更新于：2024-11-01

cyclin G1

更新于：2024-11-01

基本信息

别名

CCNG、CCNG1、CYCG1

+ [3]

简介

May play a role in growth regulation. Is associated with G2/M phase arrest in response to DNA damage. May be an intermediate by which p53 mediates its role as an inhibitor of cellular proliferation (By similarity).

关联

项与 cyclin G1 相关的药物

Rexin-G

靶点

cyclin G1

作用机制

cyclin G1抑制剂

在研机构

原研机构

在研适应症

非在研适应症

最高研发阶段批准上市

首次获批国家/地区

菲律宾

首次获批日期2007-01-01

项与 cyclin G1 相关的临床试验

NCT00572130 / Completed临床2期

A Phase II Study of Intravenous Rexin-G in Recurrent or Metastatic Osteosarcoma

Rexin-G is a tumor-targeted gene medicine that is designed to seek out and destroy both primary tumors and metastatic cancers without the side effects of standard chemotherapy. The objectives of the study are: (1) to evaluate the clinical effectiveness of intravenous injections of Rexin-G, a tumor-targeted gene vector, in controlling tumor growth and prolonging life, and (2) to evaluate its over-all safety.

开始日期2007-12-01

申办/合作机构-

NCT00505713 / Completed临床1/2期

Evaluation of Safety and Efficacy of Rexin-G as Intervention for Recurrent or Metastatic Sarcoma

Rexin-G is a tumor-targeted (pathotropic or disease-seeking) nanoparticle that when injected intravenously, seeks out and accumulates in cancerous lesions, thus enhancing local drug concentration within tumors. The goal of the adaptive trial design is to confirm the over-all safety of Rexin-G and to determine the optimal dosing regimen for Rexin-G that would document the significant clinical benefits required to support a Phase II registration protocol.

开始日期2007-07-01

申办/合作机构-

NCT00505271 / Completed临床1/2期

Phase I/II Evaluation of Safety and Efficacy of Pathotropic Nanoparticles Bearing a Dominant Negative Cyclin G1 Construct (Rexin-G) as Intervention for Recurrent or Metastatic Breast Cancer

The goal of the adaptive trial design is to confirm the over-all safety of Rexin-G and to determine the optimal dosing regimen for Rexin-G that would document the significant clinical benefits required to support a Phase II registration protocol for recurrent or metastatic breast cancer.

开始日期2007-07-01

申办/合作机构-

100 项与 cyclin G1 相关的临床结果

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100 项与 cyclin G1 相关的转化医学

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0 项与 cyclin G1 相关的专利（医药）

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836

项与 cyclin G1 相关的文献（医药）

2024-07-08·GENETICS

Translational control of MPS1 links protein synthesis with the initiation of cell division and spindle pole body duplication in Saccharomyces cerevisiae

Article

作者: Blank, Heidi M ; Loog, Mart ; Alonso, Annabel ; Winey, Mark ; Fabritius, Amy S ; Valk, Ervin ; Polymenis, Michael

AbstractProtein synthesis underpins cell growth and controls when cells commit to a new round of cell division at a point in late G1 of the cell cycle called Start. Passage through Start also coincides with the duplication of the microtubule-organizing centers, the yeast spindle pole bodies, which will form the 2 poles of the mitotic spindle that segregates the chromosomes in mitosis. The conserved Mps1p kinase governs the duplication of the spindle pole body (SPB) in Saccharomyces cerevisiae. Here, we show that the MPS1 transcript has a short upstream open reading frame (uORF) that represses the synthesis of Mps1p. Mutating the MPS1 uORF makes the cells smaller, accelerates the appearance of Mps1p in late G1, and promotes completion of Start. Monitoring the SPB in the cell cycle using structured illumination microscopy revealed that mutating the MPS1 uORF enabled cells to duplicate their SPB earlier at a smaller cell size. The accelerated Start of MPS1 uORF mutants depends on the G1 cyclin Cln3p and the transcriptional repressor Whi5p but not on the Cln1,2p G1 cyclins. These results identify growth inputs in mechanisms that control duplication of the microtubule-organizing center and implicate these processes in the coupling of cell growth with division.

2024-05-08·Radiation Research

Applicability of Gene Expression in Saliva as an Alternative to Blood for Biodosimetry and Prediction of Radiation-induced Health Effects

Article

作者: Abend, M ; Ghandhi, S A ; Stewart, S ; Amundson, S A ; Tichý, A ; Davidkova, M ; Badie, C ; Schwanke, D ; Bäumler, W ; Stroszczynski, C ; Kultova, G ; Sirak, I ; Kasper, M ; Port, M ; Stastna, M Markova ; Ostheim, P

As the great majority of gene expression (GE) biodosimetry studies have been performed using blood as the preferred source of tissue, searching for simple and less-invasive sampling methods is important when considering biodosimetry approaches. Knowing that whole saliva contains an ultrafiltrate of blood and white blood cells, it is expected that the findings in blood can also be found in saliva. This human in vivo study aims to examine radiation-induced GE changes in saliva for biodosimetry purposes and to predict radiation-induced disease, which is yet poorly characterized. Furthermore, we examined whether transcriptional biomarkers in blood can also be found equivalently in saliva. Saliva and blood samples were collected in parallel from radiotherapy (RT) treated patients who suffered from head and neck cancer (n = 8) undergoing fractioned partial-body irradiations (1.8 Gy/fraction and 50–70 Gy total dose). Samples were taken 12–24 h before first irradiation and ideally 24 and 48 h, as well as 5 weeks after radiotherapy onset. Due to the low quality and quantity of isolated RNA samples from one patient, they had to be excluded from further analysis, leaving a total of 24 saliva and 24 blood samples from 7 patients eligible for analysis. Using qRT-PCR, 18S rRNA and 16S rRNA (the ratio being a surrogate for the relative human RNA/bacterial burden), four housekeeping genes and nine mRNAs previously identified as radiation responsive in blood-based studies were detected. Significant GE associations with absorbed dose were found for five genes and after the 2nd radiotherapy fraction, shown by, e.g., the increase of CDKN1A (2.0 fold, P = 0.017) and FDXR (1.9 fold increased, P = 0.002). After the 25th radiotherapy fraction, however, all four genes (FDXR, DDB2, POU2AF1, WNT3) predicting ARS (acute radiation syndrome) severity, as well as further genes (including CCNG1 [median-fold change (FC) = 0.3, P = 0.013], and GADD45A (median-FC = 0.3, P = 0.031)) appeared significantly downregulated (FC = 0.3, P = 0.01–0.03). A significant association of CCNG1, POU2AF1, HPRT1, and WNT3 (P = 0.006-0.04) with acute or late radiotoxicity could be shown before the onset of these clinical outcomes. In an established set of four genes predicting acute health effects in blood, the response in saliva samples was similar to the expected up- (FDXR, DDB2) or downregulation (POU2AF1, WNT3) in blood for up to 71% of the measurements. Comparing GE responses (PHPT1, CCNG1, CDKN1A, GADD45A, SESN1) in saliva and blood samples, there was a significant linear association between saliva and blood response of CDKN1A (R2 = 0.60, P = 0.0004). However, the GE pattern of other genes differed between saliva and blood. In summary, the current human in vivo study, (I) reveals significant radiation-induced GE associations of five transcriptional biomarkers in salivary samples, (II) suggests genes predicting diverse clinical outcomes such as acute and late radiotoxicity as well as ARS severity, and (III) supports the view that blood-based GE response can be reflected in saliva samples, indicating that saliva is a “mirror of the body” for certain but not all genes and, thus, studies for each gene of interest in blood are required for saliva.

2023-10-04·GENETICS

Hyperactive Ras disrupts cell size control and a key step in cell cycle entry in budding yeast

Article

作者: Kellogg, Douglas R ; DeWitt, Jerry T ; Chinwuba, Jennifer C

AbstractSevere defects in cell size are a nearly universal feature of cancer cells. However, the underlying causes are unknown. A previous study suggested that a hyperactive mutant of yeast Ras (ras2G19V) that is analogous to the human Ras oncogene causes cell size defects, which could provide clues to how oncogenes influence cell size. However, the mechanisms by which ras2G19V influences cell size are unknown. Here, we found that ras2G19V inhibits a critical step in cell cycle entry, in which an early G1 phase cyclin induces transcription of late G1 phase cyclins. Thus, ras2G19V drives overexpression of the early G1 phase cyclin Cln3, yet Cln3 fails to induce normal transcription of late G1 phase cyclins, leading to delayed cell cycle entry and increased cell size. ras2G19V influences transcription of late G1 phase cyclins via a poorly understood step in which Cln3 inactivates the Whi5 transcriptional repressor. Previous studies found that yeast Ras relays signals via protein kinase A (PKA); however, ras2G19V appears to influence late G1 phase cyclin expression via novel PKA-independent signaling mechanisms. Together, the data define new mechanisms by which hyperactive Ras influences cell cycle entry and cell size in yeast. Hyperactive Ras also influences expression of G1 phase cyclins in mammalian cells, but the mechanisms remain unclear. Further analysis of Ras signaling in yeast could lead to discovery of new mechanisms by which Ras family members control expression of G1 phase cyclins.

项与 cyclin G1 相关的新闻（医药）

2024-05-29

·BioSpace

BostonGene Announces Seven Abstract Acceptances at the 2024 American Society of Clinical Oncology Annual Meeting

BostonGene will showcase its AI-powered multiomics platform and its new immune system profiling platform, which stratifies cancer patients by treatment response WALTHAM, Mass.--(BUSINESS WIRE)-- BostonGene, a leading provider of AI-driven molecular and immune profiling solutions, today announced that seven abstracts have been accepted for the 2024 ASCO Annual Meeting (ASCO), scheduled to take place May 31 – June 3, 2024, at McCormick Place Convention Center in Chicago, IL. BostonGene will deliver one oral presentation and present two posters, while four abstract presentations will be available online. BostonGene will also exhibit at booth 22157. At the event, BostonGene will feature its AI-powered multiomics platform that rapidly accelerates new research and drug development while precisely matching each patient with the best available therapy. BostonGene will also highlight its recently announced immune system profiling platform, a novel classification method and a scoring system based on this classification of systemic immunity with patient responses to various cancer treatments. This diagnostic and analytical immune system profiling framework underscores the potential of a straightforward blood test, supported by additional clinical validation, as a tool to stratify cancer patients into responders and non-responders across different treatments. Details about the abstracts selected for presentation can be found below: Oral presentation Abstract: 2015 Title: A phase Ib, window-of-opportunity study of neoadjuvant avelumab and hypofractionated proton beam therapy for recurrent radiation-relapsed meningioma Date and time: Sunday, June 2, 2024 | 11:30 AM - 1:00 PM Speaker: Jiayi Huang, MD, Washington University School of Medicine This study evaluated the immunological effects of combining avelumab, an anti-PD-L1 inhibitor, with radiation therapy (RT) for recurrent radiation-relapsed meningioma. The use of RNA-seq and MxIF on pre- and post-avelumab tumor tissues revealed that for some patients the combination (avelumab + RT) may cause an immunological response leading to prolonged remission, warranting further larger prospective studies and biomarker investigations. Research done in collaboration with the Washington University School of Medicine Poster presentations Abstract: 11523 Title: Transcriptomic analysis of novel tumor suppressor gene fusions in bone sarcomas Date and time: Saturday, June 1, 2024 | 1:30 PM - 4:30 PM Poster: 449 Speaker: Nikita Kotlov, BostonGene Transcriptomic analysis of treated bone sarcomas revealed a unique breakpoint combination in an oncogene and previously unknown gene fusions involving tumor suppressor genes. These findings highlight the importance of RNA-seq to advance research and identify potential biomarkers for sarcomas. Research done in collaboration with The University of Texas MD Anderson Cancer Center, Massachusetts General Hospital Cancer Center and the Sarcoma Oncology Center Abstract: 1044 Title: The multiomic tumor microenvironment landscape of invasive lobular carcinoma of the breast Date and time: Sunday, June 2, 2024 | 9:00 AM - 12:00 PM Poster: 22 Speaker: Jason Mouabbi, MD, The University of Texas MD Anderson Cancer Center Multiomic analysis using integrated RNA-seq and MxIF uncovered the intricate heterogeneity of the tumor microenvironment (TME) in invasive lobular carcinoma (ILC) of the breast, emphasizing the critical role of comprehensive TME profiling to understand and develop personalized treatments for ILC. Research done in collaboration with MD Anderson Cancer Center Online-only abstracts Abstract: e13168 Title: Closing classification gaps in luminal breast cancer with single-cell RNA-seq insights from normal breast lineages In this study, single-cell RNA-seq was used to investigate the connection between breast cancer classification and luminal expression pro The findings showed that compared to other breast cancer subtypes, luminal breast cancers are less similar to most luminal epithelial clusters in normal breast tissue, which suggests that the complexity of luminal-type breast cancers is not captured by traditional breast cancer classification methods. Abstract: e15138 Title: Integrated genomic and transcriptomic characterization of neuroendocrine carcinomas for improved treatment decision-making Integrated whole exome (WES) and RNA sequencing (RNA-seq) detected unique molecular features across diverse neuroendocrine tumors, indicating the potential use of comprehensive molecular profiling for therapy and clinical trial matching to improve outcomes for neuroendocrine carcinoma (NEC) patients. Research conducted in collaboration with Advanced Cancer Treatment Centers, Mayo Clinic and Duke Cancer Institute Abstract: e13593 Title: An unsupervised H&E-based machine-learning approach for precise prediction of tumor microenvironment subtypes. This study describes the development of an H&E-based machine-learning approach using colorectal cancer (CRC) samples. The results show that the H&E-based approach complements next-generation sequencing (NGS) tumor microenvironment (TME) classification, suggesting that the advanced image analysis can help refine prognostic and therapeutic strategies for CRC and warrant further expansion to other cancer types. Abstract: e15086 Title: Effect of DeltaRex-G ± DeltaRex-G Plus (an FDA-approved drug) on advanced chemoresistant pancreatic cancer, sarcoma, and breast cancer This study investigated the use of DeltaRex-G, a CCNG1 inhibitor, administered either alone or in combination with an FDA-approved drug (DeltaRex-G Plus) in advanced cancers. RNA sequencing identified enhanced CCNG1 expression in all analyzed tumors and analysis showed that the five patients treated with DeltaRex-G Plus had a partial response or stable disease, supporting the use of DeltaRex-G Plus as a promising therapy. Research conducted in collaboration with City of Hope Comprehensive Cancer Center, Sarcoma Oncology Center, Duke University and Expression Therapeutics For more information, please visit the 2024 ASCO Annual Meeting website. The abstracts will be published online in the Journal of Clinical Oncology supplement for the ASCO Annual Meeting Proceedings. About BostonGene Corporation BostonGene is a company at the intersection of technology and biology, dedicated to advancing and personalizing cancer medicine. Founded in 2015, BostonGene has continually pushed the boundaries of innovation to improve cancer patient care and accelerate research and drug development through cutting-edge solutions. Leveraging our AI-powered multiomics platform, we digitize and comprehensively analyze the molecular profiles of cancer patients, including the immune system and tumor microenvironment. Our software solutions, indication-specific cancer library and advanced bioanalytics, enable us to discover multiparametric signatures, identify targets, match them to relevant indications for biopharma and recommend the most effective treatments for patients. For more information, visit .

ASCO会议

2023-12-25

·生物谷

“神药”新发现！中山大学最新研究探明：二甲双胍能通过多途径，发挥抗衰老作用！

二甲双胍（Metformin）是治疗II型糖尿病的一线药物，可通过抑制肝脏葡萄糖的产生而发挥降糖作用。早在1957年，二甲双胍便被正式运用于临床治疗糖尿病；在我国也有着超30年的临床运用经验。全球范围内，约有1.5亿人在服用二甲双胍，可谓是目前应用最广泛的口服降糖药之一。随着科学的不断推进，对二甲双胍的研究从未停止过。除了人们熟知的降糖之外，现阶段发现的药物作用已超过20种，包括：保护心血管、减少超重/肥胖、改善血脂代谢、降低部分肿瘤风险等等。近日，来自中山大学的研究团队再一次揭示了“神药”的新发现——二甲双胍能够从细胞数量、效应功能、端粒酶含量以及基因表达等多方面抑制T细胞的衰老，从而有效预防年龄相关的疾病。难怪医学界的人戏称“二甲双胍已经不是药了，而是开启宇宙新纪元的钥匙”！https://doi.org/10.1186/s12979-023-00394-0首先，研究者从中山大学附属第一医院收集了过去6年来肺癌患者的样本，发现了个有趣的现象：与年轻人和老年人相比，中年人（45-65岁）中罹患肺癌的比例显著增加。过去六年来中山大学第一附属医院的肺癌患者样本（n=4498）事实上，这一现象的出现与衰老T细胞数量增加息息相关。代表性流式细胞术分析显示，中年患者中CD8+衰老T细胞的数量明显高于年轻组（<45岁）和老年组（>65岁），类似的情况也出现在CD4+衰老T细胞亚群中。但整体来看，CD8+衰老T细胞的比例高于CD4+T细胞。随着年龄的增长，中老年人群的胸腺会逐渐萎缩，幼稚T细胞数量减少，而记忆T细胞的数量会随之增加。当机体受到外界抗原攻击时，记忆T细胞会分化为效应记忆T细胞（Tem）。其中，衰老T细胞便是源自处于T细胞分化末期的效应T细胞（Teff）。研究者观察到，虽然老年组中Tem的比例最高，但中年组的CD57+KLRG1+双阳性细胞比例依然最高，即具有衰老T细胞表型的Tem细胞比例在45-65岁的人群中最高。FACS分析得到的中年人群中CD8+衰老T细胞比例情况衰老T细胞含量的增高自然会导致与年龄相关的疾病发生，尤其是肿瘤。如果能找到某种药物可以调节T细胞的衰老，是不是就能够有效地降低与年龄相关的疾病风险呢？于是，研究者想到了“神药”二甲双胍！考虑到二甲双胍在抗肿瘤和抗衰老方面起着重要作用，研究者进一步开展了体外研究，采用不同浓度的二甲双胍（包括0mM、5mM、10mM和20mM）对中年组中提取到的外周血单个核细胞（PBMC）进行治疗，以探究了其对于衰老T细胞的影响。结果显示，5mM二甲双胍治疗对衰老T细胞几乎没有影响；但当浓度升高到10mM时，衰老T细胞的数量显著减少，从占比47.29%降低到了34.3%，即抑制率达到了27.5%；而当再次升高浓度到20mM时，CD8+衰老T细胞的含量也出现了下降，抑制率升高至39.4%。总结来说，二甲双胍的治疗能够有效减少中年人群中衰老T细胞的含量。二甲双胍治疗后中年组CD8+衰老T细胞的数量显著减少事实上，二甲双胍对于衰老T细胞的影响，主要作用于衰老相关分泌表型（SASP）。衰老T细胞分泌出的SASP可能会对邻近的健康细胞造成损害，甚至诱导衰老的发生。比如，IFN-γ便属于SASP的范畴，在衰老T细胞中高度表达。但当研究者进一步使用20mM的二甲双胍治疗中年组PBMC，持续24小时后发现，与对照组相比，二甲双胍治疗明显抑制了衰老T细胞中IFN-γ的分泌。促炎细胞因子IL-6是存在于各类衰老细胞中的SASP因子之一，主要由先天性免疫细胞分泌，包括单核细胞和树突状细胞。分析中年组外周血CD3阴性细胞后发现，二甲双胍治疗能够有效抑制IL-6的分泌比例，甚至降低了CD3-细胞的IL-6表达水平。类似的情况也发生在T细胞中，即二甲双胍治疗同样减少了T细胞中IL-6的产生。二甲双胍抑制CD3阴性细胞中IL-6的产生当然，二甲双胍对于衰老T细胞的影响不只于上述两点，而是多方面的。研究者观察到，在二甲双胍的治疗下，CD8+衰老T细胞分泌出的肿瘤坏死因子α（TNF-α）呈现增加的趋势。TNF-α是一种有效的促炎细胞因子，在免疫系统、炎症和宿主防御的维持和平衡中发挥着重要作用。此外，二甲双胍还能增加端粒酶浓度，从对照组的0.71ng/ml升高至1.33ng/ml。端粒酶是一种具有逆转录活性的酶，负责合成端粒DNA并保持端粒长度，在保持染色体稳定性方面发挥着至关重要的作用。随着T细胞的老化，端粒缩短，端粒酶活性下降，导致其丧失增殖能力；但使用二甲双胍治疗后，端粒酶的浓度有所升高，也就意味着抗衰老的可能。免疫衰老的特点，除了老年T细胞增加外，另一个点为“具有干细胞性的幼稚T细胞的减少”。更有意思的是，二甲双胍的治疗甚至能够增加未分化T细胞的数量。二甲双胍增加了端粒酶浓度和未分化的T细胞最后，研究者的探究不局限于表面，而深入挖掘到了基因层面。对PBMC进行RNA测序后发现，二甲双胍治疗组与对照组之间存在26,089个差异表达基因（DEGs）。与对照组相比，二甲双胍治疗组中与SA-β-Gal相关的基因GLB1明显减少，DNA损伤相关基因（包括CDKN1A、CHEK2、E2F2等）出现了明显下调。相反，二甲双胍促进了细胞周期蛋白相关基因CCNG1和CCND2的表达。同时，与干性相关的TCF7、SELL、CD28、CD27基因表达的增加，也解释了“为什么未分化T细胞的数量有所升高”。也就是说，二甲双胍之所以能发挥抗衰老的作用，还得追溯到最本质的基因表达改变。与二甲双胍治疗相关的基因表达的RNA-seq分析综上所述，T细胞衰老会导致免疫功能失调和衰老相关疾病的发生，而本研究提出了二甲双胍治疗对衰老T细胞具有抗衰老作用的有力证据——二甲双胍能够减少衰老T细胞的数量、减少SASP的产生、促进端粒酶的增加以及升高未分化T细胞的数量，从而发挥抗衰老的作用。二甲双胍啊二甲双胍，你还有多少惊喜是我们不知道的？即使距二甲双胍首次合成已过去了101年，但科学家仍无法完全阐明其发挥治疗作用的各种领域以及潜在机制，也期待二甲双胍能给我们带来更多的惊喜！参考资料：Yang, J., Liu, HC., Zhang, JQ. et al. The effect of metformin on senescence of T lymphocytes. Immun Ageing 20, 73 (2023). https://doi.org/10.1186/s12979-023-00394-0撰文 | Swagpp编辑 | Swagpp来源 | 梅斯医学精彩推荐：1、柳叶刀重磅：研究表明，流感对健康的长期影响与“长新冠”影响相似2、做梦吧！Nature重磅：哈佛医学院研究发现发呆、小憩和白日梦有益于大脑发育！3、久坐伤身不用怕！《英国运动医学杂志》发现每天只需这样运动22分钟即可抵消久坐带来的死亡风险4、独处并不孤独！Science子刊：花更多时间独处的人，压力更小自主满足感更高！5、吃饭”黄金时间”出炉！Nature子刊：10万大数据研究表明早晚餐提前吃，或降低糖尿病及心脑血管风险本文仅用于学术分享，转载请注明出处。若有侵权，请联系微信：bioonSir 删除或修改！

2023-12-12

·Business Wire

Sarcoma Oncology Center Leverages BostonGene’s AI-Driven Molecular and Immune Profiling Platform to Identify Novel Treatment Options for Patients with Advanced Cancers

WALTHAM, Mass.--( BUSINESS WIRE )-- BostonGene , a leading AI-based molecular and immune profiling solutions provider, and the Sarcoma Oncology Center , announced a collaboration to expedite the availability of DeltaRex-G. This groundbreaking platform therapy, authorized by the FDA's Center for Biologics Evaluation and Research (CBER), holds immense promise for patients battling advanced pancreatic cancer, osteosarcoma, soft tissue sarcoma, and breast cancer. The designation of DeltaRex-G, a CCNG1 inhibitor, as a platform therapy with the potential to incorporate other FDA-approved drugs, was enabled by BostonGene's pivotal identification of elevated CCNG1 levels in these different cancer types. Sarcoma Oncology Center, located in Santa Monica, California, is a cancer treatment and clinical research center, recognized for its clinical trials and clinical expertise in treating patients with sarcoma. Sarcomas, rare tumors that originate in bone and connective tissue, pose a unique treatment challenge since most sarcoma subtypes have no approved standard of care treatment and are typically chemotherapy-refractory. The best treatment approach for patients with advanced sarcomas consists of understanding their unique tumor molecular profile, and selection of a therapy that is “matched” to the molecular alterations. Sarcoma Oncology Center partnered with BostonGene for its innovative computational platform, which leverages AI-based molecular and immune profiling. The BostonGene Tumor Portrait™ test uncovers intricate correlations between different “omic” profiles including genomic alterations on tumor cells, profiling of a tumor’s immune landscape, and the potential to use these findings to understand which patients are most likely to benefit from treatment . The authorization of investigational agent DeltaRex-G, a CCNG1 inhibitor, as a platform therapy open to incorporating other FDA-approved drugs and immunotherapies stems from BostonGene's pivotal identification of heightened CCNG1 levels across all tumors tested, including osteosarcoma, soft tissue sarcoma, pancreas, breast, urothelial and testicular carcinoma . " Our partnership with BostonGene provides us with an AI-driven, molecular perspective of the dynamic tumor microenvironment and immune landscape, thereby expanding the treatment horizons for our patients," said Erlinda Gordon, MD. " This collaboration has broadened our cancer treatment options, as BostonGene is the only molecular profiling company reporting on the CCNG1 expression in tumors," said Sant P. Chawla, MD, Director at Sarcoma Oncology Center. “ We are pleased to be working with the Sarcoma Oncology Center to support their efforts in personalizing treatments for their patients. Our advanced sequencing and analytical capabilities will be indispensable in guiding treatment decisions for these cancer patients who would otherwise have very limited options," said Nathan Fowler, MD, Chief Medical Officer at BostonGene. About BostonGene Corporation BostonGene has a mission to provide transformative, AI-integrated molecular analytics and biomarker discovery for precision matching of therapies to improve the lives of patients living with cancer and other immune-related diseases. BostonGene’s concierge-service model provides customized client solutions using a multi-omic approach prioritized for real-world impact to optimize standard-of-care therapies, accelerate research and provide cost-effective, measurable data-driven results. BostonGene’s tests reveal key drivers of each patient’s unique disease profile, including an in-depth profile of the immune microenvironment, actionable mutations, biomarkers of response to diverse therapies, and recommended therapies. Through these comprehensive analyses, BostonGene’s tests generate a personalized roadmap for therapeutic decision-making for each patient. For more information, visit BostonGene at http://www.BostonGene.com .

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