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cell line p53 status organism tissue type disease atcc jcrb code wi 38 wt human lung  (ATCC)
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ATCC cell line p53 status organism tissue type disease atcc jcrb code wi 38 wt human lung
PK11000 bound to and stabilized <t>p53</t> DBD. (A) Melting curve of the stabilized p53-Y220C DBD (T-p53C-Y220C) recorded via differential scanning fluorimetry in absence (blue) or in presence of 1 mM PK11000 (magenta). (B) Inhibition of T-p53C-Y220C aggregation by PK11000. Aggregation kinetics were recorded by monitoring light scattering at 500 nm with 3 μM protein at 37 °C in standard assay buffer [25 mM KPi pH 7.2, 150 mM NaCl, 1 mM TCEP, and 5% (vol/vol) DMSO]. Unlike for noncovalent binders that inhibit aggregation where the amplitude of the reaction remains unchanged and just the rate constants being lower, the amplitude of light scattering was substantially decreased at 250, 500, and 1,000 µM of PK11000, suggesting the presence of two species: unmodified p53-Y220C and a covalent adduct of PK11000 and p53. (C) Mapping of PK11000 induced peak shifts in the 15N-1H HSQC NMR spectrum onto the structure of the p53-Y220C DBD. Large peak shifts are highlighted in red; medium shifts in orange; and small shifts in yellow.
Cell Line P53 Status Organism Tissue Type Disease Atcc Jcrb Code Wi 38 Wt Human Lung, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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cell line p53 status organism tissue type disease atcc jcrb code wi 38 wt human lung - by Bioz Stars, 2026-07
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tissue status  (Novus Biologicals)
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Novus Biologicals tissue status
PK11000 bound to and stabilized <t>p53</t> DBD. (A) Melting curve of the stabilized p53-Y220C DBD (T-p53C-Y220C) recorded via differential scanning fluorimetry in absence (blue) or in presence of 1 mM PK11000 (magenta). (B) Inhibition of T-p53C-Y220C aggregation by PK11000. Aggregation kinetics were recorded by monitoring light scattering at 500 nm with 3 μM protein at 37 °C in standard assay buffer [25 mM KPi pH 7.2, 150 mM NaCl, 1 mM TCEP, and 5% (vol/vol) DMSO]. Unlike for noncovalent binders that inhibit aggregation where the amplitude of the reaction remains unchanged and just the rate constants being lower, the amplitude of light scattering was substantially decreased at 250, 500, and 1,000 µM of PK11000, suggesting the presence of two species: unmodified p53-Y220C and a covalent adduct of PK11000 and p53. (C) Mapping of PK11000 induced peak shifts in the 15N-1H HSQC NMR spectrum onto the structure of the p53-Y220C DBD. Large peak shifts are highlighted in red; medium shifts in orange; and small shifts in yellow.
Tissue Status, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sapiens source identifiers culture condition tissue source tp53 status genetic mutations cytogenetics amo 1 dsmz acc 538 rpmi 1640  (DSMZ)
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DSMZ sapiens source identifiers culture condition tissue source tp53 status genetic mutations cytogenetics amo 1 dsmz acc 538 rpmi 1640
PK11000 bound to and stabilized <t>p53</t> DBD. (A) Melting curve of the stabilized p53-Y220C DBD (T-p53C-Y220C) recorded via differential scanning fluorimetry in absence (blue) or in presence of 1 mM PK11000 (magenta). (B) Inhibition of T-p53C-Y220C aggregation by PK11000. Aggregation kinetics were recorded by monitoring light scattering at 500 nm with 3 μM protein at 37 °C in standard assay buffer [25 mM KPi pH 7.2, 150 mM NaCl, 1 mM TCEP, and 5% (vol/vol) DMSO]. Unlike for noncovalent binders that inhibit aggregation where the amplitude of the reaction remains unchanged and just the rate constants being lower, the amplitude of light scattering was substantially decreased at 250, 500, and 1,000 µM of PK11000, suggesting the presence of two species: unmodified p53-Y220C and a covalent adduct of PK11000 and p53. (C) Mapping of PK11000 induced peak shifts in the 15N-1H HSQC NMR spectrum onto the structure of the p53-Y220C DBD. Large peak shifts are highlighted in red; medium shifts in orange; and small shifts in yellow.
Sapiens Source Identifiers Culture Condition Tissue Source Tp53 Status Genetic Mutations Cytogenetics Amo 1 Dsmz Acc 538 Rpmi 1640, supplied by DSMZ, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sapiens source identifiers culture condition tissue source tp53 status genetic mutations cytogenetics amo 1 dsmz acc 538 rpmi 1640 - by Bioz Stars, 2026-07
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immunohistochemical staining status of proteins in human normal tissues, cancer tissues, and cancer cell lines  (Human Protein Atlas)
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Human Protein Atlas immunohistochemical staining status of proteins in human normal tissues, cancer tissues, and cancer cell lines
PK11000 bound to and stabilized <t>p53</t> DBD. (A) Melting curve of the stabilized p53-Y220C DBD (T-p53C-Y220C) recorded via differential scanning fluorimetry in absence (blue) or in presence of 1 mM PK11000 (magenta). (B) Inhibition of T-p53C-Y220C aggregation by PK11000. Aggregation kinetics were recorded by monitoring light scattering at 500 nm with 3 μM protein at 37 °C in standard assay buffer [25 mM KPi pH 7.2, 150 mM NaCl, 1 mM TCEP, and 5% (vol/vol) DMSO]. Unlike for noncovalent binders that inhibit aggregation where the amplitude of the reaction remains unchanged and just the rate constants being lower, the amplitude of light scattering was substantially decreased at 250, 500, and 1,000 µM of PK11000, suggesting the presence of two species: unmodified p53-Y220C and a covalent adduct of PK11000 and p53. (C) Mapping of PK11000 induced peak shifts in the 15N-1H HSQC NMR spectrum onto the structure of the p53-Y220C DBD. Large peak shifts are highlighted in red; medium shifts in orange; and small shifts in yellow.
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research tissue bank status  (Tayside Pharmaceuticals)
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Tayside Pharmaceuticals research tissue bank status
PK11000 bound to and stabilized <t>p53</t> DBD. (A) Melting curve of the stabilized p53-Y220C DBD (T-p53C-Y220C) recorded via differential scanning fluorimetry in absence (blue) or in presence of 1 mM PK11000 (magenta). (B) Inhibition of T-p53C-Y220C aggregation by PK11000. Aggregation kinetics were recorded by monitoring light scattering at 500 nm with 3 μM protein at 37 °C in standard assay buffer [25 mM KPi pH 7.2, 150 mM NaCl, 1 mM TCEP, and 5% (vol/vol) DMSO]. Unlike for noncovalent binders that inhibit aggregation where the amplitude of the reaction remains unchanged and just the rate constants being lower, the amplitude of light scattering was substantially decreased at 250, 500, and 1,000 µM of PK11000, suggesting the presence of two species: unmodified p53-Y220C and a covalent adduct of PK11000 and p53. (C) Mapping of PK11000 induced peak shifts in the 15N-1H HSQC NMR spectrum onto the structure of the p53-Y220C DBD. Large peak shifts are highlighted in red; medium shifts in orange; and small shifts in yellow.
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355 dna mutant status 189 tissue type fresh frozen fresh frozen fresh frozen formalin fixed paraffin  (Thermo Fisher)
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Thermo Fisher 355 dna mutant status 189 tissue type fresh frozen fresh frozen fresh frozen formalin fixed paraffin
PK11000 bound to and stabilized <t>p53</t> DBD. (A) Melting curve of the stabilized p53-Y220C DBD (T-p53C-Y220C) recorded via differential scanning fluorimetry in absence (blue) or in presence of 1 mM PK11000 (magenta). (B) Inhibition of T-p53C-Y220C aggregation by PK11000. Aggregation kinetics were recorded by monitoring light scattering at 500 nm with 3 μM protein at 37 °C in standard assay buffer [25 mM KPi pH 7.2, 150 mM NaCl, 1 mM TCEP, and 5% (vol/vol) DMSO]. Unlike for noncovalent binders that inhibit aggregation where the amplitude of the reaction remains unchanged and just the rate constants being lower, the amplitude of light scattering was substantially decreased at 250, 500, and 1,000 µM of PK11000, suggesting the presence of two species: unmodified p53-Y220C and a covalent adduct of PK11000 and p53. (C) Mapping of PK11000 induced peak shifts in the 15N-1H HSQC NMR spectrum onto the structure of the p53-Y220C DBD. Large peak shifts are highlighted in red; medium shifts in orange; and small shifts in yellow.
355 Dna Mutant Status 189 Tissue Type Fresh Frozen Fresh Frozen Fresh Frozen Formalin Fixed Paraffin, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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355 dna mutant status 189 tissue type fresh frozen fresh frozen fresh frozen formalin fixed paraffin - by Bioz Stars, 2026-07
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tissue biopsy to identify targetable mutation status  (AstraZeneca ltd)
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AstraZeneca ltd tissue biopsy to identify targetable mutation status
PK11000 bound to and stabilized <t>p53</t> DBD. (A) Melting curve of the stabilized p53-Y220C DBD (T-p53C-Y220C) recorded via differential scanning fluorimetry in absence (blue) or in presence of 1 mM PK11000 (magenta). (B) Inhibition of T-p53C-Y220C aggregation by PK11000. Aggregation kinetics were recorded by monitoring light scattering at 500 nm with 3 μM protein at 37 °C in standard assay buffer [25 mM KPi pH 7.2, 150 mM NaCl, 1 mM TCEP, and 5% (vol/vol) DMSO]. Unlike for noncovalent binders that inhibit aggregation where the amplitude of the reaction remains unchanged and just the rate constants being lower, the amplitude of light scattering was substantially decreased at 250, 500, and 1,000 µM of PK11000, suggesting the presence of two species: unmodified p53-Y220C and a covalent adduct of PK11000 and p53. (C) Mapping of PK11000 induced peak shifts in the 15N-1H HSQC NMR spectrum onto the structure of the p53-Y220C DBD. Large peak shifts are highlighted in red; medium shifts in orange; and small shifts in yellow.
Tissue Biopsy To Identify Targetable Mutation Status, supplied by AstraZeneca ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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PK11000 bound to and stabilized p53 DBD. (A) Melting curve of the stabilized p53-Y220C DBD (T-p53C-Y220C) recorded via differential scanning fluorimetry in absence (blue) or in presence of 1 mM PK11000 (magenta). (B) Inhibition of T-p53C-Y220C aggregation by PK11000. Aggregation kinetics were recorded by monitoring light scattering at 500 nm with 3 μM protein at 37 °C in standard assay buffer [25 mM KPi pH 7.2, 150 mM NaCl, 1 mM TCEP, and 5% (vol/vol) DMSO]. Unlike for noncovalent binders that inhibit aggregation where the amplitude of the reaction remains unchanged and just the rate constants being lower, the amplitude of light scattering was substantially decreased at 250, 500, and 1,000 µM of PK11000, suggesting the presence of two species: unmodified p53-Y220C and a covalent adduct of PK11000 and p53. (C) Mapping of PK11000 induced peak shifts in the 15N-1H HSQC NMR spectrum onto the structure of the p53-Y220C DBD. Large peak shifts are highlighted in red; medium shifts in orange; and small shifts in yellow.

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: 2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells

doi: 10.1073/pnas.1610421113

Figure Lengend Snippet: PK11000 bound to and stabilized p53 DBD. (A) Melting curve of the stabilized p53-Y220C DBD (T-p53C-Y220C) recorded via differential scanning fluorimetry in absence (blue) or in presence of 1 mM PK11000 (magenta). (B) Inhibition of T-p53C-Y220C aggregation by PK11000. Aggregation kinetics were recorded by monitoring light scattering at 500 nm with 3 μM protein at 37 °C in standard assay buffer [25 mM KPi pH 7.2, 150 mM NaCl, 1 mM TCEP, and 5% (vol/vol) DMSO]. Unlike for noncovalent binders that inhibit aggregation where the amplitude of the reaction remains unchanged and just the rate constants being lower, the amplitude of light scattering was substantially decreased at 250, 500, and 1,000 µM of PK11000, suggesting the presence of two species: unmodified p53-Y220C and a covalent adduct of PK11000 and p53. (C) Mapping of PK11000 induced peak shifts in the 15N-1H HSQC NMR spectrum onto the structure of the p53-Y220C DBD. Large peak shifts are highlighted in red; medium shifts in orange; and small shifts in yellow.

Article Snippet: Cell line p53 status Organism Tissue type Disease ATCC/JCRB code WI-38 WT Human Lung — CCL-75 HUH-6 WT Human Liver Hepatoblastoma JCRB0401 NUGC-4 WT Human Stomach Gastric adenocarcinoma JCRB0834 SJSA-1 WT Human Fibroblast (lung) Osteosarcoma CRL-2098 HCT-116 WT Human Colon Colorectal carcinoma CCL-247 SW480 R273H-P309S Human Colon Dukes’ type B, colorectal adenocarcinoma CCL-228 HUH-7 Y220C Human Liver Hepatocellular carcinoma JCRB0403 NUGC-3 Y220C Human Stomach Gastric adenocarcinoma JCRB0822 MKN1 V143A Human Stomach Adenosquamous carcinoma JCRB0252 H1299 Null Human Lung Non–small cell lung cancer CRL-5803 Open in a separate window ATCC, American Type Culture Collection; JCRB, Japanese Collection of Research Bioresources.

Techniques: Inhibition

DSF ΔTm values of different p53 mutants (8 μM) after incubation with diverse 2-sulfonylpyrimidine compounds (250 μM) for 30 min.

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: 2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells

doi: 10.1073/pnas.1610421113

Figure Lengend Snippet: DSF ΔTm values of different p53 mutants (8 μM) after incubation with diverse 2-sulfonylpyrimidine compounds (250 μM) for 30 min.

Article Snippet: Cell line p53 status Organism Tissue type Disease ATCC/JCRB code WI-38 WT Human Lung — CCL-75 HUH-6 WT Human Liver Hepatoblastoma JCRB0401 NUGC-4 WT Human Stomach Gastric adenocarcinoma JCRB0834 SJSA-1 WT Human Fibroblast (lung) Osteosarcoma CRL-2098 HCT-116 WT Human Colon Colorectal carcinoma CCL-247 SW480 R273H-P309S Human Colon Dukes’ type B, colorectal adenocarcinoma CCL-228 HUH-7 Y220C Human Liver Hepatocellular carcinoma JCRB0403 NUGC-3 Y220C Human Stomach Gastric adenocarcinoma JCRB0822 MKN1 V143A Human Stomach Adenosquamous carcinoma JCRB0252 H1299 Null Human Lung Non–small cell lung cancer CRL-5803 Open in a separate window ATCC, American Type Culture Collection; JCRB, Japanese Collection of Research Bioresources.

Techniques: Incubation

PK11000 alkylated cysteines of p53 DBD. (A) SNAr reaction mechanism for PK11000 cysteine alkylation. (B) ESI (ES+) mass spectra of 50 µM T-p53C Y220C incubated for 4 h at 20 °C with no compound (black) or 250, 500, 1,000, and 5,000 µM PK11000 (red).

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: 2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells

doi: 10.1073/pnas.1610421113

Figure Lengend Snippet: PK11000 alkylated cysteines of p53 DBD. (A) SNAr reaction mechanism for PK11000 cysteine alkylation. (B) ESI (ES+) mass spectra of 50 µM T-p53C Y220C incubated for 4 h at 20 °C with no compound (black) or 250, 500, 1,000, and 5,000 µM PK11000 (red).

Article Snippet: Cell line p53 status Organism Tissue type Disease ATCC/JCRB code WI-38 WT Human Lung — CCL-75 HUH-6 WT Human Liver Hepatoblastoma JCRB0401 NUGC-4 WT Human Stomach Gastric adenocarcinoma JCRB0834 SJSA-1 WT Human Fibroblast (lung) Osteosarcoma CRL-2098 HCT-116 WT Human Colon Colorectal carcinoma CCL-247 SW480 R273H-P309S Human Colon Dukes’ type B, colorectal adenocarcinoma CCL-228 HUH-7 Y220C Human Liver Hepatocellular carcinoma JCRB0403 NUGC-3 Y220C Human Stomach Gastric adenocarcinoma JCRB0822 MKN1 V143A Human Stomach Adenosquamous carcinoma JCRB0252 H1299 Null Human Lung Non–small cell lung cancer CRL-5803 Open in a separate window ATCC, American Type Culture Collection; JCRB, Japanese Collection of Research Bioresources.

Techniques: Incubation

ESI (ES+) mass spectra of different cysteine to p53 core DBD serine mutants after incubation without (black) and with PK11000 (red). (A) T-p53C C124S/C182S/C277S and (D) T-p53C C182S/C277S mutants showed no cysteine modification by PK11000, whereas (B) T-p53C C124S/C182S and (C) T-p53C C124S/C277S showed one cysteine modification by PK11000.

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: 2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells

doi: 10.1073/pnas.1610421113

Figure Lengend Snippet: ESI (ES+) mass spectra of different cysteine to p53 core DBD serine mutants after incubation without (black) and with PK11000 (red). (A) T-p53C C124S/C182S/C277S and (D) T-p53C C182S/C277S mutants showed no cysteine modification by PK11000, whereas (B) T-p53C C124S/C182S and (C) T-p53C C124S/C277S showed one cysteine modification by PK11000.

Article Snippet: Cell line p53 status Organism Tissue type Disease ATCC/JCRB code WI-38 WT Human Lung — CCL-75 HUH-6 WT Human Liver Hepatoblastoma JCRB0401 NUGC-4 WT Human Stomach Gastric adenocarcinoma JCRB0834 SJSA-1 WT Human Fibroblast (lung) Osteosarcoma CRL-2098 HCT-116 WT Human Colon Colorectal carcinoma CCL-247 SW480 R273H-P309S Human Colon Dukes’ type B, colorectal adenocarcinoma CCL-228 HUH-7 Y220C Human Liver Hepatocellular carcinoma JCRB0403 NUGC-3 Y220C Human Stomach Gastric adenocarcinoma JCRB0822 MKN1 V143A Human Stomach Adenosquamous carcinoma JCRB0252 H1299 Null Human Lung Non–small cell lung cancer CRL-5803 Open in a separate window ATCC, American Type Culture Collection; JCRB, Japanese Collection of Research Bioresources.

Techniques: Incubation, Modification

15N-1H HSQC NMR spectrum of the p53 Y220C core domain (red) with 1,000 µM (blue), 436 µM (yellow), and 218 µM (green) PK11000 at 293 K.

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: 2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells

doi: 10.1073/pnas.1610421113

Figure Lengend Snippet: 15N-1H HSQC NMR spectrum of the p53 Y220C core domain (red) with 1,000 µM (blue), 436 µM (yellow), and 218 µM (green) PK11000 at 293 K.

Article Snippet: Cell line p53 status Organism Tissue type Disease ATCC/JCRB code WI-38 WT Human Lung — CCL-75 HUH-6 WT Human Liver Hepatoblastoma JCRB0401 NUGC-4 WT Human Stomach Gastric adenocarcinoma JCRB0834 SJSA-1 WT Human Fibroblast (lung) Osteosarcoma CRL-2098 HCT-116 WT Human Colon Colorectal carcinoma CCL-247 SW480 R273H-P309S Human Colon Dukes’ type B, colorectal adenocarcinoma CCL-228 HUH-7 Y220C Human Liver Hepatocellular carcinoma JCRB0403 NUGC-3 Y220C Human Stomach Gastric adenocarcinoma JCRB0822 MKN1 V143A Human Stomach Adenosquamous carcinoma JCRB0252 H1299 Null Human Lung Non–small cell lung cancer CRL-5803 Open in a separate window ATCC, American Type Culture Collection; JCRB, Japanese Collection of Research Bioresources.

Techniques:

Alkylation of full-length p53 with 2-sulfonylpyrimdines does not compromise its DNA binding capability. Stabilized full-length p53 was incubated with 1 mM PK11000, PK11007, PK11010, and 5% DMSO for 2 h at 4 °C and then titrated into a cuvette containing 20 nM carboxyfluoresceine-labeled Gadd45a DNA. Fluorescence polarization data were recorded and fitted to the Hill equation including a linear drift term.

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: 2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells

doi: 10.1073/pnas.1610421113

Figure Lengend Snippet: Alkylation of full-length p53 with 2-sulfonylpyrimdines does not compromise its DNA binding capability. Stabilized full-length p53 was incubated with 1 mM PK11000, PK11007, PK11010, and 5% DMSO for 2 h at 4 °C and then titrated into a cuvette containing 20 nM carboxyfluoresceine-labeled Gadd45a DNA. Fluorescence polarization data were recorded and fitted to the Hill equation including a linear drift term.

Article Snippet: Cell line p53 status Organism Tissue type Disease ATCC/JCRB code WI-38 WT Human Lung — CCL-75 HUH-6 WT Human Liver Hepatoblastoma JCRB0401 NUGC-4 WT Human Stomach Gastric adenocarcinoma JCRB0834 SJSA-1 WT Human Fibroblast (lung) Osteosarcoma CRL-2098 HCT-116 WT Human Colon Colorectal carcinoma CCL-247 SW480 R273H-P309S Human Colon Dukes’ type B, colorectal adenocarcinoma CCL-228 HUH-7 Y220C Human Liver Hepatocellular carcinoma JCRB0403 NUGC-3 Y220C Human Stomach Gastric adenocarcinoma JCRB0822 MKN1 V143A Human Stomach Adenosquamous carcinoma JCRB0252 H1299 Null Human Lung Non–small cell lung cancer CRL-5803 Open in a separate window ATCC, American Type Culture Collection; JCRB, Japanese Collection of Research Bioresources.

Techniques: Binding Assay, Incubation, Labeling, Fluorescence

Structural effect of Cys182 modification by PK11000. Superposition of the structure of the p53 cancer mutant Y220C with (gray) and without (green) PK11000 shows that Cys182 on the surface of the L2 loop is modified by the alkylating agent, with the covalent modification pointing toward the solvent. Chain A of the asymmetric unit is shown. Alkylation fixes Cys182 in a defined conformation, but there is little interaction between the modification and the rest of the protein. The figure was generated using PyMOL (www.pymol.org).

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: 2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells

doi: 10.1073/pnas.1610421113

Figure Lengend Snippet: Structural effect of Cys182 modification by PK11000. Superposition of the structure of the p53 cancer mutant Y220C with (gray) and without (green) PK11000 shows that Cys182 on the surface of the L2 loop is modified by the alkylating agent, with the covalent modification pointing toward the solvent. Chain A of the asymmetric unit is shown. Alkylation fixes Cys182 in a defined conformation, but there is little interaction between the modification and the rest of the protein. The figure was generated using PyMOL (www.pymol.org).

Article Snippet: Cell line p53 status Organism Tissue type Disease ATCC/JCRB code WI-38 WT Human Lung — CCL-75 HUH-6 WT Human Liver Hepatoblastoma JCRB0401 NUGC-4 WT Human Stomach Gastric adenocarcinoma JCRB0834 SJSA-1 WT Human Fibroblast (lung) Osteosarcoma CRL-2098 HCT-116 WT Human Colon Colorectal carcinoma CCL-247 SW480 R273H-P309S Human Colon Dukes’ type B, colorectal adenocarcinoma CCL-228 HUH-7 Y220C Human Liver Hepatocellular carcinoma JCRB0403 NUGC-3 Y220C Human Stomach Gastric adenocarcinoma JCRB0822 MKN1 V143A Human Stomach Adenosquamous carcinoma JCRB0252 H1299 Null Human Lung Non–small cell lung cancer CRL-5803 Open in a separate window ATCC, American Type Culture Collection; JCRB, Japanese Collection of Research Bioresources.

Techniques: Modification, Mutagenesis, Solvent, Generated

Effects of diverse 2-sulfonylpyrimidines on p53 stabilization. (A) Library of diverse 2-sulfonylpyrimidines and structurally related compounds. (B and C) Time-dependent stabilization (DSF ΔTm) of T-p53C-Y220C after 15-, 30-, 60-, and 120-min incubation at room temperature with stabilizing or destabilizing/nonreactive 2-sulfonylpyrimidine compounds, respectively.

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: 2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells

doi: 10.1073/pnas.1610421113

Figure Lengend Snippet: Effects of diverse 2-sulfonylpyrimidines on p53 stabilization. (A) Library of diverse 2-sulfonylpyrimidines and structurally related compounds. (B and C) Time-dependent stabilization (DSF ΔTm) of T-p53C-Y220C after 15-, 30-, 60-, and 120-min incubation at room temperature with stabilizing or destabilizing/nonreactive 2-sulfonylpyrimidine compounds, respectively.

Article Snippet: Cell line p53 status Organism Tissue type Disease ATCC/JCRB code WI-38 WT Human Lung — CCL-75 HUH-6 WT Human Liver Hepatoblastoma JCRB0401 NUGC-4 WT Human Stomach Gastric adenocarcinoma JCRB0834 SJSA-1 WT Human Fibroblast (lung) Osteosarcoma CRL-2098 HCT-116 WT Human Colon Colorectal carcinoma CCL-247 SW480 R273H-P309S Human Colon Dukes’ type B, colorectal adenocarcinoma CCL-228 HUH-7 Y220C Human Liver Hepatocellular carcinoma JCRB0403 NUGC-3 Y220C Human Stomach Gastric adenocarcinoma JCRB0822 MKN1 V143A Human Stomach Adenosquamous carcinoma JCRB0252 H1299 Null Human Lung Non–small cell lung cancer CRL-5803 Open in a separate window ATCC, American Type Culture Collection; JCRB, Japanese Collection of Research Bioresources.

Techniques: Incubation

Biological effects of PK11007 on diverse cancer cell lines and one human fibroblast cell line. (A) Concentration-dependent viability reduction of WI-38 (fibroblast), NUGC-4 (p53 WT), HUH-6 (p53 WT), SJSA-1 (p53 WT), SW480 (p53 R273H/P309S), NUGC-3 (p53 Y220C), HUH-7 (p53 Y220C), and MKN1 (p53 V143A) cells after treatment with PK11007 for 24 h. The mutant p53 cells HUH-7, MKN1, and NUGC-3 were more sensitive to PK11007 treatment as indicated by strong viability reduction at low compound concentrations. Cell viability was measured in quadruplicate and normalized with the values of blank (viability = 1) and no cell (viability = 0) controls. Data are shown as mean ± SEM. (B) Incubation of the isogenic H1299 (p53−/−), H1299 (p53 H175), HCT116, and HCT116 p53−/− cancer cells with PK11007 yielded a comparable viability reduction after 24 h. (C) Cell viability of HUH-6, HUH-7, and MKN1 after p53 knockdown via siRNA. Cells were treated with PK11007 for 24 h (48 h for 15 µM PK11007 MKN1 sample). In HUH-6 and HUH-7, cell death was independent of p53, whereas it was partially dependent on p53 in MKN1 cells. (D) Western blots of NUGC-4, NUGC-3, MKN1, HUH-6, and HUH-7 cancer cells after 3 h (6 h for MKN1) treatment with PK11007. p53 target genes p21, PUMA, and MDM2 were up-regulated not only in MKN1 (p53-V143A), NUGC-3, and HUH-7 (both p53-Y220C), but also in HUH-6 and NUGC-4 (both p53 WT) cells. With increasing PK11007 concentration, the molecular weight of p53 gradually increased to ∼3 kDa for the mutant p53 cell lines (HUH-7, MKN1, and NUGC-3), suggesting hyperalkylation of unfolded/aggregated p53. The protein level of the antioxidative gene GSTP1 was higher in NUGC-4 (p53 WT) than in NUGC-3. The asterisks at the p53 target gene levels of HUH-6 and HUH-7 cells highlight the genes for which a different β-actin control was used. (E) Quantification of relative mRNA levels of p53 target genes via real-time PCR. Cells were treated with DMSO or 15 µM (MKN1, HUH-7) or 20 µM (NUGC-3, HUH-6) PK11007 for 6 h (4.5 h for HUH-7). p21 and PUMA mRNA levels were especially up-regulated in mutant p53 cells, whereas in p53 WT cells (HUH-6) no increased transcription was observed. Significance levels were calculated with the Student t test (***P < 0.001; **P < 0.01; *P < 0.05). (F) Western blots of protein levels of UPR key markers in MKN1, HUH-6, and HUH-7 cells. PK11007 treatment for 3 h (6 h for MKN1) increased levels of spliced XBP-1 and CHOP (especially in HUH-7). (G) Inhibition of cellular glutathione synthesis by buthionine sulfoximine strongly potentiated cell viability reduction by PK11007 in HUH-7, NUGC-3, and MKN1 mutant p53 cancer cells. (H) Determination of relative intracellular ROS levels via CellROX Deep Red fluorescence after incubating four cancer cell lines with 30 or 60 µM PK11007 for 2 h. PK11007 caused increase of ROS in all tested cell lines. However, at high doses, the increase of relative ROS levels was higher in HUH-7, NUGC-3, and MKN1 cells. Median fluorescence levels were determined in triplicate with error bars depicting the SE. Significance levels were calculated using a one-way ANOVA with the Bonferroni post hoc test for mean comparison (***P < 0.001; **P < 0.01; *P < 0.05).

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: 2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells

doi: 10.1073/pnas.1610421113

Figure Lengend Snippet: Biological effects of PK11007 on diverse cancer cell lines and one human fibroblast cell line. (A) Concentration-dependent viability reduction of WI-38 (fibroblast), NUGC-4 (p53 WT), HUH-6 (p53 WT), SJSA-1 (p53 WT), SW480 (p53 R273H/P309S), NUGC-3 (p53 Y220C), HUH-7 (p53 Y220C), and MKN1 (p53 V143A) cells after treatment with PK11007 for 24 h. The mutant p53 cells HUH-7, MKN1, and NUGC-3 were more sensitive to PK11007 treatment as indicated by strong viability reduction at low compound concentrations. Cell viability was measured in quadruplicate and normalized with the values of blank (viability = 1) and no cell (viability = 0) controls. Data are shown as mean ± SEM. (B) Incubation of the isogenic H1299 (p53−/−), H1299 (p53 H175), HCT116, and HCT116 p53−/− cancer cells with PK11007 yielded a comparable viability reduction after 24 h. (C) Cell viability of HUH-6, HUH-7, and MKN1 after p53 knockdown via siRNA. Cells were treated with PK11007 for 24 h (48 h for 15 µM PK11007 MKN1 sample). In HUH-6 and HUH-7, cell death was independent of p53, whereas it was partially dependent on p53 in MKN1 cells. (D) Western blots of NUGC-4, NUGC-3, MKN1, HUH-6, and HUH-7 cancer cells after 3 h (6 h for MKN1) treatment with PK11007. p53 target genes p21, PUMA, and MDM2 were up-regulated not only in MKN1 (p53-V143A), NUGC-3, and HUH-7 (both p53-Y220C), but also in HUH-6 and NUGC-4 (both p53 WT) cells. With increasing PK11007 concentration, the molecular weight of p53 gradually increased to ∼3 kDa for the mutant p53 cell lines (HUH-7, MKN1, and NUGC-3), suggesting hyperalkylation of unfolded/aggregated p53. The protein level of the antioxidative gene GSTP1 was higher in NUGC-4 (p53 WT) than in NUGC-3. The asterisks at the p53 target gene levels of HUH-6 and HUH-7 cells highlight the genes for which a different β-actin control was used. (E) Quantification of relative mRNA levels of p53 target genes via real-time PCR. Cells were treated with DMSO or 15 µM (MKN1, HUH-7) or 20 µM (NUGC-3, HUH-6) PK11007 for 6 h (4.5 h for HUH-7). p21 and PUMA mRNA levels were especially up-regulated in mutant p53 cells, whereas in p53 WT cells (HUH-6) no increased transcription was observed. Significance levels were calculated with the Student t test (***P < 0.001; **P < 0.01; *P < 0.05). (F) Western blots of protein levels of UPR key markers in MKN1, HUH-6, and HUH-7 cells. PK11007 treatment for 3 h (6 h for MKN1) increased levels of spliced XBP-1 and CHOP (especially in HUH-7). (G) Inhibition of cellular glutathione synthesis by buthionine sulfoximine strongly potentiated cell viability reduction by PK11007 in HUH-7, NUGC-3, and MKN1 mutant p53 cancer cells. (H) Determination of relative intracellular ROS levels via CellROX Deep Red fluorescence after incubating four cancer cell lines with 30 or 60 µM PK11007 for 2 h. PK11007 caused increase of ROS in all tested cell lines. However, at high doses, the increase of relative ROS levels was higher in HUH-7, NUGC-3, and MKN1 cells. Median fluorescence levels were determined in triplicate with error bars depicting the SE. Significance levels were calculated using a one-way ANOVA with the Bonferroni post hoc test for mean comparison (***P < 0.001; **P < 0.01; *P < 0.05).

Article Snippet: Cell line p53 status Organism Tissue type Disease ATCC/JCRB code WI-38 WT Human Lung — CCL-75 HUH-6 WT Human Liver Hepatoblastoma JCRB0401 NUGC-4 WT Human Stomach Gastric adenocarcinoma JCRB0834 SJSA-1 WT Human Fibroblast (lung) Osteosarcoma CRL-2098 HCT-116 WT Human Colon Colorectal carcinoma CCL-247 SW480 R273H-P309S Human Colon Dukes’ type B, colorectal adenocarcinoma CCL-228 HUH-7 Y220C Human Liver Hepatocellular carcinoma JCRB0403 NUGC-3 Y220C Human Stomach Gastric adenocarcinoma JCRB0822 MKN1 V143A Human Stomach Adenosquamous carcinoma JCRB0252 H1299 Null Human Lung Non–small cell lung cancer CRL-5803 Open in a separate window ATCC, American Type Culture Collection; JCRB, Japanese Collection of Research Bioresources.

Techniques: Concentration Assay, Mutagenesis, Incubation, Knockdown, Western Blot, Molecular Weight, Control, Real-time Polymerase Chain Reaction, Inhibition, Fluorescence, Comparison

Cell viability time course for (A) HUH-6 (p53 WT), HUH-7 (p53 Y220C), and (B) MKN1 cancer cells at 30 or 60 µM PK11007 (10 and 30 µM for MKN1). Cell viability was measured in quadruplicates and normalized with the values of blank (viability = 1) and no cell (viability = 0) controls. Data are shown as mean ± SEM.

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: 2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells

doi: 10.1073/pnas.1610421113

Figure Lengend Snippet: Cell viability time course for (A) HUH-6 (p53 WT), HUH-7 (p53 Y220C), and (B) MKN1 cancer cells at 30 or 60 µM PK11007 (10 and 30 µM for MKN1). Cell viability was measured in quadruplicates and normalized with the values of blank (viability = 1) and no cell (viability = 0) controls. Data are shown as mean ± SEM.

Article Snippet: Cell line p53 status Organism Tissue type Disease ATCC/JCRB code WI-38 WT Human Lung — CCL-75 HUH-6 WT Human Liver Hepatoblastoma JCRB0401 NUGC-4 WT Human Stomach Gastric adenocarcinoma JCRB0834 SJSA-1 WT Human Fibroblast (lung) Osteosarcoma CRL-2098 HCT-116 WT Human Colon Colorectal carcinoma CCL-247 SW480 R273H-P309S Human Colon Dukes’ type B, colorectal adenocarcinoma CCL-228 HUH-7 Y220C Human Liver Hepatocellular carcinoma JCRB0403 NUGC-3 Y220C Human Stomach Gastric adenocarcinoma JCRB0822 MKN1 V143A Human Stomach Adenosquamous carcinoma JCRB0252 H1299 Null Human Lung Non–small cell lung cancer CRL-5803 Open in a separate window ATCC, American Type Culture Collection; JCRB, Japanese Collection of Research Bioresources.

Techniques:

Biological effects of 2-sulfonylpyrimidines on diverse cell lines. Concentration-dependent viability reduction of WI-38 (p53 WT, noncancer), NUGC-4 (p53 WT), HUH-6 (p53 WT), SJSA-1 (p53 WT), SW480 (p53 R273H/P309S), NUGC-3 (p53 Y220C), HUH-7 (p53 Y220C), and MKN1 (p53 V143A) cells after compound treatment for 24 h. The strongest effects on cell viability were observed for PK11007 and PK11012. Mutant p53 cell lines were mostly significantly more sensitive for these compounds than p53 WT and noncancer cell lines. This behavior was also observed for PK11010 and PK11029, however only at higher compound concentrations. PK11003 led to a strong viability decrease; however, it did not distinguish clearly between mutant and WT p53 cell lines. Compounds that contain a negatively charged carboxyl group, such as PK11000 and PK11009, did not lead to a significant cell viability decrease in the tested cell lines at concentrations below 120 µM. Mutant p53 cell lines were also extra sensitive to compounds that destabilized the p53 core domain in vitro, such as PK11012 and PK11015. Cell viability was measured in quadruplicate and normalized with the values of blank (viability = 1) and no cell (viability = 0) controls. Data are shown as mean ± SEM.

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: 2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells

doi: 10.1073/pnas.1610421113

Figure Lengend Snippet: Biological effects of 2-sulfonylpyrimidines on diverse cell lines. Concentration-dependent viability reduction of WI-38 (p53 WT, noncancer), NUGC-4 (p53 WT), HUH-6 (p53 WT), SJSA-1 (p53 WT), SW480 (p53 R273H/P309S), NUGC-3 (p53 Y220C), HUH-7 (p53 Y220C), and MKN1 (p53 V143A) cells after compound treatment for 24 h. The strongest effects on cell viability were observed for PK11007 and PK11012. Mutant p53 cell lines were mostly significantly more sensitive for these compounds than p53 WT and noncancer cell lines. This behavior was also observed for PK11010 and PK11029, however only at higher compound concentrations. PK11003 led to a strong viability decrease; however, it did not distinguish clearly between mutant and WT p53 cell lines. Compounds that contain a negatively charged carboxyl group, such as PK11000 and PK11009, did not lead to a significant cell viability decrease in the tested cell lines at concentrations below 120 µM. Mutant p53 cell lines were also extra sensitive to compounds that destabilized the p53 core domain in vitro, such as PK11012 and PK11015. Cell viability was measured in quadruplicate and normalized with the values of blank (viability = 1) and no cell (viability = 0) controls. Data are shown as mean ± SEM.

Article Snippet: Cell line p53 status Organism Tissue type Disease ATCC/JCRB code WI-38 WT Human Lung — CCL-75 HUH-6 WT Human Liver Hepatoblastoma JCRB0401 NUGC-4 WT Human Stomach Gastric adenocarcinoma JCRB0834 SJSA-1 WT Human Fibroblast (lung) Osteosarcoma CRL-2098 HCT-116 WT Human Colon Colorectal carcinoma CCL-247 SW480 R273H-P309S Human Colon Dukes’ type B, colorectal adenocarcinoma CCL-228 HUH-7 Y220C Human Liver Hepatocellular carcinoma JCRB0403 NUGC-3 Y220C Human Stomach Gastric adenocarcinoma JCRB0822 MKN1 V143A Human Stomach Adenosquamous carcinoma JCRB0252 H1299 Null Human Lung Non–small cell lung cancer CRL-5803 Open in a separate window ATCC, American Type Culture Collection; JCRB, Japanese Collection of Research Bioresources.

Techniques: Concentration Assay, Mutagenesis, In Vitro

Viability reduction of APR-246 in NUGC-3 (p53 WT), HUH-6 (p53 WT), NUGC-4 (p53 Y220C), and HUH-7 (p53 Y220C) cancer cells after treatment for 24 h. Cell viability was measured in quadruplicates and normalized with the values of blank (viability = 1) and no cell (viability = 0) controls. Data are shown as mean ± SEM.

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: 2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells

doi: 10.1073/pnas.1610421113

Figure Lengend Snippet: Viability reduction of APR-246 in NUGC-3 (p53 WT), HUH-6 (p53 WT), NUGC-4 (p53 Y220C), and HUH-7 (p53 Y220C) cancer cells after treatment for 24 h. Cell viability was measured in quadruplicates and normalized with the values of blank (viability = 1) and no cell (viability = 0) controls. Data are shown as mean ± SEM.

Article Snippet: Cell line p53 status Organism Tissue type Disease ATCC/JCRB code WI-38 WT Human Lung — CCL-75 HUH-6 WT Human Liver Hepatoblastoma JCRB0401 NUGC-4 WT Human Stomach Gastric adenocarcinoma JCRB0834 SJSA-1 WT Human Fibroblast (lung) Osteosarcoma CRL-2098 HCT-116 WT Human Colon Colorectal carcinoma CCL-247 SW480 R273H-P309S Human Colon Dukes’ type B, colorectal adenocarcinoma CCL-228 HUH-7 Y220C Human Liver Hepatocellular carcinoma JCRB0403 NUGC-3 Y220C Human Stomach Gastric adenocarcinoma JCRB0822 MKN1 V143A Human Stomach Adenosquamous carcinoma JCRB0252 H1299 Null Human Lung Non–small cell lung cancer CRL-5803 Open in a separate window ATCC, American Type Culture Collection; JCRB, Japanese Collection of Research Bioresources.

Techniques:

NAC prevents PK11007-mediated ROS formation. (A) Determination of intracellular ROS levels via CellROX Deep Red fluorescence after incubating HUH-6 and HUH-7 cancer cells with 5 mM NAC, 400 µM tert-Butyl hydroperoxide (TBHP), or a combination of 30 µM PK11007 and 5 mM NAC for 1.25 h. NAC does not only decrease basal ROS levels, but also completely prevents PK11007 from increasing ROS levels. (B) Relative intracellular ROS levels via CellROX Deep Red fluorescence after incubating four cancer cell lines with 30 or 60 µM PK11007 for 2 h. PK11007 led to an increase of ROS in all tested cell lines; however, at high doses the relative ROS level was significantly higher in HUH-7 and NUGC-3 cells, whereas the ROS levels in MKN1 cells remained on the level of the p53 WT cell lines. Median fluorescence levels were determined in triplicates. Error bars depict SEM values.

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: 2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells

doi: 10.1073/pnas.1610421113

Figure Lengend Snippet: NAC prevents PK11007-mediated ROS formation. (A) Determination of intracellular ROS levels via CellROX Deep Red fluorescence after incubating HUH-6 and HUH-7 cancer cells with 5 mM NAC, 400 µM tert-Butyl hydroperoxide (TBHP), or a combination of 30 µM PK11007 and 5 mM NAC for 1.25 h. NAC does not only decrease basal ROS levels, but also completely prevents PK11007 from increasing ROS levels. (B) Relative intracellular ROS levels via CellROX Deep Red fluorescence after incubating four cancer cell lines with 30 or 60 µM PK11007 for 2 h. PK11007 led to an increase of ROS in all tested cell lines; however, at high doses the relative ROS level was significantly higher in HUH-7 and NUGC-3 cells, whereas the ROS levels in MKN1 cells remained on the level of the p53 WT cell lines. Median fluorescence levels were determined in triplicates. Error bars depict SEM values.

Article Snippet: Cell line p53 status Organism Tissue type Disease ATCC/JCRB code WI-38 WT Human Lung — CCL-75 HUH-6 WT Human Liver Hepatoblastoma JCRB0401 NUGC-4 WT Human Stomach Gastric adenocarcinoma JCRB0834 SJSA-1 WT Human Fibroblast (lung) Osteosarcoma CRL-2098 HCT-116 WT Human Colon Colorectal carcinoma CCL-247 SW480 R273H-P309S Human Colon Dukes’ type B, colorectal adenocarcinoma CCL-228 HUH-7 Y220C Human Liver Hepatocellular carcinoma JCRB0403 NUGC-3 Y220C Human Stomach Gastric adenocarcinoma JCRB0822 MKN1 V143A Human Stomach Adenosquamous carcinoma JCRB0252 H1299 Null Human Lung Non–small cell lung cancer CRL-5803 Open in a separate window ATCC, American Type Culture Collection; JCRB, Japanese Collection of Research Bioresources.

Techniques: Fluorescence

PK11007 changes the folding state of mutant p53 (Y220C) in NUGC-3 cells. PK11007 treatment led to a significant reduction of unfolded p53 (Pab 240) and a slight increase in folded p53 (Pab 1620). Hoechst 33342 dye was used to stain the nucleus. To facilitate comparison of Pab 1620 and Pab 240 fluorescence levels, we increased exposure of all raw pictures by 2 eV.

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: 2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells

doi: 10.1073/pnas.1610421113

Figure Lengend Snippet: PK11007 changes the folding state of mutant p53 (Y220C) in NUGC-3 cells. PK11007 treatment led to a significant reduction of unfolded p53 (Pab 240) and a slight increase in folded p53 (Pab 1620). Hoechst 33342 dye was used to stain the nucleus. To facilitate comparison of Pab 1620 and Pab 240 fluorescence levels, we increased exposure of all raw pictures by 2 eV.

Article Snippet: Cell line p53 status Organism Tissue type Disease ATCC/JCRB code WI-38 WT Human Lung — CCL-75 HUH-6 WT Human Liver Hepatoblastoma JCRB0401 NUGC-4 WT Human Stomach Gastric adenocarcinoma JCRB0834 SJSA-1 WT Human Fibroblast (lung) Osteosarcoma CRL-2098 HCT-116 WT Human Colon Colorectal carcinoma CCL-247 SW480 R273H-P309S Human Colon Dukes’ type B, colorectal adenocarcinoma CCL-228 HUH-7 Y220C Human Liver Hepatocellular carcinoma JCRB0403 NUGC-3 Y220C Human Stomach Gastric adenocarcinoma JCRB0822 MKN1 V143A Human Stomach Adenosquamous carcinoma JCRB0252 H1299 Null Human Lung Non–small cell lung cancer CRL-5803 Open in a separate window ATCC, American Type Culture Collection; JCRB, Japanese Collection of Research Bioresources.

Techniques: Mutagenesis, Staining, Comparison, Fluorescence

Protein levels of p53 after treatment with nontarget or p53 siRNA in MKN1, HUH-6, and HUH-7 cancer cells.

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: 2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells

doi: 10.1073/pnas.1610421113

Figure Lengend Snippet: Protein levels of p53 after treatment with nontarget or p53 siRNA in MKN1, HUH-6, and HUH-7 cancer cells.

Article Snippet: Cell line p53 status Organism Tissue type Disease ATCC/JCRB code WI-38 WT Human Lung — CCL-75 HUH-6 WT Human Liver Hepatoblastoma JCRB0401 NUGC-4 WT Human Stomach Gastric adenocarcinoma JCRB0834 SJSA-1 WT Human Fibroblast (lung) Osteosarcoma CRL-2098 HCT-116 WT Human Colon Colorectal carcinoma CCL-247 SW480 R273H-P309S Human Colon Dukes’ type B, colorectal adenocarcinoma CCL-228 HUH-7 Y220C Human Liver Hepatocellular carcinoma JCRB0403 NUGC-3 Y220C Human Stomach Gastric adenocarcinoma JCRB0822 MKN1 V143A Human Stomach Adenosquamous carcinoma JCRB0252 H1299 Null Human Lung Non–small cell lung cancer CRL-5803 Open in a separate window ATCC, American Type Culture Collection; JCRB, Japanese Collection of Research Bioresources.

Techniques: