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PubMed2002

Feeding fish meal and extruded soybeans enhances the conjugated linoleic acid (CLA) content of milk.

Twelve multiparous Holstein cows averaging 65 (33 to 122) DIM were used in a 4 x 4 Latin square for 4-wk periods to determine whether feeding fish oil as fish meal would stimulate increased amounts of milk conjugated linoleic acid (cis-9, trans-11 C18:2; CLA) and transvaccenic acid (trans-11 C18:1; TVA) when the cows were fed extruded soybeans to supply additional linoleic acid. Treatment diets were 1) control; 2) 0.5% fish oil from fish meal; 3) 2.5% soybean oil from extruded soybeans; and 4) 0.5% fish oil from fish meal and 2% soybean oil from extruded soybeans. Diets were formulated to contain 18% crude protein and were composed (dry basis) of 50% concentrate mix, 25% corn silage, and 25% alfalfa hay. Intake of DM was not affected by diet. Milk production was increased by diets 2, 3, and 4 compared with diet 1 (control). Milk fat and milk protein percentages decreased with diets 3 and 4. Milk fat yield was not affected by treatments, but yield of milk protein was increased with supplemental fish meal and extruded soybeans or their blend. When diets 2, 3, or 4 were fed, concentrations of cis-9, trans-11 CLA in milk fat increased by 0.4-, 1.4-, and 3.2-fold, and TVA concentrations in milk fat increased by 0.4-, 1.8-, and 3.5-fold compared with the control milk fat. Increases in TVA and cis-9, trans-11 CLA were 91 to 109% greater when a blend of fish meal and extruded soybeans was fed than the additive effect of fish meal and extruded soybeans. This suggested that fish oil increased the production of CLA and TVA from other dietary sources of linoleic acid such as extruded soybeans.

Animal Feed↗
PubMed2002

Effect of conjugated linoleic acid on the formation of spontaneous and PhIP-induced mutation in the colon and cecum of rats.

Conjugated linoleic acid (CLA), a mixture of positional and geometric isomers of linoleic acid, has been reported to inhibit chemically induced mammary and colon carcinogenesis in rodents. In a preliminary experiment, we found that CLA significantly reduced the induction of mutations by the dietary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in the distal colon in male rats. Here, the chemopreventive properties of CLA were further evaluated by assessing its effect on PhIP-induced mutation and aberrant crypt foci (ACF) in both male and female rats. CLA (1%, w/w) was added to the diet (1) from weaning to 50-day-old, or (2) starting 1 week prior to exposure to PhIP. The 50-day-old Big Blue and F344 rats were then exposed to 100 ppm PhIP for 47 days. No sex differences were observed in mutagenic response to the various treatments in either the distal colon or cecum. The mutation frequency (MF) in the cecum and the distal colon from control animals is 4.3+/-1.3 and 5.3+/-1.4 x 10(-5), respectively showing no statistically significant difference. Administration of PhIP induced a four-fold increase in the MF in the cecum and a seven-fold increase in the distal colon compared to the corresponding controls. Supplementation of the diet with CLA lowered the PhIP-induced MF in the distal colon by 23% (P<0.03), but had no effect in the cecum. The PhIP-induced ACF, determined 9 weeks after the termination of treatment with PhIP, were 0.75 ACF/rat, with 1.7 aberrant crypts /ACF in the colon of male rats, all located in the distal colon. This induction was completely inhibited by the addition of CLA.

Animals↗
PubMed1977

[Behavior of alpha-tocopherol during the autoxidation of linoleic acid in aqueous solution].

Addition of great quantity of alpha-tocopherol to an aqueous solution containing linoleic acid dispersed with twen 20 conduce to an important augmentation of the rate of formation of linoleic hydroperoxides. In these particular conditions, alpha-tocopherol have a prooxidant effect. In the same time, alpha-tocopherol is rapidly transformed into tocopherylquinone and a dimer of alpha-tocopherol. Transitorily there is formation of a dihydroxydimer of alpha-tocopherol. Comparison of these compounds behaviour on the oxydation rate of linoleic acid in the same conditions show a near relation between a prooxidant effect and chemical structure of these compounds as well as alpha-tocopherol. So, alpha-tocopherol and its dihydroxydimer are both prooxidant and both have a free hydroxyl on carbon 6. Dimer of alpha-tocopherol and tocopherylquinone are both antioxidant and they have neither free hydroxyl on carbon 6. alpha-tocopherol acetate in the same conditions have an antioxidant comportment. This confirms the importance of free hydroxyl on carbon 6 to obtain a prooxidant effect.

Antioxidants↗
PubMed2002

Conjugated linoleic acid differentially modifies fatty acid composition in subcellular fractions of muscle and adipose tissue but not adiposity of postweaning pigs.

This study examined the interaction between conjugated linoleic acid (CLA) and dietary fat type on the enrichment of subcellular fractions, the Delta(9) desaturase index and adiposity in pigs. Early weaned piglets (n = 6/group) were fed for 35 d diets supplemented with 15 g/100 g diet beef tallow or corn oil, or 12 g/100 g tallow or corn oil plus 3 g CLA. There were no effects of dietary fat or CLA on the mass of dissected skin, bone, muscle or adipose tissue of the 7th to 9th thoracic rib sections. Medial subcutaneous adipose tissue of pigs fed tallow had smaller adipocytes than that of pigs fed corn oil. The lateral subcutaneous site was unaffected by dietary fat type. Microsomes accumulated <50% the concentration of trans-10,cis-12, cis-11,trans-13, and cis-9,trans-11 CLA as membrane and nonmembrane fractions of adipose tissue and longissimus muscle. There was no evidence of preferential incorporation of any CLA isomer into any of the subcellular fractions. Addition of CLA to the diets reduced adipose tissue nonmembrane monounsaturated fatty acids (MUFA; g/100 g total fatty acids) by 15% in corn oil-fed pigs and by 19% in tallow-fed pigs. Total saturated fatty acids (SFA) were increased by CLA commensurately in this lipid fraction. This resulted in a reduced Delta(9) desaturase index [MUFA/(SFA + MUFA)] in the nonmembrane lipid fraction of pigs fed either the corn oil or tallow diets. Thus, in spite of marked effects on fatty acid composition and the Delta(9) desaturase index, CLA had no effect on adiposity in early weaned piglets fed high fat diets.

Adipose Tissue↗
PubMed2002

Effects of dietary conjugated linoleic acid on fatty acid composition, lipid oxidation, color, and water-holding capacity of pork loin.

The effects of dietary conjugated linoleic acid (CLA) on fatty acid composition, lipid oxidation, and pork quality were investigated. Pigs (n = 20) were fed a diet containing 0, 1, 2.5, or 5% CLA for 4 wk and slaughtered at 105 kg. The longissimus thoracis et lumborum muscle was collected at 24 h postmortem. Pork loin chops (3 cm thick) were packaged aerobically and stored at 4 degrees C for 7 d. Samples were analyzed for ultimate pH, intramuscular fat content, fatty acid composition, thiobarbituric acid-reactive substances, color (L*, a*, b*), and water-holding capacity. Dietary CLA reduced the concentration of linoleic acid and increased CLA concentration in intramuscular fat of pork loin (P < 0.05). The concentration of CLA in muscle was increased with dietary CLA level and did not change during storage. Thiobarbituric acid-reactive substance value of control was higher than that of the CLA-fed groups (P < 0.05). Intramuscular fat content was increased by dietary CLA, and less purge loss was observed with samples from CLA-fed pigs (P < 0.05). Dietary CLA improved the color stability of pork loin during cold storage. After 7 d, lightness (L*) and yellowness (b*) of the 5% CLA-fed group were significantly lower than those of control (P < 0.05). The results indicated that the water-holding capacity of pork loin was increased with increased intramuscular fat content apparently caused by dietary CLA. Also, the data indicated that color stability of pork was improved with inhibition of lipid oxidation and changing of fatty acid composition by dietary CLA.

Animals↗
PubMed1998

Dietary methionine level affects linoleic acid metabolism through phosphatidylethanolamine N-methylation in rats.

The effects of dietary methionine level on the profiles of fatty acids and phospholipids and on the plasma cholesterol concentration were investigated to confirm whether the methionine content of dietary proteins is one of the major factors that cause differential effects on lipid metabolism. The effect of dietary supplementation with eritadenine, which is shown to be a potent inhibitor of phosphatidylethanolamine (PE) N-methylation, was also investigated. Rats were fed six diets containing casein (100 g/kg) and amino acid mixture (86.4 g/kg) differing in methionine content (2.5, 4.5, and 7.5 g/kg) and without or with eritadenine supplementation (30 mg/kg) for 14 d. The ratio of arachidonic to linoleic acid of liver microsomal and plasma phosphatidylcholine (PC) was significantly increased as the methionine level of diet was elevated, indicating that dietary methionine stimulates the metabolism of linoleic acid. The PC/PE ratio of liver microsomes and the plasma cholesterol concentration were also increased by dietary methionine. These effects of methionine were completely abolished by eritadenine supplementation The S-adenosylmethionine concentration in the liver reflected the methionine level of diet. These results support the idea that the differential effects of dietary proteins on lipid metabolism might be ascribed, at least in part, to their different methionine contents, and that methionine might exert its effects through alteration of PE N-methylation.

Adenine↗
PubMed2002

Synergistic antioxidant effect of catechin and malvidin 3-glucoside on free radical-initiated peroxidation of linoleic acid in micelles.

The inhibitory effect of anthocyanins has been investigated in the peroxidation of linoleic acid in micelles in the presence and in the absence of (+)-catechin. The peroxidation was initiated by thermal decomposition of 2,2(')-azobis[2-(2-imidazolin-2-yl)propane], and the kinetics of peroxidation were followed by measuring the rate of oxygen consumption and the rate of disappearance of the antioxidant. The analysis of the antioxidant effect of various anthocyanins, alone or in the presence of catechin, demonstrates that catechin, which is relatively inefficient at inhibiting linoleic acid oxidation, regenerates the highly efficient antioxidant malvidin 3-glucoside and, at a lower extent, peonidin 3-glucoside. The malvidin 3-glucoside recycling by catechin strongly increases the antioxidant efficiency of these two antioxidants. This protective mechanism appears specific for malvidin and peonidin 3-glucosides. The high unpaired spin density of the phenolic O atoms in the radicals generated by these anthocyanins, calculated by the semiempirical quantum chemical AM1 method, may explain the observed behavior.

Anthocyanins↗
PubMed2006

Selective effect of conjugated linoleic acid isomers on atherosclerotic lesion development in apolipoprotein E knockout mice.

Research suggests that conjugated linoleic acid (CLA) may inhibit atherosclerosis, but there are contradictory results in different animal models fed heterogeneous mixtures of CLA isomers. This study addressed the hypothesis that the individual CLA isomers may exert different atherogenic properties. ApoE(-/-) mice were fed isocaloric, isonitrogenous westernized diets containing 0.15% cholesterol and enriched with 1% (w/w) cis-9,trans-11-CLA (c9,t11-CLA), trans-10,cis-12-CLA (t10,c12-CLA) or linoleic acid (control diet) for 12 weeks. At the end of the dietary intervention, the effects of CLA isomers on the development of atherosclerotic vascular lesions, lipid metabolism, inflammation and oxidative stress were assessed. The t10,c12-CLA diet had a profound pro-atherogenic effect, whereas c9,t11-CLA impeded the development of atherosclerosis. En face aortic lesion assessment showed more dorsal and lumbar extensions presenting atherosclerotic foci after the t10,c12-CLA diet. Furthermore, animals fed t10,c12-CLA had pronounced hyperlipidemia, higher 8-iso-prostaglandin F(2alpha) levels, higher vulnerable atherosclerotic plaque with a lower smooth muscle and fibre contents and higher macrophage content and activation, assayed as plasma chitotriosidase compared to the control or c9,t11-CLA dietary groups. Plasma chitotriosidase activity was more closely associated with the extent of the plaque than with MOMA staining or than monocyte chemoattractant protein-1 levels. Our results demonstrate that CLA isomers differentially modulate the development of atherosclerosis, c9,t11-CLA impedes, whereas t10,c12-CLA promotes atherosclerosis. These opposing effects may be ascribed to divergent effects on lipid, oxidative, inflammatory and fibro muscular components of this pathology. Plasma chitotriosidase is a better indicator of dietary fat interventions that alter plaque monocyte activity in this murine model.

Animals↗
PubMed2002

Antioxidant effect of beta-carotene on lipid peroxidation and synergism with tocopherol in an emulsified linoleic acid model system.

The antioxidant effect of beta-carotene was investigated in an emulsified linoleic acid model system with or without exposure to light. The effect of tocopherol on the antioxidant action of beta-carotene was also investigated. The antioxidant effect of beta-carotene was significant, and synergistically increased by the addition of rac alpha-tocopherol, in the dark but not in the light. It was#10; confirmed that superoxide anions (O(2)(-)) and hydrogen peroxide (H(2)O(2)) were formed during the light exposure, and that their formation could be significantly inhibited by the addition of tryptophan or mannitol, scavenger of hydroxyl radicals. These results strongly suggest direct participation of hydroxyl radicals, formed via the Haber-Weiss reaction, in the emulsified linoleic acid model system, with beta-carotene inhibition in the dark but an increase in the light. Regarding the mechanism of the antioxidant effect of beta-carotene, when beta-carotene is oxidized, the hydroperoxide in the acts as an electron acceptor and the hydroperoxide itself then decomposes.

Antioxidants↗
PubMed2002

Conjugated linoleic acids (CLAs) regulate the expression of key apoptotic genes in human breast cancer cells.

Conjugated linoleic acid (CLA) reduces mammary tumorigenesis in rodent models, induces apoptosis in rodent mammary tumor cell lines, and decreases expression of antiapoptotic bcl-2 in rat mammary tissue. This investigation focused on the cell mechanisms underlying the antitumor effects of CLA. Changes (mRNA, protein) in expression of major proapoptotic p53, p21WAF1/CIP1, bax, bcl-Xs genes, and the antiapoptotic bcl-2 gene were observed in malignant MCF-7 and MDA-MB-231 cells and in benign MCF-10a human mammary tumor cells in culture. CLA, but not linoleic acid (LA), inhibited proliferation in all cells; CLA mix was most effective. CLA increased DNA damage (apoptosis). CLA increased mRNA expression of p53 and p21WAF1/CIP1 (three- to fivefold and twofold, respectively) but either decreased bcl-2 by 20-30% or had no effect in MCF-7 and MCF-10a cells, respectively; protein expression reflected mRNA values. In MDA-MBA-231 (mutant p53) cells, mRNA for p53 was not changed, but p21WAF1/CIP1 and bcl-2 mRNA was increased. Protein expression largely reflected mRNA changes but, surprisingly, CLA completely suppressed mutant p53 protein in MDA-MB-231 cells. Apparent antiapoptotic effects of increased bcl-2 expression in MDA-MBA-231 cells were countered by increased proapoptotic p21WAF1/CIP1, Bax, and Bcl-Xs proteins. Findings indicate that CLA elicits mainly proapoptotic effects in human breast tumor cells through both p53-dependent and p53-independent pathways, according to cell type.

Apoptosis↗
PubMed2006

Response to conjugated linoleic acid in dairy cows differing in energy and protein status.

The trans-10, cis-12 conjugated linoleic acid (CLA) isomer inhibits milk fat synthesis, whereas milk yield and synthesis of other milk components generally remain unchanged in established lactation. However, in some CLA studies increases in milk yield, milk protein yield, or both have been observed in cows limited in energy, either in early lactation or when grazing pasture. Our objective was to evaluate the performance and monitor peripheral tissue responses to homeostatic signals regulating lipolysis and glucose uptake with CLA supplementation when cows were limited in metabolizable energy in combination with moderate or excess metabolizable protein supply. Holstein cows (n = 48; 112 +/- 5 d in milk; mean +/- SE) were provided ad libitum access to a diet that met energy and protein requirements for a 16-d standardization interval. Based on performance during this interval, the Cornell Net Carbohydrate and Protein System was used to design energy-limiting rations that provided 80% of metabolizable energy requirements, and these were fed throughout the treatment periods. Cows were randomly allocated to 4 treatments, in a 2-period crossover design. Treatments were 1) moderate metabolizable protein (MP) supply, 2) moderate MP supply + CLA, 3) excess MP supply, and 4) excess MP supply + CLA. Moderate and excess MP supply were at 88 and 117%, respectively, of the MP requirement established during the standardization period, as estimated by the Cornell Net Carbohydrate and Protein System. Each experimental period comprised 16 d, with crossover of CLA within each protein level. The lipid-encapsulated CLA supplement provided 12 g/d of trans-10, cis-12 CLA. Conjugated linoleic acid treatment reduced milk fat yield by 21% but increased milk yield and milk protein yield by 2.6 and 2.8%, respectively. Milk yield and content and yield of both milk protein and fat were unaltered by either protein treatment alone or in combination with CLA. Basal concentrations of glucose, insulin, and nonesterified fatty acids were unaffected by CLA supplementation. The fractional rate of glucose clearance in response to an insulin challenge and the nonesterified fatty acid response to an epinephrine challenge were also not altered by either CLA treatment or MP supply. Overall, the results demonstrate that CLA supplementation when cows are energy-limited allows for repartitioning of nutrients, resulting in increased yields of milk and milk protein, and this can occur without changes in whole-body glucose homeostasis and adipose tissue response to lipolytic stimuli.

Animal Feed↗
PubMed1975

Serum linoleic acid in multiple sclerosis.

Total serum fatty acids were analyzed in 30 patients with multiple sclerosis and in 33 controls. No significant decrease in linoleic acid was found in the patients with multiple sclerosis. A disturbance in linoleic acid metabolism is not inevitably associated with this disease.

Adult↗
PubMed2005

Effects of conjugated linoleic acid on liver composition and fatty acid oxidation are isomer-dependent in hamster.

OBJECTIVE: The present work was designed to study the effects of the two main isomers of conjugated linoleic acid (CLA), cis-9,trans-11 and trans-10,cis-12, on liver composition and hepatic fatty acid oxidation in hamsters. METHODS: Animals were divided into three groups that were fed atherogenic diets supplemented with 0.5% linoleic acid, cis-9,trans-11 CLA, or trans-10,cis-12 CLA for 6 wk. Liver lipids, protein, water and DNA contents, and histologic structure were analyzed. Hepatic carnitine palmitoyltransferase-I and acyl coenzyme A oxidase activities were assessed. Triacylglycerol concentration, and aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase, and alkaline phosphatase activities were evaluated in serum. CLA isomer contents were analyzed by gas chromatography in hepatic triacylglycerols. Peroxisome proliferator-activated receptor-alpha mRNA was determined by reverse transcriptase polymerase chain reaction. RESULTS: Trans-10,cis-12 CLA led to significantly greater weight, lower levels of triacylglycerol, cholesterol, and phospholipid, and larger total cell number in liver. Carnitine palmitoyltransferase-I and acyl coenzyme A oxidase activities were significantly increased by this isomer. No changes were induced by cis-9,trans-11 CLA. Trans-10,cis-12 CLA was recovered in significantly lower proportions than cis-9,trans-11 in liver triacylglycerols. Histopathologic analysis showed no abnormalities. No significant differences in serum aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase, and alkaline phosphatase activities or in hepatic mRNA peroxisome proliferator-activated receptor-alpha expression were found among the three experimental groups. CONCLUSIONS: These results suggest that the addition of 0.5% of these CLA isomers to the diet do not induce toxic effects in liver after 6 wk of feeding. Intake of trans-10,cis-12 isomer but not of cis-9,trans-11 CLA increases liver fatty acid oxidation. This effect leads to decreased hepatic and serum triacylglycerols.

Acyl-CoA Oxidase↗
PubMed1967

Adipose tissue linoleic acid as a criterion of adherence to a modified diet.

In elderly, institutionalized men on a diet of high linoleic acid content, there was little correlation after 1 yr between adipose tissue linoleic acid concentration and dining room attendance. The correlation improved thereafter, with a correlation coefficient of +0.81 after 5 yr and +0.74 after 6 yr.

Adipose Tissue↗
PubMed2005

Conjugated linoleic acid stimulates an anti-tumorigenic protein NAG-1 in an isomer specific manner.

Conjugated linoleic acids (CLAs), naturally occurring fatty acids in ruminant food products, have anti-tumorigenic and pro-apoptotic properties in animal as well as in vitro models of cancer. However, the cellular mechanism has not been fully understood. NAG-1 (non-steroidal anti-inflammatory drug-activated gene-1) is induced by several dietary compounds and belongs to a TGF-beta superfamily gene associated with pro-apoptotic and anti-tumorigenic activities. The present study was performed to elucidate the molecular mechanism by which CLA stimulates anti-tumorigenic activity in human colorectal cancer (CRC) cells. The trans-10, cis-12-CLA (t10,c12-CLA) repressed cell proliferation and induced apoptosis, whereas linoleic acid or c9,t11-CLA showed no effect on cell proliferation and apoptosis. We also found that t10,c12-CLA induced the expression of a pro-apoptotic gene, NAG-1, in human CRC cells. Inhibition of NAG-1 expression by small interference RNA (siRNA) results in repression of t10,c12-CLA-induced apoptosis. Microarray analysis using t10,c12-CLA-treated HCT-116 cells revealed that activating transcription factor 3 (ATF3) was induced and its expression was confirmed by western analysis. The t10,c12-CLA treatment followed by the overexpression of ATF3 increased NAG-1 promoter activity in HCT-116 cells. We further provide the evidence that t10,c12-CLA inhibited the phosphorylation of AKT and the blockage of GSK-3 by siRNA abolished t10,c12-CLA-induced ATF3 and NAG-1 expression. The current study demonstrates that t10,c12-CLA stimulates ATF3/NAG-1 expression and subsequently induces apoptosis in an isomer specific manner. These effects may be through inhibition of AKT/GSK-3beta pathway in human CRC cells.

Activating Transcription Factor 3↗
PubMed2001

Structure of eicosapentaenoic and linoleic acids in the cyclooxygenase site of prostaglandin endoperoxide H synthase-1.

Prostaglandin endoperoxide H synthases-1 and -2 (PGHSs) can oxygenate 18-22 carbon polyunsaturated fatty acids, albeit with varying efficiencies. Here we report the crystal structures of eicosapentaenoic acid (EPA, 20:5 n-3) and linoleic acid (LA, 18:2 n-6) bound in the cyclooxygenase active site of Co(3+) protoporphyrin IX-reconstituted ovine PGHS-1 (Co(3+)-oPGHS-1) and compare the effects of active site substitutions on the rates of oxygenation of EPA, LA, and arachidonic acid (AA). Both EPA and LA bind in the active site with orientations similar to those seen previously with AA and dihomo-gamma-linolenic acid (DHLA). For EPA, the presence of an additional double bond (C-17/C-18) causes this substrate to bind in a "strained" conformation in which C-13 is misaligned with respect to Tyr-385, the residue that abstracts hydrogen from substrate fatty acids. Presumably, this misalignment is responsible for the low rate of EPA oxygenation. For LA, the carboxyl half binds in a more extended configuration than AA, which results in positioning C-11 next to Tyr-385. Val-349 and Ser-530, recently identified as important determinants for efficient oxygenation of DHLA by PGHS-1, play similar roles in the oxygenation of EPA and LA. Approximately 750- and 175-fold reductions in the oxygenation efficiency of EPA and LA were observed with V349A oPGHS-1, compared with a 2-fold change for AA. Val-349 contacts C-2 and C-3 of EPA and C-4 of LA orienting the carboxyl halves of these substrates so that the omega-ends are aligned properly for hydrogen abstraction. An S530T substitution decreases the V(max)/K(m) of EPA and LA by 375- and 140-fold. Ser-530 makes six contacts with EPA and four with LA involving C-8 through C-16; these interactions influence the alignment of the substrate for hydrogen abstraction. Interestingly, replacement of Phe-205 increases the volume of the cyclooxygenase site allowing EPA to be oxygenated more efficiently than with native oPGHS-1.

Arachidonic Acid↗
PubMed2006

[Inhibiton of conjugated linoleic acid isomers on the proliferation of tumor cells].

OBJECTIVE: To study the effect of five conjugated linoleic acid isomers on the proliferation of human tumor cell AGS and Bel7402. METHODS: AGS, Bel7402 and Lovo cells incubated in vitro were used as model. The cell visibility was investigated after treatment with conjugated linoleic acid (CLA). RESULTS: All the five isomers had inhibitory ability to AGS, Bel7402 and Lovo cell proliferation, and the effect on AGS was more effective than that on Bel7402 and Lovo. The inhibitory effect was dose-dependent. CONCLUSION: The five isomers of CLA exhibited proliferation inhibitory effect on the tumor cell of AGS and Be17402.

Cell Line, Tumor↗