# US 2014/0193406 A1 · Methods used in identifying glioblastoma

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- Number: US 2014/0193406 A1
- Document ID: US20140193406A1
- Status: Published application
- Kind: A1
- Application number: 14/213,570
- Filed: 2014-03-14
- Published: 2014-07-10
- Earliest claimed: 2009-10-23
- Assignees: The Translational Genomics Research Institute
- Applicants: Translational Genomics Research Institute
- Inventors: NHAN TRAN
- Web page: https://patentgrep.com/patent/US20140193406A1

## CPC

- C12N 15/1137: {against enzymes (viral enzymes C12N15/1131; receptors C12N15/1138)}
- A61K 31/4188: condensed with other heterocyclic ring systems, e.g. biotin, sorbinil
- A61K 31/713: Double-stranded nucleic acids or oligonucleotides
- A61K 39/3955: {against proteinaceous materials, e.g. enzymes, hormones, lymphokines}
- A61P 35/00: Antineoplastic agents
- C12N 15/113: Non-coding nucleic acids modulating the expression of genes, e.g. antisense oligonucleotides; {Antisense DNA or RNA; Triplex- forming oligonucleotides; Catalytic nucleic acids, e.g. ribozymes; Nucleic acids used in co-suppression or gene silencing (when used in plants C12N15/8218)}
- C12Q 1/6886: for cancer (immunoassay for cancer G01N33/575)
- G01N 33/5755: of the uterine cervix, uterine corpus or endometrium
- G01N 33/57557: {of other specific parts of the body, e.g. brain}
- C12N 2310/14: interfering nucleic acids [NA]
- C12Q 2600/106: Pharmacogenomics, i.e. genetic variability in individual responses to drugs and drug metabolism
- C12Q 2600/112: Disease subtyping, staging or classification
- C12Q 2600/118: Prognosis of disease development
- G01N 2800/52: Predicting or monitoring the response to treatment, e.g. for selection of therapy based on assay results in personalised medicine; Prognosis
- C12N: MICROORGANISMS OR ENZYMES; COMPOSITIONS THEREOF; PROPAGATING, PRESERVING, OR MAINTAINING MICROORGANISMS; MUTATION OR GENETIC ENGINEERING; CULTURE MEDIA (microbiological testing media C12Q1/00)
- A61K: PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES (devices or methods specially adapted for bringing pharmaceutical products into particular physical or administering forms A61J3/00; chemical aspects of, or use of materials for deodorisation of air, for disinfection or sterilisation, or for bandages, dressings, absorbent pads or surgical articles A61L; soap compositions C11D)
- A61P: SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- C12Q: MEASURING OR TESTING PROCESSES INVOLVING ENZYMES, NUCLEIC ACIDS OR MICROORGANISMS (immunoassay G01N33/53); COMPOSITIONS OR TEST PAPERS THEREFOR; PROCESSES OF PREPARING SUCH COMPOSITIONS; CONDITION-RESPONSIVE CONTROL IN MICROBIOLOGICAL OR ENZYMOLOGICAL PROCESSES
- G01N: INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES (measuring or testing apparatus or processes other than immunoassay, involving enzymes or microorganisms C12M, C12Q)

## Abstract

The invention encompasses methods and kits used in the identification of invasive glioblastoma based upon the expression of Akt1, Akt2, and Akt3. The methods and kits also allow prediction of disease outcome and staging of patients with regard to therapy.

## Claims

### Claim 1

A method of treating a patient with cancer, the method comprising the steps of:
sensitizing the patient to a treatment by reducing an expression level of a marker selected from the group consisting of SEQ ID NO. 3 and SEQ ID NO. 4; and
administering a therapeutically effective amount of the treatment to the patient.

### Claim 2 (depends on 1)

The method of claim 1, wherein the cancer comprises glioblastoma.

### Claim 3 (depends on 2)

The method of claim 2, wherein the cancer comprises invasive glioblastoma.

### Claim 4 (depends on 1)

The method of claim 1, wherein the treatment comprises the administration of one or more compounds selected from the group consisting of TROY inhibitors, Pyk2 inhibitors, Rac1 inhibitors, Dock180 inhibitors, Dock7 inhibitors, TWEAK inhibitors, Fn14 inhibitors, BAD inhibitors, and PI3K inhibitors, TRAIL, camptothecin, temozolimide and bevacizumab.

### Claim 5 (depends on 1)

The method of claim 1, wherein reducing the expression level of the marker is enabled by small interfering RNAs targeting the nucleic acid encoding for the marker.

### Claim 6 (depends on 5)

The method of claim 5, wherein the small interfering RNAs comprise oligonucleotides.

### Claim 7

A method of characterizing a tumor as invasive and sensitizing the invasive tumor for treatment, the method comprising the steps of:
adding a first reagent capable of binding to a marker selected from the group consisting of SEQ ID NO. 3 and SEQ ID NO. 4 to a mixture comprising a sample of the tumor;
subjecting the mixture to conditions that allow detection of binding of the reagent to the marker;
classifying the tumor as invasive when the binding of the reagent to the marker is increased compared to a control sample; and
reducing an expression level of the marker to sensitize the invasive tumor to a treatment.

### Claim 8 (depends on 7)

The method of claim 7, wherein sensitizing the invasive tumor induces apoptosis in at least a portion of cells of the tumor upon administration of the treatment.

### Claim 9 (depends on 7)

The method of claim 7 and further comprising administering a therapeutically effective amount of the treatment to the patient.

### Claim 10 (depends on 9)

The method of claim 9, wherein the treatment comprises the administration of one or more compounds selected from the group consisting of TROY inhibitors, Pyk2 inhibitors, Rac1 inhibitors, Dock180 inhibitors, Dock7 inhibitors, TWEAK inhibitors, Fn14 inhibitors, BAD inhibitors, and PI3K inhibitors, TRAIL, camptothecin, temozolimide and bevacizumab.

### Claim 11 (depends on 7)

The method of claim 7, wherein the invasive tumor comprises glioblastoma.

### Claim 12 (depends on 7)

The method of claim 7, wherein the sample is selected from the group consisting of brain tissues, fluid samples, and single cells.

### Claim 13 (depends on 7)

The method of claim 7, wherein reducing the expression level of the marker is enabled by small interfering RNAs targeting the nucleic acid encoding for the marker.

### Claim 14 (depends on 13)

The method of claim 13, wherein the small interfering RNAs comprise oligonucleotides.

### Claim 15

A method of characterizing a tumor as invasive and sensitizing the invasive tumor for treatment, the method comprising the steps of:
receiving a sample from the tumor;
adding a reagent capable of binding to a marker selected from the group consisting of SEQ ID NO. 3 and SEQ ID NO. 4 to a mixture comprising the sample;
subjecting the mixture to conditions that allow detection of the binding of the reagent to the marker;
classifying the tumor as an invasive when the binding of the reagent to the marker in the sample is more than twice the binding of the reagent to a control sample; and
reducing an expression level of the marker to sensitize the invasive tumor to a treatment.

### Claim 16 (depends on 15)

The method of claim 15 and further comprising administering a therapeutically effective amount of the treatment to the patient.

### Claim 17 (depends on 16)

The method of claim 16, wherein the treatment comprises the administration of one or more compounds selected from the group consisting of TROY inhibitors, Pyk2 inhibitors, Rac1 inhibitors, Dock180 inhibitors, Dock7 inhibitors, TWEAK inhibitors, Fn14 inhibitors, BAD inhibitors, and PI3K inhibitors, TRAIL, camptothecin, temozolimide and bevacizumab.

### Claim 18 (depends on 15)

The method of claim 15, wherein the invasive tumor comprises glioblastoma.

### Claim 19 (depends on 15)

The method of claim 15, wherein reducing the expression level of the marker is enabled by small interfering RNAs targeting the nucleic acid encoding for the marker.

### Claim 20 (depends on 19)

The method of claim 19, wherein the small interfering RNAs comprise oligonucleotides.