infusion of a mixture of 520 mL of iodized oil contrast medium Lipiodol, Huaihai Pharmaceutical Factory, Shanghai, China ; , 1.0 g of 5-fluorouracil 5-Fu, Xudong Haipu Pharmaceutical Inc., Shanghai, China ; and 40-60 mg of cisplatin CDDP, Qilu Pharmaceutical Factory, Jinan, China ; or 30-50 mg of doxorubicin hydrochloride Adriamycin, Main Luck Pharmaceutical Inc., Shenzhen, China ; , and 10 mg of mitomycin Mytomycin-C C, Kyowa Hakko Kogyo, Tokyo, Japan ; , followed by 1 mm1 mm10 mm of gelatin sponge cubes Gelfoam. the 3rd Pharmaceutical Factory of Nanjing, Nanjing, China ; embolization. To preserve liver function as much as possible, we performed superselective TACE for the feeding arteries of each intrahepatic tumor. When there was an arterial portal shunt or main branch PVT, we performed TACE without lipiodol to prevent severe damage to the normal liver. TACE procedures were performed with a 4-wk interval, and the patients received 1 to 3 times. Radiotherapy Radiation treatment was given to patients placed in a supine position, with both arms raised above the head and the head in a natural position. The patients were immobilized in this position using a vacuum pillow TN-1, TOPSLANE, Shanghai, China ; with an oxygen mask 3 0005 000 cc min ; for respiratory suppression for CT simulator PQS 2000, Picker, USA ; . CT data were all transferred to a 3Dradiation treatment planning system STP 3.0, Leibinger, Freiburg, Germany ; by the network. The hepatic tumor, liver, kidneys, spinal cord, and gastroduodenal intestine of each patient were contoured and reconstructed to form a 3D representation. The radiation treatment volumes and treatment angles were designed according to the beam's-eye view technique to minimize critical organ injury. Each beam's shape was designed using a multileaf collimator or custommade block. Three-dimensional CT-based computerized treatment planning was used to determine the best combination of coplanar and noncoplanar portals. A dose-volume histogram DVH ; was generated from the stereotactic treatment planning system for each patient. Gross tumor volume GTV ; was defined as the hepatic tumor volume, visualized by three-dimensional computation of contrast CT-defined contours. Clinical target volume CTV ; was defined as GTV plus a 0.5 cm margin. Planning target volume PTV ; was defined as CTV plus a 0.5 cm margin at medial lateral ventral dorsal sides, but plus a 1.5-2 cm margin at cranial caudal sides to account for daily setup error and respiratory organ motion. Dose inhomogeneity of PTV should be within 7% of isocenter dose. Normal liver was defined as the total liver volume minus the GTV. The average volume of GTV for these 94 patients was 979623 mL. The average volume of whole liver was 1 790645 mL. The number of portals used for radiation treatment ranged from 2 to 6, with a median of 5. Ultimately, the radiotherapy volume involved a portion of the liver, and whole liver radiation was always avoided. 3D-CRT was started within 3-4 wk after TACE using a 6-MV linear accelerator CLINAC 600C D, Varian Assoc, USA.

Bleeding in the second half of pregnancy occurs in 4% of all pregnancies. In 50% of cases, vaginal bleeding is secondary to placental abruption or placenta previa. I. Clinical evaluation of bleeding second half of pregnancy A. History of trauma or pain and the amount and character of the bleeding should be assessed. B. Physical examination 1. Vital signs and pulse pressure are measured. Hypotension and tachycardia are signs of serious hypovolemia. 2. Fetal heart rate pattern and uterine activity are assessed. 3. Ultrasound examination of the uterus, placenta and fetus should be completed. 4. Speculum and digital pelvic examination should not be.
FIG. 3. Autoradiogram of polyacrylamide gels containing proteins synthesized either after mitomycin C treatment ofCloDF13: : Tnl plasmid-containing cells A and B ; or in minicells containing CloDF13 C and D ; and CloDF13: : Tnl plasmids E and F ; . A ; pC1304 + cells cloacin- B ; pC1302 + cells cloacin + C and D ; minicells containing CloDF13; E ; pC1302 + minicells; F ; pC1305 + cloacin- ; minicells and moxifloxacin.

Drugs, such as epirubicin, mitomycin C and 5-FU. These results extend studies on hematopoietic cells which demonstrate that Mcl-1 prolongs survival after exposure to chemotherapeutic drugs [52]. Our data also add to studies on other tumor types such as malignant melanoma and sarcoma, in which specific downregulation of Mcl-1 has been shown to sensitize cancer cells to chemotherapeutic drug-induced apoptosis [25, 26]. Direct targeting of Mcl-1 by antisense oligonucleotides has already been shown to sensitize the HCC cell line HepG2 as well as lung carcinoma cell lines to cisplatininduced apoptosis [18, 28]. However, in Huh7 cells, we did not observe enhanced cisplatin-induced apoptosis upon depletion of Mcl-1. This effect might be cell linespecific. Mcl-1 knockdown also augmented tumor cell death after inhibition of the pro-survival PI3K Akt pathway. This pathway contributes to apoptosis resistance in various malignancies. Active PI3K generates the phosphorylated lipid phosphatidylinositol-3, 4, 5-triphosphate PtdIns 3, 4, 5 ; P3 ; , leading to the recruitment and activation of other kinases such as Akt protein kinase B ; to the plasma membrane. Activated Akt induces strong cellular survival signals. We have already shown that the PI3K Akt pathway induces Mcl-1 expression in human hepatocytes [33]. In the current study, PI3K inhibition for 48 h led to apoptosis rates of about 20%. Downregulation of Mcl-1 significantly enhanced apoptosis induced by PI3K inhibition. Furthermore, Mcl-1 downregulation further augmented apoptosis caused by combination therapy with PI3K inhibition and chemotherapeutics. One of the downstream targets of Akt is the serine threonine kinase mTOR which is a promising candidate target in the PI3K Akt pathway in HCC [43]. In the current study, Mcl-1 downregulation slightly enhanced apoptosis induction in cells treated with chemotherapy and rapamycin. However, this treatment was not superior to the combination of Mcl-1 downregulation and chemotherapy without rapamycin. The Ras Raf MEK ERK pathway is another critical signaling cascade in HCC [38, 53]. Approaches to disable the MEK1 ERK pathway may also sensitize tumor cells to apoptosis induction. ERK phosphorylates and thereby activates downstream targets like the transcription factor c-Jun. In the current study, MEK1 inhibition by PD98059 with or without downregulation of Mcl-1 did not induce significant apoptosis rates in Huh7 cells. Mcl-1 downregulation, however, when combined with MEK1 inhibition and chemotherapy, triggered apoptosis in Huh7 cells. This treatment, however, did not induce higher apoptosis.

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