51 results about "Triple negative" patented technology

The present invention relates to a method for prognosing cancer in a subject with triple negative (TN) breast cancer, whose tumors lack expression of the estrogen receptor (ER), the progesterone receptor (PR) and normal (not amplified) levels of the human epidermal growth factor receptor 2 (HER2). Methods and biomarkers are disclosed that are useful for predicting the overall survival (OS) potential of cancer in a subject with triple negative breast cancer or for predicting metastatic disease in a subject with triple negative breast cancer. For example, the method comprises detecting in a sample from a subject one or more biomarkers selected from the group consisting of ANK3, CD24, EIF1, KLF6, KRAS, KRT1, MAP2K4, SDC4, SLC2A3, STK3, TFAP2C, and WRN. An increase or decrease in one or more biomarkers as compared to a standard is prognostic of OS of TN breast cancer. Likewise, in another example, the method comprises detecting in a sample from a subject one or more biomarkers selected from the group consisting of ANG, DICER1, EIF1, and MSH6. An increase or decrease in one or more biomarkers as compared to a standard is prognostic of metastasis of TN breast cancer.

The present invention provides methods of detecting triple negative breast cancer recurrence using biomarkers.

Methods useful in the prediction and detection of a triple negative cancer subtype using biomarkers are provided herein.

The invention relates to a miR-506 targeting PENK gene of triple negative breast cancer cells and application of the miR-506. By screening miRWalk2.0, miRBase, TargetScanHuman 7.0 databases and detecting tissue samples of triple negative breast cancer patients by using a qRT-PCR technology, it is confirmed that the expression of miR-506 in the triple negative breast cancer is decreased significantly, and is averagely down-regulated by 88.95%, a dual-luciferase reporter experiment confirms that miR-506 can directly interact with Penk, and it is indicated that miR-506 can target PENK. Accordingto the miR-506 targeting the PENK gene of the triple negative breast cancer cells and the application of the miR-506, it is proved that miR-506 affects the proliferation, metastasis and invasion of triple negative breast cancer cells by increasing the content of penk in a targeting mode; the effectiveness of miR-506 targeting penk in inhibiting the progression of the triple negative breast canceris detected through a nude mouse breast cancer model; and the results show that the miR-506 can inhibit the development of the triple negative breast cancer through targeting penk.

In one aspect, the present disclosure provides a method of predicting disease progression comprising: (a) obtaining a sample of breast tissue that is estrogen receptor negative, progesterone receptor negative and does not over-express human epidermal growth factor 2 receptor protein; and (b) determining the expression of glia maturation factor beta, wherein expression of glia maturation factor beta is indicative of lymph node metastatis. In another aspect, the present disclosure provides a method of predicting disease progression comprising: (a) obtaining a sample of breast tissue that is estrogen receptor negative, progesterone receptor negative and does not over-express human epidermal growth factor 2 receptor protein; and (b) determining the expression of glia maturation factor beta, wherein expression of glia maturation factor beta is indicative of an untreated or treated prognosis that is reduced compared to an absence of the expression.

The invention provides application of protein DEPDC1 (Dishevelled and EGL-10, Pleckstrin Domain-Containing protein 1) as a marker for diagnosing the triple negative breast cancer, and also provides application of miR-26b for preparing a medicine for treating the triple negative breast cancer. The invention also provides application of miR-26b for preparing a medicine for inhibiting DEPDC1 mRNA (Ribonucleic Acid) expression. The invention finds that DEPDC1 expression is obviously higher than a paired para-carcinoma tissue in a triple negative breast cancer tissue. In the triple negative breastcancer cell, overexpression DEPDC1 can accelerate cell growth and tumor formation through FOXM1 (Forkhead box protein M1) expression up-regulation. On the contrary, after the DEPDC1 is knocked down,an inverse function is displayed. In addition, in the triple negative breast cancer, miR-26b serves as a tumor inhibiting factor to directly inhibit DEPDC1 expression and weaken the acceleration function of the DEPDC1 for cell growth and clone formation. The invention points out a new important mechanism for the occurrence, the development, the regulation and the control of the triple negative breast cancer.

Provided are compositions and methods for the identification and treatment of cancers exhibiting reduced MRE11/RAD50/NBS1 (MRN) complex formation and/or functionality as well as methods for the identification and use of cytotoxic agents, including clastogenic agents, for the treatment of cancers exhibiting reduced MRN complex formation and/or functionality. Also provided are methods for detecting and treating cancers, in particular breast cancers, such as hormone-negative breast cancers (HNBCs) and triple-negative breast cancers (TNBCs), colorectal cancers, urothelial cancers, and other cancers that exhibit reduced MRN complex formation and/or functionality and are correspondingly sensitive to growth and/or survival inhibition by one or more cytotoxic agents.

The invention discloses a resistin polypeptide vaccine and application thereof to the treatment of a mammary cancer, and belongs to the technical field of biology. A polypeptide vaccine provided by the invention is prepared from a Resistin-protein specific polypeptide segment and an immunologic adjuvant, and becomes the Resistin polypeptide vaccine. Through multiple subcutaneous injections, the vaccine can be used for activating the lymphocyte of an organism, and generates an immune neutralizing antibody aiming at Resistin protein. The Resistin polypeptide vaccine does not influence the sugartolerance and insulin tolerance levels of the organism at all. The Resistin polypeptide vaccine can be used for obviously inhibiting the growth of an ER (Estrogen Receptor) positive mammary tumor anda triple-negative mammary tumor under a mouse model; in addition, the Resistin polypeptide vaccine can be used for obviously inhabiting the growth of the ER positive mammary tumor and the triple-negative mammary tumor of a mouse under an obesity model induced by a high fat diet, and a new way is provided for ameliorating a current treatment method of the mammary cancer by the resistin polypeptidevaccine.

A method for the diagnosis of breast cancer using an anti-LAT1 monoclonal antibody. Among intraductal breast neoplastic lesions, duct carcinoma in situ, which is malignant, expresses LAT1 at a significantly high level, as compared to intraductal breast papilloma, which is benign. An anti-LAT1 monoclonal antibody is useful for the discrimination between these two lesions. Further, LAT1 is expressed at a high level in most of triple negative infiltrating carcinomas, which are negative for all of ER, PgR, and HER2 that are conventional molecular targeting markers for breast cancer. Therefore, LAT1 can be used as a novel molecular targeting marker for the triple negative breast cancer.

Provided herein are methods for diagnosing and/or treating a new subtype of triple negative breast cancers (TNBC), as well as compositions and kits that can be used in such methods.

The present invention relates to a method for treating breast cancer in a subject having a breast cancer of the triple-negative type, which method comprises the step of administering to said subject a therapeutically effective amount of a modulator of the protein tyrosine phosphatase, non-receptor type 11 (PTPN11) gene or of its gene product (Shp2). The present invention also relates to a method for treating breast cancer in a subject having a breast cancer over-expressing the “SHP2 signature” genes, as compared to normal breast tissue samples, which method comprises the step of administering to said subject a therapeutically effective amount of a modulator of the protein tyrosine phosphatase, non-receptor type 11 (PTPN11) gene or of its gene product (Shp2), wherein said “SHP2 signature” genes consist of the genes SGCB, ZSCAN12, ID4, ZIC3, CPVL, HLA-A, MCOLN3, SPATA18, TMEM45A, GNAL, CYBRD1, TSPAN7, ZEB1, CNTLN, NEFL, CENPV, ARL6, HPRT1, LRRC34, PDPN, BEND7, SLC16A10, FAM27E1, PLEKHA1, HERC5, CHIC1, PHF6, ELOVL4, ANTXR1, PRAME, SCML1, CLIP4, CECR2, CNOT10, IGF2BP3, NAP1L3, GPC3, KIAA1804, DGKE, FAS, EPHA6, KDELC1, CRISPLD1, DOCK3, ACSL4, CNTNAP3, PLEKHM3, RDX, TBX18, RRAGD, HOXB5, SNCA, FUNDC2, ITGA8, HFM1, IGF2BP2, CCND2, SGTB, MKX, CRYBG3, WBP5, LPHN3, BEX4, CPNE8, GLDC, SLC35F1, HOXA13, SERPINF1, NEFM, SYCP2L, FHL1, APOBEC3C, CALD1, FKBP10, HOXD11, DENND2C, LRRC49, FAM55C, KIAA0408, HOXB9, C160RF62, ACN9, TUSC3, ELOVL2, SPOCK3, HOXB6, WDR35, MPP1, FBX038, PRKAA2, SLAIN1, NPHP3, KIAA1524, PRPS1, GJC1, AMOT, SLC9A6, KCTD12, NUP62CL, DZIP3, JAM3, HOXA9, ANKRD19, CDKN2A, BCAT1, OAT, LPHN2, CCDC82, HSD17B11, SAMHD1, WDR17, STK33, GSTP1, TRPC1, CKB, LIN28B, ALDH1L2, SACS, CLGN, MY03A, EPB41L3, SLC25A27, VCAN, GPX8, GALNT13, PVRL3, MOXD1, HEY1, MAP7D3, ESD, MPP6, EYA4, SPG20, ZDBF2, ZNF204, IFT57, AKR1B1, ADAT2, ZNF717, CCDC88A, ZNF215, MIDI, FBN2, LOC100130876, TCEAL8, IGF2BP1, ANKRD18B, PLAGL1, PM20D2, LDHB, C150RF51, PTPN11, EPB41L2, TLE4, GOLM1, C60RF192, HOXD13, SLIT2, UCHL1, DYNC2H1, CPS1, GPR180, PYGL, NRN1, PRTFDC1, SLC16A1, DSC3, TMC01, LRCH2, SLC6A15, DZIP1, HOXA5, HSPA4L, CDR1, PLS3, ECHDC1, SMARCA1, CXORF57, HOXD10, and IRS4.