IP Library Granted Patent US 9,452,182
Granted Patent B2
US 9,452,182 · App. 14/365,367 · Granted Sep 27, 2016

Collateral gene inactivation biomarkers and targets for cancer therapy

Inventors: Florian L. Muller (Houston, TX); Eliot Fletcher-Sananikone (Houston, TX); Simona Colla (Houston, TX); Elisa Aquilanti (Boston, MA); Ronald DePinho (Houston, TX)
Assignees: Board of Regents, The University of Texas System; Dana-Farber Cancer Institute, Inc.
A61K31/713A61K31/191A61K31/198A61K31/35A61K31/352A61K31/357A61K31/5685A61K31/661A61K31/662A61K45/06C12N15/1137C12Q1/6886G01N33/5038G01N33/5743G01N33/57407A61K48/00C12N2310/14C12N2310/531C12N2320/31C12Q2600/106C12Q2600/156C12Y402/01001C12Y402/01011G01N2333/988G01N2800/52
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Quick Facts
Patent No.
US 9,452,182
App. No.
14/365,367
Granted
Sep 27, 2016
Kind
B2
Abstract

Methods for treating a subject determined to have a cancer comprising a heterozygous inactivation of a housekeeping gene (or a homozygous deletion of a functionally redundant housekeeping gene) by treating the subject with an inhibitor of the gene. For example, a subject having a cancer with an ENO gene deletion can be treated with a glycolysis inhibitor, such as an enolase inhibitor. In some aspects, a subject having a cancer with an ARS gene deletion can be treated with an ARS inhibitor.

Claims (29)

1. A method of treating cancer in a subject, comprising administering to the subject an effective amount of an inhibitor of a functionally redundant homologue of a housekeeping gene, said cancer in the subject having been determined to have a homozygous deletion in the housekeeping gene.

2. The method of claim 1 , wherein the inhibitor is a nucleic acid that inhibits the expression or activity of the redundant homologue, an antibody that specifically binds the redundant homologue or a small molecule inhibitor of the redundant homologue.

3. The method of claim 1 , further comprising administering a chemotherapeutic agent to the subject.

4. The method of claim 3 , wherein the chemotherapeutic agent interferes with DNA homeostasis.

5. The method of claim 1 , wherein:

a) the housekeeping gene is enolase 1 (ENO1) and the redundant homologue is enolase 2 (ENO2);

b) the housekeeping gene is hexose-6-phosphate dehydrogenase (H6PD) and the redundant homologue is glucose-6 dehydrogenase (G6PD);

c) the housekeeping gene is kinesin family member 1B (KIF1B) and the redundant homologue is kinesin family member 1A (KIF1A) or kinesin family member 1C (KIF1C);

d) the housekeeping gene is Nicotinamide nucleotide adenylyl transferase 1 (NMNAT1) and the redundant homologue is Nicotinamide nucleotide adenylyl transferase 2 (NMNAT2) or nicotinamide nucleotide adenylyl transferase 3 (NMNAT3);

e) the housekeeping gene is ubiquitination factor E4B (UBE4B) and the redundant homologue is ubiquitination factor 4A (UBE4A);

f) the housekeeping gene is aconitase 1 (ACO1) and the redundant homologue is aconitase 2 (ACO2) or aconitase 3 (ACO3);

g) the housekeeping gene is kelch-like 9 (KLHL9) and the redundant homologue is kelch-like 13 (KLHL13);

h) the housekeeping gene is pantothenate kinase 1 (PANK1) and the redundant homologue is pantothenate kinase 3 (PANK3); or

i) the housekeeping gene is kinase family member 20B (KIF20B) and the redundant homologue is kinase family member 20A (KIF20A).

6. The method of claim 5 , wherein the housekeeping gene is ENO1 and the redundant homologue is ENO2 and wherein the inhibitor is a glycolysis inhibitor.

7. The method of claim 6 , wherein the glycolysis inhibitor is an enolase inhibitor.

8. The method of claim 7 , the enolase inhibitor is a small molecule enolase inhibitor.

9. The method of claim 8 , wherein the enolase inhibitor comprises D-tartronate semialdehyde phosphate; 3-aminoenolpyruvate-2-phosphate; phosphonoacetohydroaxamate (PhAH); 2-fluoro-2-phosphonoacetohydroxamate; (3-hydroxy-2-nitropropyl)phosphonate; (nitroethyl)phosphonate; d -(phosphonoethyl)nitrolate or a prodrug thereof.

10. The method of claim 7 , wherein the glycolysis inhibitor is 2-deoxyglucose, 6-aminonicotinamide, tetrose diphosphate, koningic acid or MJE3 or a prodrug thereof.

11. The method of claim 5 , wherein the housekeeping gene is H6PD and the redundant homologue is G6PD and wherein the inhibitor is dehydroepiandrosterone or a prodrug thereof.

12. The method of claim 5 , wherein the housekeeping gene is NMNAT1 and the redundant homologue is NMNAT2 or NMNAT3 and wherein the inhibitor is Np2AD, Np4AD or Nap4AD or a prodrug thereof.

13. The method of claim 5 , wherein the housekeeping gene is ACO1 and the redundant homologue is ACO2 or ACO3 and wherein the inhibitor is fluorocitrate or a prodrug thereof.

14. The method of claim 5 , wherein the housekeeping gene is PANK1 and the redundant homologue is PANK3 and wherein the inhibitor is hopantenate or a prodrug thereof.

15. The method of claim 1 , further comprising measuring the level of one or more metabolites of the metabolic pathway of the housekeeping gene in a sample from the subject, wherein an accumulation of the metabolite indicates that the treatment is efficacious.

16. The method of claim 15 , wherein the housekeeping gene is enolase and the metabolite is glyerate.

17. The method of claim 1 , wherein the cancer was determined to have a homozygous deletion in the housekeeping gene by DNA sequencing.

18. A method of treating a subject having a cancer comprising, administering an effective amount of a glycolysis inhibitor to the subject, said cancer in the subject having been previously determined to comprise a heterozygous mutation that inactivates one copy of the Enolase 1 (ENO1) gene.

19. The method of claim 18 , wherein the glycolysis inhibitor comprises D-tartronate semialdehyde phosphate; 3-aminoenolpyruvate-2-phosphate; phosphonoacetohydroaxamate (PhAH); 2-fluoro-2-phosphonoacetohydroxamate; (3-hydroxy-2-nitropropyl)phosphonate; (nitroethyl)phosphonate; d-(phosphonoethyl)nitrolate or a prodrug thereof.

20. A method of treating a subject having a cancer comprising, administering an effective amount of an ARS inhibitor, or a prodrug thereof, to the subject, said cancer in the subject having been determined to comprise a heterozygous mutation that inactivates one copy of a tRNA synthetase (ARS) gene.

Assignments (2)
CONFIRMATORY LICENSE Recorded Oct 24, 2017
From: UNIVERSITY OF TX MD ANDERSON CAN CTR
To: NATIONAL INSTITUTES OF HEALTH (NIH), U.S. DEPT. OF HEALTH AND HUMAN SERVICES (DHHS), U.S. GOVERNMENT
Reel/Frame 044279/0952 →
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Dec 1, 2014
From: MULLER, FLORIAN L.; FLETCHER-SANANIKONE, ELIOT; COLLA, SIMONA; AQUILANTI, ELISA; DEPINHO, RONALD
To: BOARD OF REGENTS, THE UNIVERSITY OF TEXAS SYSTEM; DANA-FARBER CANCER INSTITUTE, INC.
Reel/Frame 034288/0008 →
Continuity (3)
Provisional Application 61570366 · Dec 14, 2011
Provisional Application 61652738 · May 29, 2012
Related Publication 20140378529A1 · Dec 25, 2014