CN111420033A - Use of human interferon in tumor treatment - Google Patents
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Abstract
The invention discloses an application of interferon in preparing a medicament for treating tumors, and due to the expression characteristics of the interferon in epithelial cells and mucosal tissues, the interferon is found to have a remarkable effect in treating melanoma, so that the interferon has a good application prospect in the aspect of tumor treatment, provides a certain theoretical basis for the anti-cancer effect of the interferon in treating tumors, particularly solid tumors of melanoma, and also provides a new thought and treatment means for the tumor treatment, particularly the solid tumor treatment represented by the melanoma.
Description
Technical Field
The invention relates to the technical field of tumor treatment, in particular to application of interferon in preparing a medicament for treating tumors.
Background
Currently, malignant tumor (cancer) has become one of the major public health problems seriously threatening the global population health, and according to the statistical data of the latest World Health Organization (WHO) international agency for research on cancer (IARC), the number of people suffering from cancer worldwide is rapidly increasing, 1810 ten thousand cases are newly added in 2018 for one year, and the number of death people is up to 960 ten thousand. By the end of this century, cancer will likely become the world's first number "killer". Cancer is still one of the most lethal diseases in China at present. According to the latest cancer data released by the national cancer center, about 392.9 ten thousand cases of malignant tumors occur in China in 2015, and the incidence rate is 285.8/10 ten thousand; the number of deaths was 233.8 million, with an average of 7.5 diagnosed as cancer per minute. In the past ten years, the survival rate of cancer in China is on a gradually rising trend, and the relative survival rate of cancer in 5 years is about 40.5 percent at present. But still has a big gap compared with developed countries in europe and america.
Melanoma, the most aggressive skin cancer in the world, is one of the common skin cancers caused by melanin gene mutation, and can occur in many parts of the human body, such as skin, eyes, inner ear, head and neck. Statistically, about one person is diagnosed with melanoma every 2 minutes, and 1 person dies from the disease every 10 minutes. Melanoma has a very high mortality rate in skin cancer because it is more likely to spread to other parts of the body, and ordinary surgery and chemotherapy do not help to provide help. Although many drugs and therapeutic approaches have been developed to date, their efficacy, high cost and unpleasant side effects remain major challenges for the treatment of melanoma. Melanoma thus remains one of the major disease burdens in humans.
Cervical cancer is the second cancer to occur and die in women, with an estimated 570,000 new cases in 2018 accounting for 6.6% of all women's cancers. Approximately 90% of cervical cancer deaths occur in low and moderate income countries. Although vaccines are currently available that can prevent the common oncogenic types of human papillomaviruses and can greatly reduce the risk of cervical cancer. However, for patients already suffering from cervical cancer, treatment remains a significant burden for women suffering from cervical cancer, and therefore, new drugs and treatment regimens are continually being developed and perfected.
Interferons were the first gene drugs to be marketed and have been widely used since 1989. The internationally approved treatment indications are about dozens, and since the treatment indications are put into the market, the medicine becomes one of the most extensive medicines for resisting cancers and viruses, and great social and economic benefits are obtained. Interferon is a glycoprotein with low relative molecular mass and various biological activities, has various biological functions of resisting virus, resisting tumor, regulating immune activity, inhibiting cell proliferation and the like, and forms a first line of defense against pathogens in animal bodies. Therefore, interferons have been widely used for the treatment of various diseases. Interferons are classified into two categories according to their structure, physicochemical properties, biological properties (including the location of genes and the signal transduction mode of receptors bound thereto, etc.): type I and type II interferons. Interferonepsilon is a later-found member of the interferon family, belonging to the type I interferon. Although interferon-has some common biological effects with other members, it has its own characteristics. Attempts have been made to treat viral infectious diseases such as condyloma acuminatum, hepatitis b, hepatitis c, etc.,
under the condition that interferons such as α, β and the like are widely applied to clinical treatment, the research on the interferon remains in the basic research stage, and the action and mechanism of the interferon are not completely clear at present.
In view of this, the invention is particularly proposed.
Disclosure of Invention
In view of the disadvantages of the prior art, the present invention aims to provide the use of interferon in the preparation of a medicament for treating tumors.
As a further improvement, the interferon is used for preparing a medicament for treating tumors and an activator for inducing innate immune response.
As a further refinement, the activator of inducing an innate immune response comprises an activator for activating type I and type II interferon signaling pathways.
As a further improvement, for the use of the medicament for the treatment of tumors, for the preparation of an activator of gene expression of one or more of OAS, IFI, IFIT, IFIH, IFITM, DHX, DDX, IRF, EPSTI, ISG, HE Z, HERC, STAT, RP-572P 18.1, RP-468E 2.4, PARP, SAMD, XAGE1, EPSTI, HE Z, CMPK, USP, REC, SAMHD, pcscr;
or/and the application of preparing the antagonist of the gene expression of one or more of TXNDC5, AC016739.2, RP L5P 34 and UBE2Q2P 6.
As a further improvement, the application of the compound as an activator of gene expression in one or more of IFI27, IFI 44L, IFI6, OAS2, IFI44, ISG15, SAMD 9L, OAS1, OAS3, P L SCR1, PARP9, DDX60, HERC6 and IFIT1 in the epithelial tumor treatment medicine.
As one mode of use of the present invention, the tumor comprises melanoma.
As an application mode of the invention, the interferon is applied to the preparation of an inhibitor for inhibiting the proliferation of melanoma cells.
As an application mode of the invention, the interferon is applied to the preparation of the accelerant for promoting the apoptosis of melanoma cells.
As an application mode of the invention, the interferon-is applied to the preparation of a promoter for promoting the nuclear fragmentation of melanoma and the formation of apoptotic bodies.
As an application mode of the invention, the effective dose is 100-1000 ng/ml.
As an application mode of the invention, the effective dose is 500-1000 ng/ml.
As an application mode of the invention, the effective dose is 800 ng/ml.
The invention has the advantages that the invention provides a new application of interferon, and the interferon-application in tumor treatment, because of the expression characteristics of interferon-on epithelial cells and mucosal tissues, the interferon-application in the treatment of melanoma is found to have a remarkable effect, in addition, although the interferon-belonging to type I interferon, the interferon-belonging to type I interferon is found to be capable of promoting tumor immune response by regulating signaling pathways of type I and type II interferons for anti-tumor treatment, and the interferon-capable of remarkably inhibiting the proliferation of SK-ME L103 melanoma cells and changing the morphology of tumor cells is also found to be capable of regulating the interferon-application in the tumor treatment, so that the invention provides a certain theoretical basis for the anti-cancer effect of the interferon-in the treatment of tumors, especially solid tumors represented by melanoma, and simultaneously provides a new thought and treatment means for the tumor treatment, especially for the treatment of solid tumors represented by melanoma.
Drawings
FIG. 1 shows the results of the effect of interferon on the proliferation of melanoma cells provided in example 1 of the present invention, FIG. 1a shows the effect of interferon with different concentration gradients on the proliferation of melanoma cells; FIG. 1b shows interferon-and H2O2Effect of treatment on melanoma cell proliferation separately, fig. 1c is interferon-effect of different treatment times on melanoma cell proliferation;
FIG. 2 is a graph of the interferon-versus-melanoma cell morphology provided in example 2 of the present invention, after 48 hours of treatment with 800ng/ml interferon, cells were imaged by an inverted microscope set at 200 Xmagnification; the markers indicate (1) normal cells, (2) nuclear condensation, (3) cell contraction, (4) membrane blebbing, (5) apoptotic bodies, (6) nuclear fragmentation, (7) blebbing, (8) spinous processes;
FIG. 3 is a normalized boxplot of the distribution of read counts in RNA sequences, plotted on the ordinate against log2(normalized or non-normalized counts), the x-axis represents each group, control (MCl, MC2, MC3) and experimental (MT1, MT2, MT 3). (A) Distribution of non-normalized read counts. (B) The distribution of read counts was normalized.
FIG. 4 is a volcano plot of differentially expressed genes in example 3, with the abscissa representing log2(fold change) value, ordinate represents log10(Padj) Average expression value of (a);
FIG. 5 is the functional analysis of differentially expressed genes of example 3, wherein the first 7 are enriched molecular function terms (p < 0.05) and the second 17 are enriched biological processes;
FIG. 6 is an enrichment analysis of the Reactome pathway of example 3;
FIG. 7 is a volcano plot of differentially expressed genes in example 4, with the abscissa representing log2(fold change) value, ordinate represents log10(Padj) Average expression value of (a);
FIG. 8 is the functional analysis of differentially expressed genes of example 4, wherein the first 2 are enriched molecular function terms (p < 0.05) and the second 6 are enriched biological processes;
FIG. 9 is an enrichment analysis of the Reactome pathway of example 4.
Detailed Description
The present invention will be further described below with reference to examples and effect examples, which are carried out under conventional conditions or conditions recommended by the manufacturer, without limiting the scope of the present invention. The reagents or instruments used are not indicated by the manufacturer, and are all conventional products available commercially. The use of interferon-in the present invention in tumor therapy is specifically described below.
Cell lines and major reagents:
melanoma cell line (SK-ME L103) was cultured in DMEM (5% fetal bovine serum) at 37 deg.C and 5% C02The recombinant human interferon- (purity > 90%) was purchased from Bio-Techno in North America and made into a 250. mu.g/m L preparation with sterile water for use according to the manufacturer's instructions.
Example 1 Effect of Interferon-on proliferation of SK-ME L103 melanoma cells
Detection of cell proliferation by WST method
To optimize interferon-optimal dose, cell viability was assessed using the WST-1 cell proliferation and cytotoxicity assay kit (Beyotime, Shanghai) SK-ME L103 cells at 2 × 10 per well3The density of individual cells was seeded in 96-well cell plates until complete attachment, and then the cells were treated with a gradient of interferon concentration from 0 to 1000ng/ml for 24 hours, with an equal volume of sterile water added as a control group (i.e., control group). To each well, 10. mu.l of the WST-1 mixed solution was added, and incubated in an incubator at 37 ℃ for 4 hours, and the absorbance (OD) value at 450nm was measured by a microplate reader (Biotek, USA). The plots show cell viability. In the cell viability assay, 3 wells per group were repeated 5 times, and the results are expressed as (mean ± sem).
The results in FIG. 1a show that treatment of SK-ME L103 melanoma cells with a gradient of interferon- (0-1000ng/ml) for 24 hours exposed the optimal dose of interferon to melanoma cells (800ng/ml), e.g., a decrease in cell viability of 7% after 24 hours of 800ng/ml interferon-stimulation compared to the control group (P < 0.05).
To further verify the inhibitory effect of interferon on cells, the cells were treated with a gradient of interferon (0-1000ng/ml) for 24 hours and then treated with 300. mu.M/L H2O2Incubate for 4 hours. Cell viability was determined by WST-1 analysis. The data in FIG. 1b show that: treatment with interferon alone (800ng/ml) still showed significant inhibition of melanoma cell activity (P < 0.01) compared to the control group. Interestingly, with the use of H alone2O2Treatment in contrast, after 800ng/ml interferon-pretreatment, 300. mu.M/L H was added2O2Treatment significantly reduced the level of cell viability from 67% to 49% (P < 0.0001). The loss of cell viability increased to 11% compared to 7% when interferon-treated alone (figure 1 b). These results indicate that interferon-has a significant inhibitory effect on the proliferation of melanoma cells.
To further investigate the effect of interferon-on melanoma cells at different treatment time points, melanoma cells were treated with 800ng/ml interferon for 24 hours, 48 hours, 72 hours, and 96 hours, respectively. The data in FIG. 1c show that: interferon-showed the most significant inhibition of melanoma cell viability at 48 hours compared to the control, with a reduction of about 10% in cell viability after 48 hours of treatment (P < 0.0001). As described above, interferon-capable of inhibiting the proliferation of melanoma cell lines and effective at a treatment time of 48 hours is preferred.
Example 2 Effect of Interferon-on SK-ME L103 melanoma cell morphology
To investigate the reason that may affect cell proliferation, we performed morphological change examination on cancer cells 1 × 104Individual cells were seeded in 35mm cell culture dishes (thermolfisher) and incubated for 24 hours. After discarding the medium, the cells were washed twice with pbs (hyclone tm). The cells were infiltrated with 1ml of fresh complete medium and treated with 800ng/ml interferon-for 48 hours, and an equal volume of sterile water was added as a control group (i.e., control group). Examination of the shape of cancer cells by using an inverted microscope (Nikon, Japan) at 200X magnificationThe state changes. All experiments were repeated three times.
The results in FIG. 2 show that: the melanoma cells underwent significant morphological changes compared to the control group. Visualization of control (untreated) cells indicated that the cells grew and adhered well. At the same time, the cells remain in the original state, and only a few cells show a nuclear contraction state. In contrast, the number of cells in the same field treated with interferon- (800ng/ml) was significantly reduced and the cell morphology revealed typical abnormal features such as nuclear fragmentation, apoptotic bodies, effervescence and spinous processes, especially the frequency of apoptotic bodies was high. This suggests that interferon-may affect the morphology of melanoma cells, leading to apoptosis of melanoma cells.
Example 3 Effect of Interferon on Gene expression levels in melanoma cells
Assessment of transcript abundance and differential expression analysis of melanoma cells before comparing the expression profiles of the two sets of samples, we normalized all samples and the results are shown in figure 3. The normalization data indicated that the normalization of the six samples worked well and that the data was suitable for comparative differential expression analysis. After comparing the expression profiles of the control (MC) and the treatment (MT) groups, we succeeded in identifying 34 differentially expressed genes (P < 0.05) consisting of 31 up-regulated genes and 3 down-regulated genes when the threshold of fold change was > 2 (FIG. 4A). As shown in FIG. 4B, when a more relaxed threshold was used (fold change ≧ 1.5), 68 genes with significantly different expression could be identified, including 54 up-regulated genes and 14 down-regulated genes. We found that the two sets of genes generated by setting two critical thresholds are substantially similar. Therefore, we decided to use genes set in a strict threshold (fold change ≧ 2) for downstream analysis.
The volcano plot results for the differentially expressed genes are shown in FIG. 4, with the abscissa representing log2(fold change) value, ordinate represents log10(Padj) 34 differentially expressed genes specifically as shown in Table 1, out of the 31 upregulated genes in interferon-treated melanoma cells, we found a number of interferon-inducible protein family members, including OAS2, IFI 44L, IFI6. It is also well known that IFIT1, IFI27, IRF9, IFIT3, IFI44 and the protein members associated with innate immunity, ISG15, PARP9 and IRF7, among others, are significantly induced, OAS2 and IFI 44L exhibit significant induction of changes of about 16 fold in interferon-induced proteins OAS2 protein is a dsRNA-activated antiviral enzyme that mediates antiviral action by activating RNASE L, causing cellular viral RNA degradation, thereby inhibiting protein synthesis and terminating viral replication, in addition to which it has been reported to play a key role in cellular processes such as proliferation, differentiation, apoptosis and gene regulation, effective induction of OAS2 may reveal interferons-a potential function in inhibiting cancer cell proliferation.
TABLE 1
Functional enrichment analysis to better understand the function of differentially expressed genes, we used the PANTERH classification system on the GeneOntology (GO) website for functional enrichment analysis. Our results show that GO molecular function and GO biological progression are significantly enriched in interferon-treated melanoma samples compared to control samples, as shown in figure 5. For biological processes, the most important term is the type I interferon signaling pathway, which is assigned 41% of the genes. Interferon-gamma mediated signaling pathways and negative regulation of viral genome replication were also significantly enriched, accounting for 24%, 21% and 17%, respectively. In addition, 10% of the genes were assigned to innate immune responses and other type I or type II signaling pathways (fig. 5). The first five most important genes are most involved in innate anti-viral responses as well as proliferation, differentiation and gene regulation, demonstrating that they are involved in a variety of mechanisms that mediate the immune response of tumor hosts. In particular, most of the genes associated with type I signaling pathways, such as OAS2, ISG15, STAT1, IFI6, IRF9, etc., are involved in the mechanism of mediating cancer immune responses. These results indicate that interferon-exerts an effect on melanoma cells by inducing innate immunity, including type I and type II interferon signaling pathways. For molecular function, DEG is primarily assigned to binding and enzymatic activity (fig. 5). The top panel represents carbohydrate derivative binding, nucleotide binding, purine ribonucleoside triphosphate binding and double-stranded RNA binding, 38%, 34% and 21%, respectively. The genes represented at the top include RNA helicase activity, NAD + ADP-ribosyltransferase activity and 2'-5' -oligoadenylate synthetase activity mapped to 14%, l 0% and 10%, respectively.
Our analysis indicates that differentially expressed genes (41%) are largely enriched for interferon α/β signaling, followed by type II signaling, DDX85/IFIH 1-mediated interferon α/β induction and ISG15 antiviral mechanisms (fig. 6). activated interferon signaling may play an important anti-cancer role by activating the JAK-STAT pathway of the immune response.
Example 4 Effect of Interferon on Gene expression levels in cervical carcinoma cells
Transcript abundance assessment and differential expression analysis of cervical cancer cells before comparing the expression profiles of the two sets of samples, we normalized all samples and the results are shown in figure 3. The normalization data indicated that the normalization of the six samples worked well and that the data was suitable for comparative differential expression analysis. After comparing the expression profiles of the control group (HC) and the experimental group (HT), we successfully identified 18 differentially expressed genes (P < 0.05) consisting of 17 up-regulated genes and 1 down-regulated gene when the threshold of fold change was greater than or equal to 2.
The volcano plot results for the differentially expressed genes are shown in FIG. 7, with the abscissa representing log2(fold change) value, ordinate represents log10(Padj) Average expression value of (1).
Specifically, as shown in Table 2, among 17 upregulated genes in interferon-treated cervical cancer cells, we found that a number of interferon-inducible protein family members, including OAS2, IFI27, IFI 44L 44L 6, IFI27, IFIT3, IFIT5, IFITM1, IFI44 and the innate immunity-related protein members ISG15 and PARP9, were significantly induced among interferon-inducible proteins, IFI27 and IFI 44L showed significant induction with fold change of about 11.14-18 fold. IFI 24 is an inducible protein of type I interferon and is capable of activating interferon-related pathways to inhibit proliferation of cancer cells. furthermore, cytokines and enzymes such as SAMD 9L, P9 SCR 6862, PARP9, DDX60, HERC6, and the like, are significantly induced to down-regulate cell proliferation and cell proliferation by NDC-mediated DNA damage, innate immunity signal transduction genes, NDC-mediated by NDC-mediated proliferation and NDC-mediated by NDC-inducible genes to promote cell proliferation and proliferation of cancer cells.
TABLE 2
Functional enrichment analysis to better understand the function of differentially expressed genes, we used the PANTERH classification system on the GeneOntology (GO) website for functional enrichment analysis. Our results show a significant enrichment of GO molecular function and GO biological processes in interferon-treated cervical cancer samples compared to control samples, as shown in figure 8. For biological processes, the most important term is the virus defense response, which is assigned 76% of the genes. Type I interferon-gamma mediated signaling pathways and negative regulation of viral genome replication were also significantly enriched, accounting for 47% and 41%, respectively. In addition, 18% of the genes were assigned to the type II signaling pathway (fig. 8). The first five most important genes are most involved in innate anti-viral responses as well as proliferation, differentiation and gene regulation, demonstrating that they are involved in a variety of mechanisms that mediate the immune response of tumor hosts. In particular, genes associated with the type I and type II interferon signaling pathways, such as OAS2, ISG15, IFI6, and the like, are involved in the mechanism that mediates cancer immune responses. These results indicate that interferon-exerts an effect on cervical cancer cells by inducing innate immunity, including type I and type II interferon signaling pathways.
To further determine the pathways in which differentially expressed genes participate, the differentially expressed genes were analyzed by the PANTIER Classification System (GENEONTO L Y) and Reactome pathway annotation We chose the two pathways that are most enriched and analyzed, which indicated that the differentially expressed genes (47%) were mostly rich in interferon α/β signaling, followed by type II signaling (18%) (FIG. 9). Activated interferon signaling may play an important anti-cancer role through the JAK-STAT pathway that activates the immune response.
By way of example 3 and example 4, the interferon-acting melanoma cells and cervical carcinoma cells had 14 identical regulatory genes when compared, as shown in table 3, further revealing that the 14 identical regulatory genes act on epithelial tumor cells by inducing innate immune responses.
TABLE 3
Conclusion
On a molecular level, interferons-kill cancer cells, particularly epithelial tumor cells, by modulating the immune response by activating interferon-/modulating tumor signaling pathways that regulate expression of the OAS, STAT1, IRF7, and IRF9 genes, enriching for interferon-gamma mediated signaling pathways and interferon gamma signaling. Interferon-gamma signaling induces tumor ischemia and an in vivo homeostasis program, resulting in tumor clearance.
The above is only a preferred embodiment of the present invention, and the protection scope of the present invention is not limited to the above-mentioned embodiments, and all technical solutions belonging to the idea of the present invention belong to the protection scope of the present invention. It should be noted that modifications and embellishments within the scope of the invention may occur to those skilled in the art without departing from the principle of the invention, and are considered to be within the scope of the invention.
Claims (11)
1. Use of interferon-for the manufacture of a medicament for the treatment of a tumour.
2. Use of interferon according to claim 1 for the preparation of a medicament for the treatment of tumors, for the preparation of an activator for inducing an innate immune response.
3. The interferon of claim 2, wherein said activator of inducing an innate immune response comprises an activator of type I and type II interferon signaling pathways.
4. The use of an interferon according to claim 2 for the preparation of a medicament for the treatment of tumors for the preparation of an agent for activating the expression of one or more genes selected from OAS2, OAS1, OAS3, IFI 44L, IFI44, IFI3, IFI27, IFI6, IFIT1, IFIT5, IFIH1, IFITM1, DHX58, DDX60, IRF9, EPSTI1, ISG15, HE L Z2, HERC6, STAT1, RP11-572P18.1, RP11-468E2.4, PARP9, PARP12, PARP14, SAMD 9L, XAGE1E, EPSTI1, HE L Z2, CMPK2, USP18, REC8, samp 1, hd L SCR 1;
or/and the application of preparing the antagonist of the gene expression of one or more of TXNDC5, AC016739.2, RP L5P 34 and UBE2Q2P 6.
5. The use of interferon-according to claim 4, characterized by the use as an activator of gene expression of one or more of IFI27, IFI 44L, IFI6, OAS2, IFI44, ISG15, SAMD 9L, OAS1, OAS3, P L SCR1, PARP9, DDX60, HERC6, IFIT1 in a medicament for the treatment of epithelial tumors.
6. The interferon of claim 1, wherein the tumor comprises a melanoma.
7. Use of an interferon according to claim 6, characterized in that the use of an interferon for the preparation of an inhibitor for inhibiting the proliferation of melanoma cells.
8. Use of an interferon according to claim 6, characterized in that the use of an interferon for the preparation of a promoter for promoting the fragmentation of melanoma nuclei to form apoptotic bodies.
9. The interferon-use according to claim 1, wherein the effective amount is 100-1000 ng/ml.
10. The interferon-use according to claim 1, wherein the effective amount is 500-1000 ng/ml.
11. The interferon of claim 10, in which the effective dose is 800 ng/ml.
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Cited By (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN114480608A (en) * | 2020-10-27 | 2022-05-13 | 细胞图谱有限公司 | Peripheral blood sample analysis method and kit |
| WO2023245771A1 (en) * | 2022-06-23 | 2023-12-28 | 江苏康可得生物技术股份有限公司 | Use of helz2 gene in drugs for prevention and treatment of tumors |
Citations (6)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| GB2123835A (en) * | 1982-07-12 | 1984-02-08 | Damon Biotech Inc | Interferon E |
| WO1999029863A1 (en) * | 1997-12-08 | 1999-06-17 | Genentech, Inc. | Human interferon-epsilon: a type i interferon |
| WO2000017361A2 (en) * | 1998-09-18 | 2000-03-30 | Zymogenetics, Inc. | Interferon-epsilon |
| US20110151469A1 (en) * | 2008-06-10 | 2011-06-23 | Piramal Life Sciences Limited | Interferon epsilon (ifne1) as a marker for targeted cancer therapy |
| CN107596350A (en) * | 2017-11-01 | 2018-01-19 | 哈尔滨欧替药业有限公司 | A kind of recombinant human interferon alpha 2 ε vaginal expansion plugs and preparation method thereof |
| CN110831962A (en) * | 2017-01-30 | 2020-02-21 | 哈德森医学研究院 | Method of treatment |
-
2020
- 2020-03-30 CN CN202010240579.4A patent/CN111420033A/en active Pending
Patent Citations (7)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| GB2123835A (en) * | 1982-07-12 | 1984-02-08 | Damon Biotech Inc | Interferon E |
| WO1999029863A1 (en) * | 1997-12-08 | 1999-06-17 | Genentech, Inc. | Human interferon-epsilon: a type i interferon |
| US20020172660A1 (en) * | 1997-12-08 | 2002-11-21 | Genentech, Inc. | Human interferon-epsilon: a type I interferon |
| WO2000017361A2 (en) * | 1998-09-18 | 2000-03-30 | Zymogenetics, Inc. | Interferon-epsilon |
| US20110151469A1 (en) * | 2008-06-10 | 2011-06-23 | Piramal Life Sciences Limited | Interferon epsilon (ifne1) as a marker for targeted cancer therapy |
| CN110831962A (en) * | 2017-01-30 | 2020-02-21 | 哈德森医学研究院 | Method of treatment |
| CN107596350A (en) * | 2017-11-01 | 2018-01-19 | 哈尔滨欧替药业有限公司 | A kind of recombinant human interferon alpha 2 ε vaginal expansion plugs and preparation method thereof |
Non-Patent Citations (5)
| Title |
|---|
| ABDEL-FATTAH MANAL等: "The Arabian camel, Camelus dromedarius interferon epsilon: Functional expression, in vitro refolding, purification and cytotoxicity on breast cancer cell lines", 《PLOS ONE》, vol. 14, no. 9 * |
| DANIEL MARRERO-RODRÍGUEZ等: "Interferon epsilon mRNA expression could represent a potential molecular marker in cervical cancer", 《INT J CLIN EXP PATHOL》, vol. 11, no. 4, pages 1979 - 1988 * |
| YANG LIMIN等: "Molecular and Functional Characterization of Canine Interferon-Epsilon", 《JOURNAL OF INTERFERON AND CYTOKINE RESEARCH》, vol. 33, no. 12, XP055606811, DOI: 10.1089/jir.2013.0037 * |
| ZOE R C MARKS等: "PROPERTIES AND FUNCTIONS OF THE NOVEL TYPE I INTERFERON EPSILON", 《SEMIN IMMUNOL》, vol. 43, pages 101328 * |
| 李虹霖、陈艳萍: "宫颈癌患者外周血中干扰素Epsilon的表达及临床意义", 《标记免疫分析与临床》, pages 300 - 302 * |
Cited By (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN114480608A (en) * | 2020-10-27 | 2022-05-13 | 细胞图谱有限公司 | Peripheral blood sample analysis method and kit |
| WO2023245771A1 (en) * | 2022-06-23 | 2023-12-28 | 江苏康可得生物技术股份有限公司 | Use of helz2 gene in drugs for prevention and treatment of tumors |
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