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| Achieving clinical success with BET inhibitors as anti-cancer agents | Among five patients with MYC-positive DLBCL, only one showed a favourable outcome to BETi exposure. We also outline the logic of incorporating BETi into combination therapies to enhance its efficacy. References Hanahan, D. This sensitivity translated well in vivo, with prostate xenografts responding to as low a dose as 4. Postel-Vinay, S. Paris Saint Germain Andrew ГОООЛ! |
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Гол или Асистенция: Галин Иванов. Гол или Асистенция или Картон: Ивелин Попов. Голмайстор: Джонатан Дейвид. It should therefore not be surprising that in some cancers, such as AML and triple-negative breast cancer, epigenetic reprogramming to maintain the expression of these oncogenic networks is a mechanism of both intrinsic and acquired resistance.
Many types of cancer are characterised by increased transduction through these classical oncogenic networks. Notably, numerous studies found that BETi inactivate transcriptional programmes involved in RTK signalling exclusively in sensitive cells.
On nearly half of these active enhancers, an enrichment for BRD4 binding was concurrently observed. Notably, based on understanding this underlying mechanism of resistance, it was revealed that these neuroblastoma cell models were sensitive to PI3K inhibitors in combination with BETi.
Likewise, ovarian cancer cells acquiring BETi resistance through long-term culture reprogrammed their kinome to elevate signalling through PI3K and RAS pathways. However, exome sequencing was not carried out, so de novo activating mutations cannot be excluded.
In colorectal cancer models, KRAS mutations do not appear to render tumour cells more resistant to BETi. In KRAS -mutant-carrying NSCLC models, sensitivity to BETi was reported, but 2. mTOR is a key downstream effector of the PI3K pathway, regulating diverse processes including protein synthesis and cytoskeletal remodelling.
In this model, loss of LKB1 is expected to increase mTOR signalling thereby imparting resistance to BETi. Together, these data suggest that gain-of-function mutations and constitutive activity through the PI3K and RAS signalling axes might act as biomarkers of resistance to BETi in specific types of cancer Fig.
As described below, this information points towards the use of rational combination therapies to overcome this resistance. The stability of BET proteins might also influence their susceptibility to inhibitors. Remarkably, in endometrial cancer, some SPOP SRD mutations, such as RQ, lead to an enhanced association between SPOP and BET-family members, which results in increased ubiquitylation, decreased BET protein levels and enhanced sensitivity to BETi.
Overall, SPOP mutations hold great promise as biomarkers of both resistance and sensitivity to BETi. These studies reinforce the notion that BRD4 levels within tumours modulate the responsiveness to BETi.
The data also suggest that the activity of BET proteins might be regulated by proteasomal degradation across tissue types, which opens new therapeutic perspectives.
Especially relevant might be targeting BET proteins, either individually or combinatorially, using a proteolysis targeting chimera PROTAC, reviewed in ref.
Pharmacodynamic biomarkers enable the clinical monitoring of drug activity in vivo, ideally using simple PCR or ELISA-based assays that act in lieu of more complex approaches to measure the accumulation of an administered drug within plasma or the tumour itself.
Identifying robust pharmacodynamic biomarkers for BETi in preclinical settings will undoubtedly facilitate the optimisation of their clinical utility. Generating such biomarkers might be enhanced through the preclinical use of orthotopic xenografts that mimic a relevant tumour microenvironment, thereby more accurately predicting drug response in a time- and dose-dependent manner.
Upregulation of HEXIM1 has been identified as a potential pharmacodynamic biomarker in numerous tumour xenografts and whole blood samples in response to ABBV treatment Fig.
A small clinical trial showed a trend for both MYC repression and an increase in HEXIM1 in the plasma of patients treated with the BETi BAY for mixed, refractory malignancies. This is below administered drug levels eliciting dose-limiting toxicities. This may cast some doubt on the necessity for BETi to lower MYC transcription in order to provoke an anti-tumour response.
Another preclinical study reported that MYC and HEXIM1 act most robustly as tumour-based pharmacodynamic biomarkers for BETi and that the corresponding mRNAs did not show optimal correlation with drug accumulation within blood samples.
The study from Yeh et al. This is especially relevant for CCR2, that is known to recruit myeloid-derived suppressor cells to the tumour niche, which in turn, promotes tumour growth. After extensive preclinical evaluation, but in the absence of robust predictive biomarkers, multiple clinical trials of BETi against solid and haematological types of cancer have been initiated.
To date, ~25 clinical trials are either ongoing or have been completed Table 2. With the exception of NMC, these trials are not targeting specific molecular subtypes, and this lack of biological rationale, plus unexpected toxicities, might limit clinical efficacy in the short term.
Strong results from the preclinical evaluation of BETi in multiple myeloma mled to elevated expectations for achieving clinical responses in this malignancy. The first published clinical trials of BETi all used the widely studied drug OTX MK Among five patients with MYC-positive DLBCL, only one showed a favourable outcome to BETi exposure.
However, this dose might not be universally achievable because almost all of the patients in this trial displayed dose-limiting toxicities, including thrombocytopenia, anaemia, neutropenia, gastrointestinal events and fatigue.
Based on published clinical data, these toxicities appear to be common for this class of drugs regardless of the type of cancer being treated or the chemical structure of the BETi being tested.
Once maximum drug activity is identified in the plasma or intratumorally, higher doses are likely to elicit strong off-target effects. As described above, NMC is characterised by BRD4 fusions leading to aberrant BRD4 activity.
Again, based on preclinical data, expectations that BETi would show efficacy against these tumours were high and, consequently, the first published clinical trial using BETi was focused on NMC. Clinical responses were observed in two patients, but all four patients succumbed to their disease between 5 and 19 months post-diagnosis.
Complementing this study, Lewin et al. Partial responses have also been described for NMC patients treated with the I-BETA molibresib. In addition to MYC and BRD4—NUT-driven malignancies, BETi have been tested against several AMLs and diverse solid tumours. In an initial study of OTX in a cohort of 41 patients with AML, 59 three patients showed partial responses and two patients showed a complete response lasting 2—5 months.
Notably, however, an attempt to identify potential biomarkers including mutations in 42 genes failed to uncover any clear molecular pathologies among responders. Although published reports of the use of BETi against solid tumours have not met expectations, responses have been observed, again underscoring a need for predictive biomarkers.
Perhaps the most promising preclinical data against solid tumours beyond NMC have come from prostate cancer models. This study included patient cohorts harbouring both solid and haematological tumours. In total, 65 patients were enrolled, including those with NMC, small cell- and non-small lung cancer, triple-negative breast cancer TNBC , CRPC, colorectal cancer, neuroblastoma and multiple myeloma.
While complete responses were not reported, four NMC patients had confirmed and unconfirmed partial responses and one TNBC patient achieved unconfirmed partial response. Based on these data, we predict that BETi might play an important clinical role in the management of NMC.
However, it is clear that predictive biomarkers and, most likely, combinatorial approaches, will be essential moving forward and, perhaps more importantly, it will be critical to overcome in-class dose-limiting toxicities.
BET proteins are important for multiple cellular processes required for homoeostasis, which might explain why complete bromodomain inhibition leads to unexpected toxicities.
Advances in the medicinal chemistry of BETi might be required to dissociate anti-cancer effects from the inhibition of physiological pathways required for homoeostasis.
The necessity of using such high doses to combat cancer proliferation strongly suggests a high level of intrinsic resistance to these compounds across tumour types that has not been widely studied or appreciated. The precise mechanisms of intrinsic resistance to BETi remain unclear, but multiple studies suggest that the activation of oncogenic signalling pathways including those mediated by PI3K and RAS might be involved and that repression of these pathways might act as key mediators of BETi activity.
We suggest that, consequently, these pathways also play a role in intrinsic BETi resistance and could therefore be targeted in conjunction with the use of BETi. Several studies report the PI3K pathway as a determining factor influencing BETi both intrinsic and acquired resistance, and suggest that this resistance could be successfully overcome through the combination treatment using BETi and PI3K inhibitors.
As described below, a better understanding the mechanisms of resistance mediated by constitutive signalling through PI3K and MAPK pathways will probably reveal new therapeutic options for these patients.
Multiple studies demonstrate that combining BETi with tyrosine kinase inhibitors effectively overcomes both intrinsic and acquired resistance to these drugs in several types of cancer.
A chemical combinatorial screening of JQ1 with around compounds aimed at finding effective small molecule combination therapies with BETi revealed PI3K inhibitors to be the most potent partners against neuroblastoma both in vitro and in animal models.
Melanomas bearing NRAS mutations frequently have high BRD4 mRNA and protein expression levels, which are associated with a poor outcome.
The combined treatment downregulated proteins implicated in cell cycle regulation and apoptosis. Recent evidence indicates that cell cycle regulation resulting from the combination of BETi with MAPK inhibitors may stem from a broad repression of nucleotide metabolism in ovarian cancers.
Moving forward, it will be important to examine whether this mechanism is relevant to other cancer models sensitive to this combination.
About half of all recurrent TNBC express high levels of n-MYC. It remains to be experimentally proven which, if any, of these correlates are responsible for the observed growth inhibition. In PDX models of TNBC, intermediate or high levels of n-MYC predicted response to the synergistic combination of trametinib with either JQ1 or another BETi, INCB, whereas PDX models with low levels of n-MYC were more resistant.
As stated above, the half-life of JQ1 in vivo is quite short, and high doses are generally required to achieve effects. Additional combinations using BETi also show promise. KRAS mutations are very prevalent in pancreatic ductal adenocarcinoma PDAC and is associated with a very poor prognosis.
That being said, independent reports have supported the applicability of this combination in vivo, using either a MYC-driven lymphoma model or against a neuroblastoma model. As stated previously, BET proteins might act as oncogenes, at least in part, through the activation of genes involved in cell cycle progression.
As such, it would be logical to combine BETi with inhibitors of CDKs. This approach has been explored successfully in NMC. An interesting combination of BETi with vitamin C was demonstrated to be effective using both in vitro and in vivo TNBC models.
In this study, simultaneous treatment resulted in a decrease in histone acetylation, perhaps consistent with the findings of efficacy between BETi and HDAC inhibitors. This strategy of combining BETi with vitamin C not only in TNBC, but also in melanoma significantly improved the EC50 of BETi by reducing it to a nanomolar range.
Even though responses differ across tissue types, the cell response to BETi is generally cytostatic in nature, resulting in delayed cell cycle progression. Thus, it might be logical to complement this cytostatic response with promoters of an apoptotic response.
Supporting this idea are a number of studies showing synergy between several BETi and the BCL-2 inhibitor venetoclax ABT against haematopoietic malignancies. The combination of inhibitors of poly-ADP ribose polymerase PARP with BETi has shown great promise, instigating a loss of proliferation across many cell types, including ovarian, breast and pancreatic cancer models both in vitro and in vivo.
The development of BETi has provided important insights into the key role of BET proteins in the transcriptional control of proto-oncogenes, and highlighted the potential of these proteins as therapeutic targets.
Preclinical studies have demonstrated a remarkable anti-proliferative activity of BETi against tumours, including several incurable subtypes. It is our opinion that a lack of biomarkers predicting sensitivity to BETi, coupled with the use of non-clinically relevant doses in preclinical studies, is limiting the application of these agents in clinical practice.
Further research and mechanistic studies will help to identify such biomarkers, and the development of novel, highly selective bromodomain inhibitors will help prevent toxicities. Finally, exciting new data indicate that, in the long term, BETi are likely to hold the most clinical potential as a part of combinatorial regimens.
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Genes Dev. Kouzarides, T. Chromatin modifications and their function. Wilson, V. Cancer Res. Cameron, E. Synergy of demethylation and histone deacetylase inhibition in the re-expression of genes silenced in cancer.
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Structure and ligand of a histone acetyltransferase bromodomain. Nature , — Jung, M. Affinity map of bromodomain protein 4 BRD4 interactions with the histone H4 tail and the small molecule inhibitor JQ1.
Loven, J. Selective inhibition of tumor oncogenes by disruption of super-enhancers. Filippakopoulos, P. Histone recognition and large-scale structural analysis of the human bromodomain family. Bhagwat, A. BET bromodomain inhibition releases the mediator complex from select cis-regulatory elements.
Cell Rep. Jang, M. The bromodomain protein Brd4 is a positive regulatory component of P-TEFb and stimulates RNA polymerase II-dependent transcription. Cell 19 , — Gilan, O. Selective targeting of BD1 and BD2 of the BET proteins in cancer and immunoinflammation.
Science , — Yang, Z. Brd4 recruits P-TEFb to chromosomes at late mitosis to promote G1 gene expression and cell cycle progression. Cell Biol. Sinha, A. Bromodomain analysis of Brd2-dependent transcriptional activation of cyclin A. Mochizuki, K.
The bromodomain protein Brd4 stimulates G1 gene transcription and promotes progression to S phase. Chapuy, B. Discovery and characterization of super-enhancer-associated dependencies in diffuse large B cell lymphoma. Cancer Cell 24 , — Delmore, J. BET bromodomain inhibition as a therapeutic strategy to target c-Myc.
Peng, J. Brd2 is a TBP-associated protein and recruits TBP into E2F-1 transcriptional complex in response to serum stimulation. Cell Biochem. French, C. NUT Carcinoma: clinicopathologic features, pathogenesis, and treatment. Lee, J. Complex chromosomal rearrangements by single catastrophic pathogenesis in NUT midline carcinoma.
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Natl Acad. USA , — Wu, X. Inhibition of BRD4 suppresses cell proliferation and induces apoptosis in renal cell carcinoma. Cell Physiol. Dawson, M. Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia.
Lu, L. Inhibition of BRD4 suppresses the malignancy of breast cancer cells via regulation of Snail. Cell Death Differ. Nicodeme, E. Suppression of inflammation by a synthetic histone mimic.
Dey, A. BRD4 directs hematopoietic stem cell development and modulates macrophage inflammatory responses. EMBO J. Belkina, A. BET protein function is required for inflammation: Brd2 genetic disruption and BET inhibitor JQ1 impair mouse macrophage inflammatory responses. Wienerroither, S.
Regulation of NO synthesis, local inflammation, and innate immunity to pathogens by BET family proteins. Baud, M. Chemical biology. A bump-and-hole approach to engineer controlled selectivity of BET bromodomain chemical probes.
Bardini, M. Cancer Ther. Mirguet, O. Discovery of epigenetic regulator I-BET lead optimization to afford a clinical candidate inhibitor of the BET bromodomains.
Wyce, A. Inhibition of BET bromodomain proteins as a therapeutic approach in prostate cancer. Oncotarget 4 , — Bailey, D. RVX a small molecule that increases apolipoprotein A-I and high-density lipoprotein cholesterol in vitro and in vivo.
Stubbs, M. The novel bromodomain and extraterminal domain inhibitor INCB induces vulnerabilities in myeloma cells that inform rational combination strategies. Endo, J. A phenotypic drug discovery study on thienodiazepine derivatives as inhibitors of T cell proliferation induced by CD28 co-stimulation leads to the discovery of a first bromodomain inhibitor.
Cochran, A. Drug Discov. Zaware, N. Bromodomain biology and drug discovery. Zuber, J. RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukaemia.
Bandopadhayay, P. BET bromodomain inhibition of MYC-amplified medulloblastoma. Shu, S. Response and resistance to BET bromodomain inhibitors in triple-negative breast cancer. Klingbeil, O. Inhibition of BET bromodomain-dependent XIAP and FLIP expression sensitizes KRAS-mutated NSCLC to pro-apoptotic agents.
Cell Death Dis. Boi, M. The BET bromodomain inhibitor OTX affects pathogenetic pathways in preclinical B-cell tumor models and synergizes with targeted drugs. Clin Cancer Res. Finley, A. Small molecule control of chromatin remodeling. Seal, J. Identification of a novel series of BET family bromodomain inhibitors: binding mode and profile of I-BET GSKA.
Odore, E. Phase I population pharmacokinetic assessment of the oral bromodomain inhibitor OTX in patients with haematologic malignancies. Potent activity of the bromodomain inhibitor OTX in multiple myeloma. Henssen, A. Targeting MYCN-driven transcription By BET-bromodomain inhibition.
Vázquez, R. Cancer , — PubMed Google Scholar. Xie, F. The BET inhibitor I-BET inhibits pancreatic ductal adenocarcinoma cell proliferation and enhances the therapeutic effect of gemcitabine. Chaidos, A.
Potent antimyeloma activity of the novel bromodomain inhibitors I-BET and I-BET Blood , — Tarantelli, C.
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