[Survival analysis for laryngeal carcinoma patients with no surgery, radiotherapy or chemotherapy].

OBJECTIVE: To investigate the survival rate and prognostic factors of laryngeal carcinoma patients with no surgery, radiotherapy or chemotherapy. METHODS: One hundred and sixty-seven laryngeal carcinoma cases with no surgery, radiotherapy or chemotherapy were analyzed retrospectively. Survival rates were calculated by Kaplan-Meier product-limit method. With univariate analysis, comparisons among/between groups were performed using Log-rank test. Multivariate analysis was carried out using Cox proportional hazard model. RESULTS: Overall survival time was (16.0 ± 1.4) months (x(-) ± s), overall 1- and 2-year survival rates were 56.4% and 26.5%, respectively. No patient survived over 5 years in these cases who had been diagnosed more than 5 years (except for those who lost). Univariate analysis showed that primary site, pathological grade, T-stage, N-stage and clinical stage were significant prognostic factors for the survival of the patients (P < 0.05). The survival rates of laryngeal carcinoma whether with tracheotomy were no statistically significant (P > 0.05). Multivariate analysis showed survival rates statistically correlated with T stage and N stage (hazard ratio were 1.812 and 1.557, P < 0.05). CONCLUSIONS: The development of laryngeal carcinoma course was faster, without treatment to the tumor itself, even if palliative surgical such as tracheostomy would not improve the survival rate. In laryngeal carcinoma patients with no surgery, radiotherapy or chemotherapy, the factors affecting the survival rates include primary site, pathological grade, T-stage, N-stage and clinical stage, and of them, T-stage and N-stage are the independent prognostic factors.

[RNA interference targeting c-Met inhibits proliferation of human laryngeal carcinoma Hep-2 cell line in vitro and in its xenografts in nude mice].

OBJECTIVE: The proto-oncogene c-Met was found to express on human laryngeal carcinoma Hep-2 cell line in previous research. In the present study, the author further examined whether inhibition of c-Met by RNA interference (RNAi) might inhibit biologic activity of Hep-2 cell line in vitro and proliferation using a murine laryngeal carcinoma model. METHODS: RNAi plasmid that can express small interfering RNA targeting c-Met or siRNA that did not match any known human coding mRNA(control siRNA plasmid)was designed, constructed, and transfected into Hep-2 cell line by using cationic liposome Lipofectamine2000 as transfecting agent. In vitro, the transfection efficacy was tested by RT-PCR and Western Blot method, then elected the most inhibitive c-Met-siRNA sequence. Cell proliferation, movement and invasion were studied using MTT, cell migration assay and cell invasion assay, respectively. The Hep-2 cells were transplanted into nude mice, then the time of tumor formation and growth were observed. After tumor formation, c-Met-siRNA was given as the anti-tumor therapy. Expression of c-Met, MMP-9 and VEGF were detected by Western Blot method. RESULTS: After the pSilencer2.0/c-Met-shRNA recombinant plasmid transfection into laryngeal carcinoma Hep-2 cells, the expression of mRNA and protein of c-Met decreased significantly in Hep-2 cells. On the 35th day after tumor vaccination, the tumor volume was (138 ± 27) mm³ in c-Met-siRNA transfection group, Which was diminished significantly in contrast with control group (P < 0.01). The expression of c-Met, MMP-9 and VEGF in the tumor of experiment group was decreased significantly, respectively (P < 0.05). CONCLUSIONS: The results indicated that c-Met-siRNA can down-regulate the expression of c-Met and markedly inhibit laryngeal carcinoma Hep-2 cell proliferation, movement and invasion and the growth of transplantation tumor of nude mice. The siRNA expressing plasmid mediated gene therapy might be a new strategy in targeting molecular therapy of cancer of larynx.

The interaction between interferon-induced protein with tetratricopeptide repeats-1 and eukaryotic elongation factor-1A.

It has been shown previously that in mammalian cells, interferon-induced protein with tetratricopeptide repeats-1(IFIT1) is rapidly synthesized in response to viral infection, functions as an inhibitor of translation by binding to the eukaryotic initiation factor-3, and consequently assigns resistive activity against viral invasion to cells. It has also been reported that IFIT1 is rapidly produced in response to other cell stress agents with no direct relation to virus such as bacterial lipopolysaccharide and interleukin-1, but its function under these non-viral infection cell stress conditions has yet to be elucidated. Here, we demonstrate an interaction between IFIT1 and eukaryotic elongation factor-1A (eEF1A) both in vitro, using recombinant proteins as bait in pull-down assays, and in vivo, using laser confocal microscopy and immunoprecipitation. In addition, we report the initial determination of the domain of IFIT1 that mediates this interaction. We also display that both IFIT1 and eEF1A protein levels are rapidly elevated, prolonged in tumor necrosis factor alpha pre-treated Raw264.7 cells, and most of those cells are induced to death by the end of investigations. Our results imply that under some stressful stimulations IFIT1 may participate in cell death pathways by interaction with eEF1A.

{N'-[(E)-(5-Bromo-2-oxidophen-yl)(phen-yl)methyl-ene]benzohydrazidato}pyridine-copper(II).

The asymmetric unit of title complex, [Cu(C(20)H(13)BrN(2)O(2))(C(5)H(5)N)], contains two independent mol-ecules. In each mol-ecule, the central Cu(II) atom has a square-planar environment formed by the tridentate hydrazone and the monodentate pyridine ligands, with the N atoms in a trans arrangement about the Cu(II) atom.

(meso-5,7,7,12,14,14-Hexamethyl-1,4,8,11-tetra-azacyclo-tetra-deca-4,11-diene)nickel(II) bis-[O,O'-bis(4-methyl-phen-yl) dithio-phosphate].

In the title compound, [Ni(C(16)H(32)N(4))](C(14)H(14)O(2)PS(2))(2) or [Ni(trans[14]dien)][S(2)P(OC(6)H(4)Me-4)(2)](2), where trans[14]dien is meso-5,7,7,12,14,14-hexa-methyl-1,4,8,11-tetra-azacyclo-tetra-deca-4,11-diene, the Ni(II) ion lies across a centre of inversion and is four-coordinated in a relatively undistorted square-planar arrangement by the four N atoms of the macrocyclic ligand trans[14]dien. The two O,O'-di(4-methyl-phen-yl)dithio-phos-phates act as counter-ions to balance the charge. Important geometric data include Ni-N = 1.9135 (16) and 1.9364 (15) Å.

{N'-[(E)-(5-Bromo-2-oxidophen-yl)(phenyl)-methyl-ene]-4-chloro-benzo-hydrazidato}pyridine-nickel(II).

The asymmetric unit of title complex, [Ni(C(20)H(12)BrClN(2)O(2))(C(5)H(5)N)], contains one complex with the central Ni atom in a slightly distorted square-planar environment, formed by the tridentate hydrazone and the monodentate pyridine ligands, with N atoms in a trans arrangement about the Ni atom.

N'-[(E)-(5-Bromo-2-hydroxy-phen-yl)(phen-yl)methyl-ene]benzohydrazide.

In the title compound, C(20)H(15)BrN(2)O(2), the C=N double bond displays a trans configuration. The crystal structure features an intra-molecular O-H⋯N hydrogen bond.

{N'-[(E)-1-(5-Bromo-2-oxidophen-yl)ethyl-idene]-4-chloro-benzohydrazidato}pyridinenickel(II).

The title complex, [Ni(C(15)H(10)BrClN(2)O(2))(C(5)H(5)N)], displays a square-planar coordination geometry around the Ni(II) ion, formed by the tridentate hydrazone and monodentate pyridine ligands, with the N atoms in a trans arrangement about the Ni center.

{N'-[(E)-(5-Bromo-2-oxidophen-yl)(phen-yl)methyl-ene]benzohydrazidato}pyridine-nickel(II).

The asymmetric unit of title complex, [Ni(C(20)H(13)BrN(2)O(2))(C(5)H(5)N)], contains two independent mol-ecules. In each mol-ecule, the central Ni(II) atom has a square-planar environment, formed by the tridentate hydrazone and the monodentate pyridine ligands, with the N atoms in a trans arrangement about the Ni(II) atom.

N'-[(E)-(5-Bromo-2-hydroxy-phen-yl)(phen-yl)methyl-idene]-4-chloro-benzo-hydrazide.

The Schiff base, C(20)H(14)BrClN(2)O(2), displays a trans conformation with respect to the C=N double bond. The aromatic rings at either end of the -C(=O)-NH-N=C- fragment are nearly parallel [dihedral angle = 3.4 (5)°]. The hydr-oxy group forms an intra-molecular hydrogen bond to the imino N atom.

(5-Bromo-2-hydroxy-phen-yl)(phen-yl)methanone.

In the title compound, C(13)H(9)BrO(2), the dihedral angle between the aromatic ring planes is 53.6 (1)°. The crystal structure is stabilized by intra-molecular O-H⋯O and inter-molecular C-H⋯O hydrogen bonding and C-H⋯π inter-actions.

N'-[(E)-1-(5-Bromo-2-hydroxy-phen-yl)ethyl-idene]benzohydrazide.

The C=N double bond in the title compound, C(15)H(13)BrN(2)O(2), is transE configured and the dihedral angle between the aromatic ring planes is 22.3 (1)°. The crystal structure is stabilized by intra-molecular O-H⋯O and inter-molecular N-H⋯O hydrogen bonds.

[Tuberculosis of pharynx and larynx: a report of 32 cases].

OBJECTIVE: To evaluate the trends and the clinical changes in tuberculosis of pharynx and larynx. METHODS: The clinical data of 32 patients with tuberculosis of pharynx and larynx from Jan. 1982 to Dec. 2000 in Daping hospital were studied retrospectively. RESULTS: (1) The local manifestations were mainly single lesion that commonly involved the vocal cord (10 cases). (2) The lesions appearances were mainly the proliferation such as mass (11 cases) or granulation(8 cases). (3) anti-tuberculosis is the main treatment, the operation is the second. Twelve patients cured in clinic, six patients received operation and cured without any complications. Fourteen patients condition controlled. CONCLUSION: The classical manifestations with tuberculosis of pharynx and larynx were not exited, the new clinical manifestations were associated with local lesion in nowadays.