Cell cycle arrest is an active response to stresses that enables organisms to survive under fluctuating environmental conditions. While signalling pathways that inhibit cell cycle progression have been elucidated, the putative core module orchestrating cell cycle arrest in response to various stresses is still elusive. Here we report that in Arabidopsis, the NAC-type transcription factors ANAC044 and ANAC085 are required for DNA damage-induced G2 arrest. Under genotoxic stress conditions, ANAC044 and ANAC085 enhance protein accumulation of the R1R2R3-type Myb transcription factor (Rep-MYB), which represses G2/M-specific genes. ANAC044/ANAC085-dependent accumulation of Rep-MYB and cell cycle arrest are also observed in the response to heat stress that causes G2 arrest, but not to osmotic stress that retards G1 progression. These results suggest that plants deploy the ANAC044/ANAC085-mediated signalling module as a hub which perceives distinct stress signals and leads to G2 arrest.
A human pancreatic cancer cell line (SUIT-2) and four sublines cloned in vitro (S2-007, S2-013, S2-020 and S2-028) were inoculated into nude mice for assessment of metastatic potentials. After 16 weeks of subcutaneous injection, the parent SUIT-2 line metastasized to the lungs and lymph nodes in three of six mice. S2-007 cells presented the highest metastatic potential in pulmonary (5/6) and lymph node (2/6) metastases among the four sublines. No metastasis was found in S2-028. The incidence of spontaneous pulmonary metastasis was correlated with that of pulmonary colonization after intravenous (i.v.) injection of cell clusters (r = 0.87, P = 0.056). Pulmonary colonization potential using single cells, however, did not always reflect a spontaneous metastatic ability. Type I collagenolytic activity in serum-free conditioned media of these cells was correlated effectively with the incidence of spontaneous pulmonary metastasis (r = 0.92, P = 0.026) and pulmonary colonization after i.v. injection of cell clusters (r = 0.95, P = 0.013). Thus, type I collagenolytic activity may possibly be essential to spontaneous cancer metastasis.
The production of carcino-embryonic antigen (CEA) and carbohydrate antigen 19-9 (CA19-9) were investigated in 28 clones isolated from a human pancreatic cancer cell line (SUIT-2) and related to in vitro morphology of the clones and in vivo tumorigenicity. Clones of fusiform and polygonal cells could be morphologically distinguished in confluent cultures. There was no significant difference in CEA production between fusiform-cell clones (2.10 +/- 2.70 ng/L x 10(6) per 24 h) and polygonal-cell clones (6.01 +/- 7.30 ng/L x 10(6) per 24 h), but polygonal-cell clones had higher production of CA19-9 (1176.1 +/- 1628.4 U/L x 10(6) per 24 h) than fusiform (6.0 +/- 7.3 U/L x 10(6) per 24 h; P < 0.01). Production of CA19-9 in vitro correlated with the histological grade of differentiation in vivo in nude mice (r = 0.73, P < 0.001), but CEA production did not. The polygonal-cell clones developed well-differentiated carcinomas in vivo and produced significantly more CA19-9 (P < 0.001) than fusiform-cell clones, which generally developed into poorly differentiated tubular adenocarcinomas in vivo. This cell line may provide an appropriate system for further studies of the biology and therapy of pancreatic cancer.
Sequential computed tomography (CT) scans were obtained in 30 patients with acute cerebral infarction. In some cases, infarction was seen on the scans as early as three to six hours after onset of symptoms. Although small areas of petechial hemorrhagic infarction are not easily detected by currently available equipment, positive contrast enhancement helps locate petechial hemorrhagic infarction, which is usually in the cortical gray matter of the cerebral mantle and the central gray matter of the deep central gray matter. Contrast-enhanced CT scans are a useful method for detecting small infarctions. However, when a CT scan is performed within five days of ictus, contrast enhancement is usually not required.
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