Biomedical subjects

P Lin

Publications and source records attributed to P Lin.

At least 127 records · Page 7Linked to original sources

PubMed1994

Failure to observe a relationship between bis-(beta-chloroethyl)sulfide-induced NAD depletion and cytotoxicity in the rat keratinocyte culture.

It has been proposed that the activation of poly(ADP-ribose) polymerase (Papirmeister et al., 1985), which results from the presence of strand breaks in bis-(beta-chloroethyl)sulfide (BCES) damaged DNA, causes depletion in the level of nicotinamide adenine dinucleotide (NAD) leading to cell death. This hypothesis has now been evaluated in the primary submerged culture of rat keratinocytes. The DNA content, the viable cell number, and the proliferative capability (measured by thymidine incorporation) of the culture were all reduced 48 h after exposure to 10 microM BCES. However, the total NAD level, that is, NAD+ plus NADH, was not changed at a dose of BCES lower than 50 microM. This observation was the same in both proliferating and early differentiating cultures. To further test this hypothesis, the modifying effect of inhibiting poly(ADP-ribose) polymerase on cytotoxicity in BCES-exposed cells was investigated. After exposure to 250 microM BCES, the NAD level was reduced to approximately 26 pmol/micrograms DNA. This value was increased to 34-49 pmol/micrograms DNA at both 24 and 48 h postexposure when the cultures were incubated in medium supplemented with 1-10 mM nicotinamide. Nevertheless, the decrease in the DNA content of the culture was not reversed. These results suggest that in the rat keratinocyte culture exposed to BCES, depletion of NAD is not a prerequisite for cell death.

Animals↗

PubMed1994

[Immunohistochemical observation of anti-human hepatocellular carcinoma monoclonal antibody HL2 in cancers].

Molecular weight of human hepatocellular carcinoma (HCC)-associated antigen-HL2 antigen was detected to be about 50,000 dalton by SDS-PAGE and Western blot. One hundred and twenty-seven paraffin sections of cancers and pathological liver tissue were tests by ABC immunohistochemical staining. MAb HL2 reacted with 62.7% HCC and also with 8 of the 10 stomach carcinomas but only with a few other digestive system carcinomas (pancreas carcinoma, rectum carcinoma and duodenum carcinoma) and hepatitis. MAb HL2 was negative in hepatocirrhosis and other tumors (vesica carcinoma, skin carcinoma, breast carcinoma, neurogliocytoma and carcinoma of the lung). The results suggest that MAb HL2 has values in diagnosis of HCC and differential diagnosis between HCC and other tumours. HL2 antigen might be a new tumor-associated antigen (TAA). Further study of HL2 antigen will significantly show the actions of TAA in the occurrence and development of tumor.

Antibodies, Monoclonal↗

PubMed1993

Humanized Mik beta 1, a humanized antibody to the IL-2 receptor beta-chain that acts synergistically with humanized anti-TAC.

Mik beta 1 is a mouse mAb directed at the beta-subunit of the human IL-2R (Tac) that inhibits IL-2 binding and inhibits IL-2 induction of large granular lymphocytes (LGL). Mik beta 1 alone does not inhibit IL-2-induced T-cell proliferation, but acts synergistically with anti-Tac to inhibit IL-2-induced proliferation of activated T cells. To evaluate these effects for possible therapy in humans, we constructed two humanized Mik beta 1 antibodies by combining the complementarity-determining regions of the murine antibody with human framework and constant regions. Compared with murine Mik beta 1, the two humanized Mik beta 1 antibodies, which differ in their degree of humanization, had similar affinities for IL-2R beta. The murine Mik beta 1 and one of the humanized Mik beta 1 antibodies were equivalent in competing for IL-2 binding to IL-2R beta and inhibiting IL-2 induction of LGL cytotoxicity. The activity of the second humanized antibody was significantly reduced. The three Mik beta 1 antibodies act synergistically to varying degrees with humanized anti-Tac to prevent IL-2-induced proliferation of activated T cells. This capacity to synergize paralleled their abilities to inhibit IL-2 binding. In addition, both humanized antibodies directed antibody-dependent cell-mediated cytotoxicity. We hope that humanized Mik beta 1 in combination with humanized anti-Tac will provide a new immunosuppressive therapy for the treatment of autoimmune diseases, graft-versus-host disease, and prevention of allograft rejection.

Amino Acid Sequence↗

PubMed1993

Purification and characterization of human recombinant IgE-Fc fragments that bind to the human high affinity IgE receptor.

The Fc-region of immunoglobulin E (IgE) comprising C epsilon 2, C epsilon 3, and C epsilon 4 domains is sufficient for binding to the alpha chain of the high affinity IgE-Fc receptor (Fc epsilon RI alpha). In order to identify the smallest Fc fragment capable of binding to the Fc epsilon RI alpha with high affinity, various regions of the IgE-Fc molecule were expressed in COS cells and investigated for their ability to bind Fc epsilon RI alpha. The smallest fragment that showed Fc epsilon RI alpha binding activity spans amino acids 329-547 and lacks the entire C epsilon 2 domain. Two active fragments, viz. Fc epsilon(315-547) (containing Cys328 which is responsible for interchain S-S bonding) and Fc epsilon(329-547), have been overexpressed in CHO cells and purified to homogeneity. The purified proteins bind to the Fc epsilon RI alpha with high affinity, similar to native IgE. SDS-polyacrylamide gel electrophoresis analyses indicate that Fc epsilon(315-547) is an S-S-linked dimer of apparent molecular mass of 68 kDa. Fc epsilon(329-547) appears on SDS-gel as three distinct bands at approximately 32 kDa, both under reducing and nonreducing conditions. However, size exclusion chromatography and analytical ultracentrifugation studies suggest that Fc epsilon(329-547) also remains associated as a dimer. The presence of N-linked glycosylation was detected in both proteins. The deglycosylated form of Fc epsilon(315-547) was isolated after Endo F/N-glycosidase F digestion and demonstrated to have binding activity comparable to that of the mock-digested protein. These results suggest that the presence of N-linked sugars is not necessary for Fc epsilon RI alpha binding. Both proteins blocked the release of histamine from RBL cells expressing human Fc epsilon RI alpha in a dose-dependent manner. The availability of these recombinant IgE-Fc proteins will be helpful in elucidating the key epitopes essential for the binding of IgE to its high affinity receptor.

Animals↗

PubMed1993

A comparison of flow cytometric and absorption cytometric DNA values as prognostic indicators for pancreatic carcinoma.

BACKGROUND: The DNA content of 30 adenocarcinomas of the head of the pancreas was measured by flow and absorption cytometric analysis. METHODS: Each of the patients in this study had curative pancreatoduodenectomy. The absorption cytometric measurements were done in a research laboratory, and the flow cytometric measurements were performed in a commercial laboratory. The DNA measurements were done on nuclei disaggregated from pancreatic cancer tissue blocks without the examiner knowing whether the patient had survived. RESULTS: Twenty-one of the 30 cancers were found to be aneuploid by absorption cytometric analysis, whereas only 1 of the 30 cancers was aneuploid by flow cytometric analysis. This difference was statistically significant (P < 0.001). CONCLUSIONS: Univariate and multivariate analyses showed that the absorption cytometric DNA measurements were stronger prognostic determinants for patient survival than were the flow cytometric DNA measurements, indicating that some caution may be warranted in the interpretation of commercially obtained DNA distributions of pancreatic carcinomas.

Analysis of Variance↗

PubMed1993

Disposition of SK&F L-190144 in rats and monkeys after oral, intravenous or ocular administration.

The objective of the study was to investigate the systemic disposition of 14C-SK&F L-190144 after single intravenous (10 mg kg-1) and oral (200 mg kg-1) doses to rats and after single intravenous and ocular doses (0.33 mg kg-1) to monkeys. After the intravenous dose, the blood concentration-time profile of 14C-SK&F L-190144 followed a rapid triexponential decline with half-lives of 2.5, 15, and 246 min in rats and 3, 19, and 2520 min in monkeys. The 14C-label in blood was mainly the parent compound. The terminal elimination half-life detected in rats using the urinary excretion rate-time data was 700 min. The total body clearance values were 17.6 +/- 2.1 (mean +/- SD, n = 6) and 1.11 +/- 0.41 (n = 4) ml min-1 kg-1 for rats and monkeys, respectively. Both species had similar values of volume of distribution at the terminal phase, 4 to 6 l kg-1, and similar excretion patterns, approximately 60 per cent and 30 per cent of the dose were excreted in the urine and feces, respectively. 14C-SK&F L-190144 was not absorbed orally in rats with the majority of the dose recovered in the feces. Following ocular administration to monkeys, the plasma drug concentrations peaked at 8 h post-dosing but did not reach a biexponential elimination phase until 18 h post-dosing, suggesting slow systemic absorption of drug from the ocular site. The monkeys excreted 42 per cent of the dose in urine and 50 per cent in feces after ocular administration. This increase in fecal excretion compared to the intravenous route of administration may have been due to the slow absorption by the ocular and nasal tissues altering the relative proportions of drug elimination via the renal and hepatic routes, or to a proportion of the dose passing into the gastrointestinal tract and exiting unabsorbed. Study results demonstrate similar excretion patterns and volume of distribution after intravenous administration in both species. The slow terminal elimination phase in monkeys was attributed to the low body clearance. The low oral bioavailability was possibly due to the poor partitioning behavior of the drug (logarithm of partition coefficient -2.6). A significant fraction of the dose was absorbed in the body via the ocular route.

Administration, Oral↗

PubMed1993

Evidence for altered cell-cycle traverse of the non-modal cells of the heteroploid MCa-11 line.

Classic stem cell theory states that the growth of heteroploid cell populations is due to the proliferation of 'main stemline' cells with modal DNA content and chromosome number. Cells with non-modal DNA content and chromosome number are thought to be blocked and/or destroyed at mitosis. To test this, we studied two chromosomally stable cell populations (mouse bone marrow and WCHE-5 cells) and one heteroploid, chromosomally diverse cell line (MCa-11). The heteroploid MCa-11 cells showed significant [3H]dT labelling for cells with DNA contents below the modal G0/G1 peak and above the modal G2 peaks (P < 0.001). This was consistent with the presence of cells with the non-modal DNA content that were engaged in replicative DNA synthesis. A percentage labelled mitosis analysis showed that MCa-11 cells with non-modal DNA content and chromosome number were able to complete mitosis, although with prolonged pre-karyokinetic time. These results suggest that many non-modal cells present in heteroploid cell populations are capable of continued proliferation.

Aneuploidy↗

PubMed1993

Measurement of DNA content and of tritiated thymidine and bromodeoxyuridine incorporation by the same cells.

We tested a method of measuring DNA content (Feulgen) and tritiated thymidine ([3H]-T) and bromodeoxyuridine (BrdU) incorporation by the same cell. Initial experiments showed that Feulgen hydrolysis denatured the DNA of fixed cells sufficiently to allow detection of incorporated BrdU with monoclonal antibodies. MCa-11 cells were then double-labeled with [3H]-T and BrdU, placed on slides, and Feulgen stained. Next, absorption cytometry was performed to measure the DNA content of randomly selected cells. Feulgen staining and the development and removal of either the [3H]-T or the BrdU grains after DNA measurements did not interfere with subsequent detection of the grains from the other label, and BrdU and [3H]-T can be used reliably in combination for identification of S-phase cells. This method may eventually allow the use of microscope-based image analysis to selectively measure the DNA contents and the BrdU/[3H]-T labeling of non-transformed stromal and cancer cells in solid tumors, thereby providing new insights into the growth kinetics of these heterogeneous cell populations.

Animals↗

PubMed1992

Phosphatidylcholine-specific phospholipase D-derived 1,2-diacylglycerol does not initiate protein kinase C activation in the RBL 2H3 mast-cell line.

We examined the role of phosphatidylcholine-specific phospholipase D (PC-PLD) in the IgE-dependent activation of protein kinase C (PKC) in RBL 2H3 cells (a model for mast-cell function). Cells were sensitized with mouse monoclonal anti-trinitrophenol (TNP) IgE (0.5 micrograms/ml) and were then triggered with an optimal concentration (10 ng/ml) of TNP-ovalbumin conjugate (TNP-OVA). This resulted in an immediate biphasic increase in the production of 1,2-diacylglycerol (DAG) and activation of PKC. The initial increase in DAG production reached a peak within 30 s, and the second phase reached a plateau within 5 min after stimulation. TNP-OVA-induced PC-PLD activation followed the initial increase in DAG formation in response to IgE-receptor cross-bridging, but coincided with the second peak. Phosphatidic acid (PA), derived from the PC-PLD pathway, is metabolized to DAG by the action of PA phosphohydrolase (PAPase). Propranolol (0.3 mM), which inhibits PAPase, blocked the IgE-dependent increase in DAG, activation of PKC, and subsequently degranulation. The PKC inhibitor staurosporine (0.1 microM) inhibited the second, but not first, peak of DAG accumulation, reversed PKC translocation after 10 min and inhibited subsequent mediator release. Taken together, these results demonstrate that PC-PLD does not initiate, but may play a latent role in, IgE-dependent DAG production, PKC activation and mediator release from RBL 2H3 cells.

Alkaloids↗

PubMed1992

The role of calcium and protein kinase C in the IgE-dependent activation of phosphatidylcholine-specific phospholipase D in a rat mast (RBL 2H3) cell line.

Our previous studies have suggested that phosphatidylcholine-specific phospholipase D (PtdCho-PLD) plays a role in IgE-dependent diacylglycerol production, protein kinase C activation and mediator release in the RBL 2H3 mast cell line. We have extended these studies to examine the mechanisms by which PtdCho-PLD may be regulated in these cells. RBL 2H3 cellular lipids were labeled with [14C]arachidonic acid or [3H]myristic acid, then PtdCho-PLD activity was monitored by the formation of radiolabeled phosphatidylethanol when ethanol was included in the incubation medium. Trinitrophenol-ovalbumin conjugate (10 ng/ml), when added to cells previously sensitized with anti-(trinitrophenelated mouse IgE) (0.5 microgram/ml), ionomycin (1 microM) and thapsigargin (0.1 microM), stimulated PtdCho-PLD activation and mediator release in cells incubated in buffer containing 1.8 mM calcium, but not in cells incubated in calcium-free, buffer. Phorbol 12-myristate 13-acetate (0.1 microM) activated PtdCho-PLD in both buffers, but on its own did not trigger mediator release. When intracellular calcium was chelated with 5,5'-dimethyl-1,2-bis(2- aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, trinitrophenol-ovalbumin conjugate failed to activate PtdCho-PLD and histamine release. Similarly, down-regulation of protein kinase C activity by long-term exposure to the phorbol ester (0.1 microM) and preincubation of the cells with protein kinase inhibitors resulted in the loss of the trinitrophenol-ovalbumin response on PtdCho-PLD activity and histamine release. Taken together, the above results suggest that IgE-dependent PtdCho-PLD activation is dependent on both activation of protein kinase C and a rise in the intracellular free calcium concentration.

Alkaloids↗

PubMed1992

Activation of human factor VII by the prothrombin activator from the venom of Oxyuranus scutellatus (Taipan snake).

The crude venom of Oxyuranus scutellatus (Taipan snake) was found to cleave single-chain human factor VII to yield a two-chain molecule indistinguishable from authentic factor VIIa by SDS-polyacrylamide gel electrophoresis. A protease that activates factor VII was purified from this venom by a combination of gel permeation and ion-exchange chromatography. Characterization of the venom factor VII activator revealed its apparent identity with the Oxyuranus scutellatus prothrombin activator. The purified venom prothrombin activator was observed to activate factor VII by limited proteolysis in a reaction that was greatly potentiated by calcium and phospholipids (75% phosphatidyl choline/25% phosphatidylserine). Treatment of the venom protease with 0.8 M NaSCN weakly inhibited its ability to activate factor VII indicating that, in contrast to prothrombin activation, the factor Va-like component of this oligomeric enzyme complex was not essential for the activation of factor VII.

Amino Acid Sequence↗

PubMed1991

Reduced immunogenicity and improved pharmacokinetics of humanized anti-Tac in cynomolgus monkeys.

The anti-Tac mAb has been shown to bind to the p55 chain of the IL-2R, block IL-2 binding and inhibit T cell proliferation. A humanized form of anti-Tac (HAT) has been constructed that retains the binding properties of murine anti-Tac (MAT). These two mAb were evaluated in cynomolgus monkeys to compare relative immunogenicity and pharmacokinetic properties. Monkeys treated with HAT daily for 14 days exhibited anti-HAT antibody titers which were 5- to 10-fold lower than their MAT-treated counterparts and these antibodies developed later than in the MAT-treated monkeys. Two of four monkeys receiving a single injection of MAT developed anti-MAT antibodies, whereas none of four monkeys developed antibodies after a single treatment with HAT. In monkeys injected with either HAT or MAT daily for 14 days, the anti-antibody titers induced were inversely related to the amount of anti-Tac administered. Antibodies that developed against MAT were both anti-isotypic and anti-idiotypic, whereas those developed against HAT appeared to be predominantly anti-idiotypic. The pharmacokinetic properties, that is the half-life and area under the curve values, of HAT were also significantly different from those of MAT. The area under the curve values for HAT in naive monkeys were approximately twofold more than those for MAT, and the mean serum half-life of HAT was 214 h, approximately four- to fivefold more than MAT. These pharmacokinetic values were reduced in monkeys previously sensitized with HAT or MAT suggesting that the presence of anti-antibodies altered these parameters.

Animals↗

PubMed1991

High affinity human IgE receptor (Fc epsilon RI). Analysis of functional domains of the alpha-subunit with monoclonal antibodies.

The binding of IgE to the high affinity Fc epsilon receptor (Fc epsilon RI) on mast cells and basophils is mediated by the alpha-subunit of the tetrameric receptor complex. Based on sequence homologies, the 50-kDa alpha-subunit is a member of the immunoglobulin superfamily of proteins and has two predicted disulfide-bonded loops. Monoclonal antibodies specific for the human alpha-subunit have been identified and separated into two major classes: inhibitory and noninhibitory antibodies. Inhibitory antibodies (i.e. 15A5) block 125I-IgE binding to a recombinant chimeric alpha-subunit (ch-alpha-protein) expressed on Chinese hamster ovary cells and immunoprecipitate 125I-labeled purified ch-alpha-protein. Noninhibitory antibodies (i.e. 22E7) immunoprecipitate both 125I-labeled ch-alpha-protein and the soluble complex of 125I-IgE cross-linked to ch-alpha-protein but do not block 125I-IgE binding to the ch-alpha-protein expressed on Chinese hamster ovary cells. Both classes of antibodies bind to natural Fc epsilon RI present on human basophils and induce histamine release from these cells. Inhibitory antibody 15A5 specifically binds to a peptide corresponding to amino acids 125-140 of the putative second domain of the alpha-subunit sequence. All the inhibitory antibodies compete with 125I-15A5 for binding to the ch-alpha-protein, indicating that these antibodies recognize inhibitory epitopes that are either identical or sterically overlapping. Noninhibitory antibodies (i.e. 22E7) do not block 125I-15A5 binding to the ch-alpha-protein. These data suggest that antibodies binding to the predicted second domain of the alpha-subunit can inhibit IgE binding to the alpha-subunit, while antibodies binding at a distance from this site do not inhibit IgE binding. These inhibitory antibodies may block IgE binding to the ch-alpha-protein by direct overlap, steric inhibition, or induced conformational changes of the receptor contact points for IgE.

Animals↗

PubMed1991

Excitation of nitrogen by fast H3+ ions.

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Journal Article↗

PubMed1991

Establishment and preliminary application of spermidine radioimmunoassay with 125I-labelled monoclonal antibody and solid phase antigen.

Purified anti-spermidine monoclonal antibody was labelled with radioactive iodine by the Iodogen method and spermidine-bovine serum albumin (SPD-BSA) conjugate was used to coat polystyrene beads as solid phase antigen. The new solid phase 125I-labelled spermidine radioimmunoassay (RIA) depends on the competition between spermidine in the sample and the solid phase antigen for the limited amount of 125I-labelled monoclonal antibody. The sensitivity of this assay was 10 ng/ml higher than that of liquid RIA for spermidine with 14C-labelled spermidine. The coefficients of variation (CV) within and among batches were 4% and 13% respectively. The sample-batch capacity was increased from 20 (liquid RIA with 14C-labelled spermidine) to 150-200 by using this method. Because of its simplicity, the solid phase RIA kit is very convenient for population survey. This RIA could be used to determine spermidine in saliva for the diagnosis of precancerous lesions. In a preliminary study saliva spermidine levels in different populations were measured among 130 normal subjects, 202 esophageal epithelial hyperplasia cases treated with anti-tumor B for 5 years, 207 esophageal epithelial hyperplasia cases as control, and 55 esophageal cancer patients. The levels were 1,795 +/- 1,481, 3,470 +/- 6,981, 9,753 +/- 17,641 and 18,090 +/- 21,509 ng/ml, respectively, with the saliva spermidine levels in precancerous and cancer patients being significantly higher than that of normal subjects (P less than 0.001); the level in patients treated with anti-tumor B was significantly lower than that of controls (P less than 0.001). This decreased saliva spermidine content was coincident with the 47.3% reduction of canceration rate seen in precancerous patients after a 5-year treatment with anti-tumor B.

Antibodies, Monoclonal↗

PubMed1991

Progress in studies on the antimutagenicity and anticarcinogenicity of green tea epicatechins.

An antioxidative fraction was extracted from green tea and the major compounds in the fraction identified as epicatechins. Experimental results showed that green tea epicatechin compounds (GTEC) inhibited the mutagenicity and/or chromosomal damage caused by different carcinogens in both bacterial and mammalian cells. In vitro, GTEC inhibited transformation of BALB/3T3 cells induced by BP, X-rays, or MCA/TPA. In vivo, green tea extract decreased the incidence of carcinoma in the forestomach and esophagus of mice induced by sarcosine and NaNO2. GTEC inhibited the development of gamma-glutamyl transpeptidase-positive foci in the livers of rats treated with diethyl nitrosamine (DEN) or DEN/phenobarbital. Our investigations indicate that the antimutagenic and anticarcinogenic mechanisms of GTBC are related to the following: increased glutathione-S-transferase activity; inhibition of edema, hyperplasia, and ODC activity induced by TPA; free radical scavenging; blocked tumor promoter-induced inhibition of intercellular communication; and enhanced cell-mediated immunity. GTEC might be useful in the prevention of some kinds of cancer and a variety of oxidation-related diseases.

Animals↗

PubMed1990

Studies on medicamentous inhibitory therapy for esophageal precancerous lesions--3- and 5-year inhibitory effects of antitumor-B, retinamide and riboflavin.

Since 1983, we have been conducting inhibitory therapy for precancerous lesions of the esophagus in two regions of Henan Province considered high-risk areas of esophageal carcinoma. Our goal was to effect a 50% reduction in the canceration rate of marked esophageal dysplasia. By means of a cytological survey, 2531 cases of marked esophageal dysplasia and 3393 cases of mild esophageal dysplasia were selected. The former were randomly divided into 3 groups for antitumor-B (ATB, a mixture of Chinese herbs), retinamide (4-ethoxycarbophenylretinamide) and placebo treatment respectively, and the latter into 2 groups treated with riboflavin and placebo respectively. Treatment was continued for 3 or 5 years (administration rate greater than 90% in all groups) and esophageal cytology reexamined (reexamination rates were 94.1% and 92.5% respectively). Our results were as follows: 1) ATB 3- and 5-year subjects saw the canceration rate of marked esophageal dysplasia drop by 52.2% and 47.3% respectively as compared to control (P less than 0.01). 2) Retinamide lowered the canceration rate by 37.3% after a 3-year treatment period, with this reduction reaching 43.2% after an additional 2 years of treatment with increased dosages (P less than 0.05, P less than 0.01). 3) In the riboflavin group, the canceration rate of mild esophageal dysplasia was reduced by 22.2% and 34.8% after 3 and 5 years of treatment respectively, but these differences were not statistically significant. The above results verify the efficacy of medicamentous inhibitory therapy for esophageal precancerous lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

[Medicamentous inhibitory therapy of precancerous lesions of the esophagus--3 and 5 year inhibitory effect of antitumor B, retinamide and riboflavin].

9633 subjects aged 40 to 65 were sampled from high-risk areas for esophageal cancer and examined by esophageal exfoliative cytology. 2531 and 3393 cases of markedly and mildly dysplastic patients were screened out respectively. Those with marked dysplasia were randomized into 3 groups and given respective medications: antitumor B (Chinese herbs), 4-ethoxycarbophenylretinamide (retinamide) and placebo. The subjects with mild dysplasia were randomly divided into 2 groups for riboflavin and placebo treatment. After medication for 3 or 5 years the subjects were reexamined by esophageal exfoliative cytology. The incidence of esophageal cancer in the antitumor B group after taking medication for 3 and 5 years was reduced by 52.2% and 47.3% respectively as compared with the placebo group. These differences were statistically significant (chi 2 = 8.9115, P less than 0.01; chi 2 = 10.9573, P less than 0.01). The incidence of esophageal cancer in the retinamide group after 3 years of medication was reduced by 37.3% as compared with control, while the incidence among patients treated for 5 years dropped by 43.2% relative to control. This difference was statistically significant (chi 2 = 9.2836, P less than 0.01). The incidence of esophageal cancer in the riboflavin group was reduced by 22.2% and 34.8% respectively. The above results indicate that secondary prevention of esophageal cancer is possible and that inhibitory therapy of precancerous lesions of the esophagus is effective in preventing esophageal cancer. This method needs further trial and study in high risk areas of esophageal cancer. The reliability of the experimental results is critically discussed.

Adult↗