Herbert Haack from Newburyport, MA, age 63

Us Patents

Protein Markers Of Responsiveness To Type Iii Receptor Tyrosine Kinase Inhibitors
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US Patent:

7833736, Nov 16, 2010
Filed:

Apr 2, 2007
Appl. No.:

11/731984
Inventors:

Herbert Haack - Holliston MA, US
Laura Sullivan - Beverly MA, US
Assignee:

Cell Signaling Technology, Inc. - Danvers MA
International Classification:

G01N 33/574
US Classification:

435 723
Abstract:

The invention discloses ten (10) protein markers predictive of cancer resistance or responsiveness to Type III Receptor Tyrosine Kinase (RTK) inhibitors, and provides methods for identifying a cancer that is likely to be resistant to a Type III RTK-inhibiting therapeutic by examining expression and/or activity of one or more of the disclosed biomarkers in a biological sample from the cancer. Methods for identifying a compound that inhibits a cancer resistant to a Type III RTK-inhibiting therapeutic by determining the effect of the compound on one or more of the disclosed marker proteins are also provided.

Gene Defects And Mutant Alk Kinase In Human Solid Tumors
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US Patent:

8168383, May 1, 2012
Filed:

Oct 19, 2009
Appl. No.:

12/589176
Inventors:

Klarisa Rikova - Reading MA, US
Herbert Haack - South Hamilton MA, US
Laura Sullivan - Shrewsbury MA, US
Ailan Guo - Lexington MA, US
Anthony Possemato - Worcester MA, US
Joan MacNeill - Litchfield NH, US
Jian Yu - Hamilton MA, US
Assignee:

Cell Signaling Technology, Inc. - Danvers MA
International Classification:

C12Q 1/68
C12Q 1/48
C07H 21/00
C12N 9/12
US Classification:

435 61, 435194, 435 15, 536 231, 536 232, 536 235
Abstract:

Novel gene deletions and translocations involving chromosome 2 resulting in fusion proteins combining part of Anaplastic Lymphoma Kinase (ALK) kinase with part of a secondary protein have now been identified in human solid tumors, e. g. non-small cell lung carcinoma (NSCLC). Secondary proteins include Echinoderm Microtubule-Associated Protein-Like 4 (EML-4) and TRK-Fusion Gene (TFG). The EML4-ALK fusion protein, which retains ALK tyrosine kinase activity, was confirmed to drive the proliferation and survival of NSCLC characterized by this mutation. The invention therefore provides, in part, isolated polynucleotides and vectors encoding the disclosed mutant polypeptides, probes for detecting it, isolated mutant polypeptides, and reagents for detecting the fusion and truncated polypeptides. The invention also provides methods for determining the presence of these mutant polypeptides in a biological sample, methods for screening for compounds that inhibit the proteins, and methods for inhibiting the progression of a cancer characterized by the mutant polynucleotides or polypeptides.

Gene Defects And Mutant Alk Kinase In Human Solid Tumors
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US Patent:

8232060, Jul 31, 2012
Filed:

Sep 3, 2009
Appl. No.:

12/584353
Inventors:

Klarisa Rikova - Reading MA, US
Herbert Haack - Holliston MA, US
Laura Sullivan - Beverly MA, US
Ailan Guo - Burlington MA, US
Anthony Possemato - Framingham MA, US
Joan MacNeill - Derry NH, US
Assignee:

Cell Signaling Technology, Inc. - Danvers MA
International Classification:

G01N 33/53
C12P 21/00
C07K 14/00
C12Q 1/48
C12N 9/12
US Classification:

435 71, 435194, 435 691, 435 15, 530350
Abstract:

In accordance with the invention, novel gene deletions and translocations involving chromosome 2 resulting in fusion proteins combining part of Anaplastic Lymphoma Kinase (ALK) kinase with part of a secondary protein have now been identified in human solid tumors, e. g. non-small cell lung carcinoma (NSCLC). Secondary proteins include Echinoderm Microtubule-Associated Protein-Like 4 (EML-4) and TRK-Fusion Gene (TFG). The EML4-ALK fusion protein, which retains ALK tyrosine kinase activity, was confirmed to drive the proliferation and survival of NSCLC characterized by this mutation. The invention therefore provides, in part, isolated polynucleotides and vectors encoding the disclosed mutant ALK kinase polypeptides, probes for detecting it, isolated mutant polypeptides, recombinant polypeptides, and reagents for detecting the fusion and truncated polypeptides. The disclosed identification of this new fusion protein enables new methods for determining the presence of these mutant ALK kinase polypeptides in a biological sample, methods for screening for compounds that inhibit the proteins, and methods for inhibiting the progression of a cancer characterized by the mutant polynucleotides or polypeptides, which are also provided by the invention.

Gene Defects And Mutant Alk Kinase In Human Solid Tumors
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US Patent:

8288102, Oct 16, 2012
Filed:

Feb 27, 2010
Appl. No.:

12/714457
Inventors:

Klarisa Rikova - Reading MA, US
Herbert Haack - Holliston MA, US
Laura Sullivan - Beverly MA, US
Ailan Guo - Burlington MA, US
Anthony Possemato - Framingham MA, US
Joan MacNeill - Derry NH, US
Jian Yu - Hamilton MA, US
Assignee:

Cell Signaling Technology, Inc. - Danvers MA
International Classification:

C12Q 1/68
C12N 9/12
C07H 21/00
US Classification:

435 612, 435 61, 435194, 536 234, 536 243
Abstract:

In accordance with the invention, novel gene deletions and translocations involving chromosome 2 resulting in fusion proteins combining part of Anaplastic Lymphoma Kinase (ALK) kinase with part of a secondary protein have now been identified in human solid tumors, e. g. non-small cell lung carcinoma (NSCLC). Secondary proteins include Echinoderm Microtubule-Associated Protein-Like 4 (EML-4) and TRK-Fusion Gene (TFG). The EML4-ALK fusion protein, which retains ALK tyrosine kinase activity, was confirmed to drive the proliferation and survival of NSCLC characterized by this mutation. The invention therefore provides, in part, isolated polynucleotides and vectors encoding the disclosed mutant ALK kinase polypeptides, probes for detecting it, isolated mutant polypeptides, recombinant polypeptides, and reagents for detecting the fusion and truncated polypeptides. The disclosed identification of this new fusion protein enables new methods for determining the presence of these mutant ALK kinase polypeptides in a biological sample, methods for screening for compounds that inhibit the proteins, and methods for inhibiting the progression of a cancer characterized by the mutant polynucleotides or polypeptides, which are also provided by the invention.

Gene Defects And Mutant Alk Kinase In Human Solid Tumors
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US Patent:

8377642, Feb 19, 2013
Filed:

Sep 28, 2010
Appl. No.:

12/891987
Inventors:

Klarisa Rikova - Reading MA, US
Herbert Haack - South Hamilton MA, US
Laura Sullivan - Beverly MA, US
Ailan Guo - Lexington MA, US
Anthony Possemato - Worcester MA, US
Joan MacNeill - Litchfield NH, US
Jian Yu - Hamilton MA, US
Assignee:

Cell Signaling Technology, Inc. - Danvers MA
International Classification:

C12Q 1/68
C07H 21/00
C12N 9/12
US Classification:

435 618, 435 614, 435 612, 435 611, 435194, 536 231, 536 232
Abstract:

In accordance with the invention, novel gene deletions and translocations involving chromosome 2 resulting in fusion proteins combining part of Anaplastic Lymphoma Kinase (ALK) kinase with part of a secondary protein have now been identified in human solid tumors, e. g. non-small cell lung carcinoma (NSCLC). Secondary proteins include Echinoderm Microtubule-Associated Protein-Like 4 (EML-4) and TRK-Fusion Gene (TFG). The EML4-ALK fusion protein, which retains ALK tyrosine kinase activity, was confirmed to drive the proliferation and survival of NSCLC characterized by this mutation. The invention therefore provides, in part, isolated polynucleotides and vectors encoding the disclosed mutant ALK kinase polypeptides, probes for detecting it, isolated mutant polypeptides, recombinant polypeptides, and reagents for detecting the fusion and truncated polypeptides. The disclosed identification of this new fusion protein enables new methods for determining the presence of these mutant ALK kinase polypeptides in a biological sample, methods for screening for compounds that inhibit the proteins, and methods for inhibiting the progression of a cancer characterized by the mutant polynucleotides or polypeptides, which are also provided by the invention.

Methods Of Treating Lung Cancer Using Inhibitors Anaplastic Lymphoma Kinase
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US Patent:

8481279, Jul 9, 2013
Filed:

Feb 6, 2012
Appl. No.:

13/366679
Inventors:

Klarisa Rikova - Reading MA, US
Herbert Haack - South Hamilton MA, US
Laura Sullivan - Shrewsbury MA, US
Ailan Guo - Lexington MA, US
Anthony Possemato - Worcester MA, US
Joan MacNeill - Litchfield NH, US
Jian Yu - Hamilton MA, US
Assignee:

Cell Signaling Technology, Inc. - Danvers MA
International Classification:

C12Q 1/48
A61K 31/00
C12N 9/12
US Classification:

435 15, 435194, 514 1
Abstract:

In accordance with the invention, novel gene deletions and translocations involving chromosome 2 resulting in fusion proteins combining part of Anaplastic Lymphoma Kinase (ALK) kinase with part of a secondary protein have now been identified in human solid tumors, e. g. non-small cell lung carcinoma (NSCLC). Secondary proteins include Echinoderm Microtubule-Associated Protein-Like 4 (EML-4) and TRK-Fusion Gene (TFG). The EML4-ALK fusion protein, which retains ALK tyrosine kinase activity, was confirmed to drive the proliferation and survival of NSCLC characterized by this mutation. The invention therefore provides, in part, isolated polynucleotides and vectors encoding the disclosed mutant ALK kinase polypeptides, probes for detecting it, isolated mutant polypeptides, recombinant polypeptides, and reagents for detecting the fusion and truncated polypeptides. The disclosed identification of this new fusion protein enables methods for screening for compounds that inhibit the proteins, and methods for inhibiting the progression of a cancer characterized by the mutant polynucleotides or polypeptides.

Gene Defects And Mutant Alk Kinase In Human Solid Tumors
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US Patent:

8486645, Jul 16, 2013
Filed:

Apr 3, 2012
Appl. No.:

13/438218
Inventors:

Klarisa Rikova - Reading MA, US
Herbert Haack - South Hamilton MA, US
Laura Sullivan - Shrewsbury MA, US
Ailan Guo - Lexington MA, US
Anthony Possemato - Worcester MA, US
Joan MacNeill - Litchfield NH, US
Jian Yu - Hamilton MA, US
Assignee:

Cell Signaling Technology, Inc. - Danvers MA
International Classification:

G01N 33/53
G01N 33/563
C12Q 1/48
C12N 9/12
G01N 35/08
US Classification:

435 71, 435 15, 435194, 436512, 436513, 436 52
Abstract:

Novel gene deletions and translocations involving chromosome 2 resulting in fusion proteins combining part of Anaplastic Lymphoma Kinase (ALK) kinase with part of a secondary protein have now been identified in human solid tumors, e. g. non-small cell lung carcinoma (NSCLC). Secondary proteins include Echinoderm Microtubule-Associated Protein-Like 4 (EML-4) and TRK-Fusion Gene (TFG). The EML4-ALK fusion protein, which retains ALK tyrosine kinase activity, was confirmed to drive the proliferation and survival of NSCLC characterized by this mutation. The invention therefore provides, in part, isolated polynucleotides and vectors encoding the disclosed mutant polypeptides, probes for detecting it, isolated mutant polypeptides, and reagents for detecting the fusion and truncated polypeptides. The invention also provides methods for determining the presence of these mutant polypeptides in a biological sample, methods for screening for compounds that inhibit the proteins, and methods for inhibiting the progression of a cancer characterized by the mutant polynucleotides or polypeptides.

Gene Defects And Mutant Alk Kinase In Human Solid Tumors
view source
US Patent:

20090156475, Jun 18, 2009
Filed:

Apr 13, 2007
Appl. No.:

11/787132
Inventors:

Klarisa Rikova - Reading MA, US
Herbert Haack - Holliston MA, US
Laura Sullivan - Shrewsbury MA, US
Ailan Guo - Burlington MA, US
Anthony Possemato - Framingham MA, US
Joan MacNeill - Derry NH, US
Jian Yu - Hamilton MA, US
International Classification:

A61K 38/16
C07H 21/04
C12N 15/74
C07K 14/00
C07K 16/00
G01N 33/53
C12Q 1/68
A61P 35/00
US Classification:

514 12, 536 237, 4353201, 435471, 530350, 530402, 5303871, 435 71, 435 6
Abstract:

In accordance with the invention, novel gene deletions and translocations involving chromosome 2 resulting in fusion proteins combining part of Anaplastic Lymphoma Kinase (ALK) kinase with part of a secondary protein have now been identified in human solid tumors, e.g. non-small cell lung carcinoma (NSCLC). Secondary proteins include Echinoderm Microtubule-Associated Protein-Like 4 (EML-4) and TRK-Fusion Gene (TFG). The EML4-ALK fusion protein, which retains ALK tyrosine kinase activity, was confirmed to drive the proliferation and survival of NSCLC characterized by this mutation. The invention therefore provides, in part, isolated polynucleotides and vectors encoding the disclosed mutant ALK kinase polypeptides, probes for detecting it, isolated mutant polypeptides, recombinant polypeptides, and reagents for detecting the fusion and truncated polypeptides. The disclosed identification of this new fusion protein enables new methods for determining the presence of these mutant ALK kinase polypeptides in a biological sample, methods for screening for compounds that inhibit the proteins, and methods for inhibiting the progression of a cancer characterized by the mutant polynucleotides or polypeptides, which are also provided by the invention.