T24 HRAS transformed NIH/3T3 mouse cells (GhrasT-NIH/3T3) in serial tumorigenic in vitro/in vivo passages give rise to increasingly aggressive tumorigenic cell lines T1-A and T2-A and metastatic cell lines T3-HA and T4-PA
Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progressi...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Ray, Durwood B. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2016transfer abstract |
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| Schlagwörter: |
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| Umfang: |
11 |
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| Übergeordnetes Werk: |
Enthalten in: 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS - 2012, ECR, Orlando, Fla |
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| Übergeordnetes Werk: |
volume:340 ; year:2016 ; number:1 ; day:1 ; month:01 ; pages:1-11 ; extent:11 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.yexcr.2015.07.029 |
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| Katalog-ID: |
ELV030080908 |
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| 245 | 1 | 0 | |a T24 HRAS transformed NIH/3T3 mouse cells (GhrasT-NIH/3T3) in serial tumorigenic in vitro/in vivo passages give rise to increasingly aggressive tumorigenic cell lines T1-A and T2-A and metastatic cell lines T3-HA and T4-PA |
| 264 | 1 | |c 2016transfer abstract | |
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| 520 | |a Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ... | ||
| 520 | |a Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ... | ||
| 650 | 7 | |a Tansformed |2 Elsevier | |
| 650 | 7 | |a In vitro/in vivo tumorigenic progression |2 Elsevier | |
| 650 | 7 | |a NIH/3T3 |2 Elsevier | |
| 650 | 7 | |a GhrasT-NIH/3T3 |2 Elsevier | |
| 650 | 7 | |a Metastasis |2 Elsevier | |
| 650 | 7 | |a Doubling time method |2 Elsevier | |
| 650 | 7 | |a Punctuated evolution |2 Elsevier | |
| 650 | 7 | |a Chromoplexy |2 Elsevier | |
| 650 | 7 | |a HRAS |2 Elsevier | |
| 650 | 7 | |a Chromothripsis |2 Elsevier | |
| 700 | 1 | |a Merrill, Gerald A. |4 oth | |
| 700 | 1 | |a Brenner, Frederic J. |4 oth | |
| 700 | 1 | |a Lytle, Laurie S. |4 oth | |
| 700 | 1 | |a Lam, Tan |4 oth | |
| 700 | 1 | |a McElhinney, Aaron |4 oth | |
| 700 | 1 | |a Anders, Joel |4 oth | |
| 700 | 1 | |a Rock, Tara Tauber |4 oth | |
| 700 | 1 | |a Lyker, Jennifer Kier |4 oth | |
| 700 | 1 | |a Barcus, Scott |4 oth | |
| 700 | 1 | |a Leslie, Kara Hust |4 oth | |
| 700 | 1 | |a Kramer, Jill M. |4 oth | |
| 700 | 1 | |a Rubenstein, Eric M. |4 oth | |
| 700 | 1 | |a Pryor Schanz, Karen |4 oth | |
| 700 | 1 | |a Parkhurst, Amy J. |4 oth | |
| 700 | 1 | |a Peck, Michelle |4 oth | |
| 700 | 1 | |a Good, Kimberly |4 oth | |
| 700 | 1 | |a Granath, Kristi Lemke |4 oth | |
| 700 | 1 | |a Cifra, Nicole |4 oth | |
| 700 | 1 | |a Detweiler, Jessalee Wantz |4 oth | |
| 700 | 1 | |a Stevens, Laura |4 oth | |
| 700 | 1 | |a Albertson, Richard |4 oth | |
| 700 | 1 | |a Deir, Rachael |4 oth | |
| 700 | 1 | |a Stewart, Elisabeth |4 oth | |
| 700 | 1 | |a Wingard, Katherine |4 oth | |
| 700 | 1 | |a Richardson, Micah Rose |4 oth | |
| 700 | 1 | |a Blizard, Sarah B. |4 oth | |
| 700 | 1 | |a Gillespie, Lauren E. |4 oth | |
| 700 | 1 | |a Kriley, Charles E. |4 oth | |
| 700 | 1 | |a Rzewnicki, Daniel I. |4 oth | |
| 700 | 1 | |a Jones, David H. |4 oth | |
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10.1016/j.yexcr.2015.07.029 doi GBVA2016021000016.pica (DE-627)ELV030080908 (ELSEVIER)S0014-4827(15)30060-4 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 610 VZ 44.44 bkl Ray, Durwood B. verfasserin aut T24 HRAS transformed NIH/3T3 mouse cells (GhrasT-NIH/3T3) in serial tumorigenic in vitro/in vivo passages give rise to increasingly aggressive tumorigenic cell lines T1-A and T2-A and metastatic cell lines T3-HA and T4-PA 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ... Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ... Tansformed Elsevier In vitro/in vivo tumorigenic progression Elsevier NIH/3T3 Elsevier GhrasT-NIH/3T3 Elsevier Metastasis Elsevier Doubling time method Elsevier Punctuated evolution Elsevier Chromoplexy Elsevier HRAS Elsevier Chromothripsis Elsevier Merrill, Gerald A. oth Brenner, Frederic J. oth Lytle, Laurie S. oth Lam, Tan oth McElhinney, Aaron oth Anders, Joel oth Rock, Tara Tauber oth Lyker, Jennifer Kier oth Barcus, Scott oth Leslie, Kara Hust oth Kramer, Jill M. oth Rubenstein, Eric M. oth Pryor Schanz, Karen oth Parkhurst, Amy J. oth Peck, Michelle oth Good, Kimberly oth Granath, Kristi Lemke oth Cifra, Nicole oth Detweiler, Jessalee Wantz oth Stevens, Laura oth Albertson, Richard oth Deir, Rachael oth Stewart, Elisabeth oth Wingard, Katherine oth Richardson, Micah Rose oth Blizard, Sarah B. oth Gillespie, Lauren E. oth Kriley, Charles E. oth Rzewnicki, Daniel I. oth Jones, David H. oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:340 year:2016 number:1 day:1 month:01 pages:1-11 extent:11 https://doi.org/10.1016/j.yexcr.2015.07.029 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 340 2016 1 1 0101 1-11 11 045F 570 |
| spelling |
10.1016/j.yexcr.2015.07.029 doi GBVA2016021000016.pica (DE-627)ELV030080908 (ELSEVIER)S0014-4827(15)30060-4 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 610 VZ 44.44 bkl Ray, Durwood B. verfasserin aut T24 HRAS transformed NIH/3T3 mouse cells (GhrasT-NIH/3T3) in serial tumorigenic in vitro/in vivo passages give rise to increasingly aggressive tumorigenic cell lines T1-A and T2-A and metastatic cell lines T3-HA and T4-PA 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ... Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ... Tansformed Elsevier In vitro/in vivo tumorigenic progression Elsevier NIH/3T3 Elsevier GhrasT-NIH/3T3 Elsevier Metastasis Elsevier Doubling time method Elsevier Punctuated evolution Elsevier Chromoplexy Elsevier HRAS Elsevier Chromothripsis Elsevier Merrill, Gerald A. oth Brenner, Frederic J. oth Lytle, Laurie S. oth Lam, Tan oth McElhinney, Aaron oth Anders, Joel oth Rock, Tara Tauber oth Lyker, Jennifer Kier oth Barcus, Scott oth Leslie, Kara Hust oth Kramer, Jill M. oth Rubenstein, Eric M. oth Pryor Schanz, Karen oth Parkhurst, Amy J. oth Peck, Michelle oth Good, Kimberly oth Granath, Kristi Lemke oth Cifra, Nicole oth Detweiler, Jessalee Wantz oth Stevens, Laura oth Albertson, Richard oth Deir, Rachael oth Stewart, Elisabeth oth Wingard, Katherine oth Richardson, Micah Rose oth Blizard, Sarah B. oth Gillespie, Lauren E. oth Kriley, Charles E. oth Rzewnicki, Daniel I. oth Jones, David H. oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:340 year:2016 number:1 day:1 month:01 pages:1-11 extent:11 https://doi.org/10.1016/j.yexcr.2015.07.029 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 340 2016 1 1 0101 1-11 11 045F 570 |
| allfields_unstemmed |
10.1016/j.yexcr.2015.07.029 doi GBVA2016021000016.pica (DE-627)ELV030080908 (ELSEVIER)S0014-4827(15)30060-4 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 610 VZ 44.44 bkl Ray, Durwood B. verfasserin aut T24 HRAS transformed NIH/3T3 mouse cells (GhrasT-NIH/3T3) in serial tumorigenic in vitro/in vivo passages give rise to increasingly aggressive tumorigenic cell lines T1-A and T2-A and metastatic cell lines T3-HA and T4-PA 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ... Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ... Tansformed Elsevier In vitro/in vivo tumorigenic progression Elsevier NIH/3T3 Elsevier GhrasT-NIH/3T3 Elsevier Metastasis Elsevier Doubling time method Elsevier Punctuated evolution Elsevier Chromoplexy Elsevier HRAS Elsevier Chromothripsis Elsevier Merrill, Gerald A. oth Brenner, Frederic J. oth Lytle, Laurie S. oth Lam, Tan oth McElhinney, Aaron oth Anders, Joel oth Rock, Tara Tauber oth Lyker, Jennifer Kier oth Barcus, Scott oth Leslie, Kara Hust oth Kramer, Jill M. oth Rubenstein, Eric M. oth Pryor Schanz, Karen oth Parkhurst, Amy J. oth Peck, Michelle oth Good, Kimberly oth Granath, Kristi Lemke oth Cifra, Nicole oth Detweiler, Jessalee Wantz oth Stevens, Laura oth Albertson, Richard oth Deir, Rachael oth Stewart, Elisabeth oth Wingard, Katherine oth Richardson, Micah Rose oth Blizard, Sarah B. oth Gillespie, Lauren E. oth Kriley, Charles E. oth Rzewnicki, Daniel I. oth Jones, David H. oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:340 year:2016 number:1 day:1 month:01 pages:1-11 extent:11 https://doi.org/10.1016/j.yexcr.2015.07.029 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 340 2016 1 1 0101 1-11 11 045F 570 |
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10.1016/j.yexcr.2015.07.029 doi GBVA2016021000016.pica (DE-627)ELV030080908 (ELSEVIER)S0014-4827(15)30060-4 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 610 VZ 44.44 bkl Ray, Durwood B. verfasserin aut T24 HRAS transformed NIH/3T3 mouse cells (GhrasT-NIH/3T3) in serial tumorigenic in vitro/in vivo passages give rise to increasingly aggressive tumorigenic cell lines T1-A and T2-A and metastatic cell lines T3-HA and T4-PA 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ... Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ... Tansformed Elsevier In vitro/in vivo tumorigenic progression Elsevier NIH/3T3 Elsevier GhrasT-NIH/3T3 Elsevier Metastasis Elsevier Doubling time method Elsevier Punctuated evolution Elsevier Chromoplexy Elsevier HRAS Elsevier Chromothripsis Elsevier Merrill, Gerald A. oth Brenner, Frederic J. oth Lytle, Laurie S. oth Lam, Tan oth McElhinney, Aaron oth Anders, Joel oth Rock, Tara Tauber oth Lyker, Jennifer Kier oth Barcus, Scott oth Leslie, Kara Hust oth Kramer, Jill M. oth Rubenstein, Eric M. oth Pryor Schanz, Karen oth Parkhurst, Amy J. oth Peck, Michelle oth Good, Kimberly oth Granath, Kristi Lemke oth Cifra, Nicole oth Detweiler, Jessalee Wantz oth Stevens, Laura oth Albertson, Richard oth Deir, Rachael oth Stewart, Elisabeth oth Wingard, Katherine oth Richardson, Micah Rose oth Blizard, Sarah B. oth Gillespie, Lauren E. oth Kriley, Charles E. oth Rzewnicki, Daniel I. oth Jones, David H. oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:340 year:2016 number:1 day:1 month:01 pages:1-11 extent:11 https://doi.org/10.1016/j.yexcr.2015.07.029 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 340 2016 1 1 0101 1-11 11 045F 570 |
| allfieldsSound |
10.1016/j.yexcr.2015.07.029 doi GBVA2016021000016.pica (DE-627)ELV030080908 (ELSEVIER)S0014-4827(15)30060-4 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 610 VZ 44.44 bkl Ray, Durwood B. verfasserin aut T24 HRAS transformed NIH/3T3 mouse cells (GhrasT-NIH/3T3) in serial tumorigenic in vitro/in vivo passages give rise to increasingly aggressive tumorigenic cell lines T1-A and T2-A and metastatic cell lines T3-HA and T4-PA 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ... Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ... Tansformed Elsevier In vitro/in vivo tumorigenic progression Elsevier NIH/3T3 Elsevier GhrasT-NIH/3T3 Elsevier Metastasis Elsevier Doubling time method Elsevier Punctuated evolution Elsevier Chromoplexy Elsevier HRAS Elsevier Chromothripsis Elsevier Merrill, Gerald A. oth Brenner, Frederic J. oth Lytle, Laurie S. oth Lam, Tan oth McElhinney, Aaron oth Anders, Joel oth Rock, Tara Tauber oth Lyker, Jennifer Kier oth Barcus, Scott oth Leslie, Kara Hust oth Kramer, Jill M. oth Rubenstein, Eric M. oth Pryor Schanz, Karen oth Parkhurst, Amy J. oth Peck, Michelle oth Good, Kimberly oth Granath, Kristi Lemke oth Cifra, Nicole oth Detweiler, Jessalee Wantz oth Stevens, Laura oth Albertson, Richard oth Deir, Rachael oth Stewart, Elisabeth oth Wingard, Katherine oth Richardson, Micah Rose oth Blizard, Sarah B. oth Gillespie, Lauren E. oth Kriley, Charles E. oth Rzewnicki, Daniel I. oth Jones, David H. oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:340 year:2016 number:1 day:1 month:01 pages:1-11 extent:11 https://doi.org/10.1016/j.yexcr.2015.07.029 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 340 2016 1 1 0101 1-11 11 045F 570 |
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Enthalten in 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS Orlando, Fla volume:340 year:2016 number:1 day:1 month:01 pages:1-11 extent:11 |
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Enthalten in 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS Orlando, Fla volume:340 year:2016 number:1 day:1 month:01 pages:1-11 extent:11 |
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Tansformed In vitro/in vivo tumorigenic progression NIH/3T3 GhrasT-NIH/3T3 Metastasis Doubling time method Punctuated evolution Chromoplexy HRAS Chromothripsis |
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72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS |
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Ray, Durwood B. @@aut@@ Merrill, Gerald A. @@oth@@ Brenner, Frederic J. @@oth@@ Lytle, Laurie S. @@oth@@ Lam, Tan @@oth@@ McElhinney, Aaron @@oth@@ Anders, Joel @@oth@@ Rock, Tara Tauber @@oth@@ Lyker, Jennifer Kier @@oth@@ Barcus, Scott @@oth@@ Leslie, Kara Hust @@oth@@ Kramer, Jill M. @@oth@@ Rubenstein, Eric M. @@oth@@ Pryor Schanz, Karen @@oth@@ Parkhurst, Amy J. @@oth@@ Peck, Michelle @@oth@@ Good, Kimberly @@oth@@ Granath, Kristi Lemke @@oth@@ Cifra, Nicole @@oth@@ Detweiler, Jessalee Wantz @@oth@@ Stevens, Laura @@oth@@ Albertson, Richard @@oth@@ Deir, Rachael @@oth@@ Stewart, Elisabeth @@oth@@ Wingard, Katherine @@oth@@ Richardson, Micah Rose @@oth@@ Blizard, Sarah B. @@oth@@ Gillespie, Lauren E. @@oth@@ Kriley, Charles E. @@oth@@ Rzewnicki, Daniel I. @@oth@@ Jones, David H. @@oth@@ |
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3570 |
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Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. 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T24 HRAS transformed NIH/3T3 mouse cells (GhrasT-NIH/3T3) in serial tumorigenic in vitro/in vivo passages give rise to increasingly aggressive tumorigenic cell lines T1-A and T2-A and metastatic cell lines T3-HA and T4-PA |
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T24 HRAS transformed NIH/3T3 mouse cells (GhrasT-NIH/3T3) in serial tumorigenic in vitro/in vivo passages give rise to increasingly aggressive tumorigenic cell lines T1-A and T2-A and metastatic cell lines T3-HA and T4-PA |
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t24 hras transformed nih/3t3 mouse cells (ghrast-nih/3t3) in serial tumorigenic in vitro/in vivo passages give rise to increasingly aggressive tumorigenic cell lines t1-a and t2-a and metastatic cell lines t3-ha and t4-pa |
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T24 HRAS transformed NIH/3T3 mouse cells (GhrasT-NIH/3T3) in serial tumorigenic in vitro/in vivo passages give rise to increasingly aggressive tumorigenic cell lines T1-A and T2-A and metastatic cell lines T3-HA and T4-PA |
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Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ... |
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Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ... |
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Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ... |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV030080908</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625180504.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2016 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.yexcr.2015.07.029</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2016021000016.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV030080908</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0014-4827(15)30060-4</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">570</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">570</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.44</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Ray, Durwood B.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">T24 HRAS transformed NIH/3T3 mouse cells (GhrasT-NIH/3T3) in serial tumorigenic in vitro/in vivo passages give rise to increasingly aggressive tumorigenic cell lines T1-A and T2-A and metastatic cell lines T3-HA and T4-PA</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2016transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">11</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. A new photomicrographic technique to follow growth rates within six preselected 2×2mm2 grids per ...</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Cancer cells often arise progressively from “normal” to “pre-cancer” to “transformed” to “local metastasis” to “metastatic disease” to “aggressive metastatic disease”. Recent whole genome sequencing (WGS) and spectral karyotyping (SKY) of cancer cells and tumorigenic models have shown this progression involves three major types of genome rearrangements: ordered small step-wise changes, more dramatic “punctuated evolution” (chromoplexy), and large catastrophic steps (chromothripsis) which all occur in random combinations to generate near infinite numbers of stochastically rearranged metastatic cancer cell genomes. This paper describes a series of mouse cell lines developed sequentially to mimic this type of progression. This starts with the new GhrasT-NIH/Swiss cell line that was produced from the NIH/3T3 cell line that had been transformed by transfection with HRAS oncogene DNA from the T24 human bladder carcinoma. These GhrasT-NIH/Swiss cells were injected s.c. into NIH/Swiss mice to produce primary tumors from which one was used to establish the T1-A cell line. T1-A cells injected i.v. into the tail vein of a NIH/Swiss mouse produced a local metastatic tumor near the base of the tail from which the T2-A cell line was established. T2-A cells injected i.v. into the tail vein of a nude NIH/Swiss mouse produced metastases in the liver and one lung from which the T3-HA (H=hepatic) and T3-PA (P=pulmonary) cell lines were developed, respectively. T3-HA cells injected i.v. into a nude mouse produced a metastasis in the lung from which the T4-PA cell line was established. PCR analysis indicated the human T24 HRAS oncogene was carried along with each in vitro/in vivo transfer step and found in the T2-A and T4-PA cell lines. Light photomicrographs indicate that all transformed cells are morphologically similar. GhrasT-NIH/Swiss cells injected s.c. produced tumors in 4% of NIH/Swiss mice in 6–10 weeks; T1-A cells injected s.c. produced tumors in 100% of NIH/Swiss mice in 7–10 days. T1-A, T-2A, T3-HA and T4-PA cells when injected i.v. into the tail produced local metastasis in non-nude or nude NIH/Swiss mice. T4-PA cells were more widely metastatic than T3-HA cells when injected i.v. into nude mice. Evaluation of the injected mice indicated a general increase in metastatic potential of each cell line in the progression as compared to the GhrasT-NIH/3T3 transformed cells. 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