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#PDAC

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victorjavierlo

We’re excited to share our latest research: “ELOVL6 as a Therapeutic Target: Disrupting c-MYC-Driven Lipid Metabolism to Enhance Chemotherapy in Pancreatic Cancer.”

biorxiv.org/content/10.1101/20

Targeting metabolic dependencies like ELOVL6 in c-MYC-driven cancers could open new avenues in PDAC treatment, offering hope for better patient outcomes. Follow us for updates as we continue exploring the therapeutic potential of lipid metabolism in cancer

bioRxiv · ELOVL6 as a Therapeutic Target: Disrupting c-MYC-Driven Lipid Metabolism to Enhance Chemotherapy in Pancreatic CancerPancreatic ductal adenocarcinoma (PDAC) is a devastating disease, marked by a survival rate of only 12%. Consequently, the exploration of novel therapeutic strategies becomes a critical clinical imperative. Among the genetic alterations contributing to PDAC, c-MYC overexpression arises due to upstream mutations, amplifications, and copy number alterations. c-MYC serves as a key regulator in the tumor's metabolic reprogramming, playing a pivotal role in proliferation, migration, and metastasis. This study delves into the investigation of the role of the elongase ELOVL6 in c-MYC-induced cell transformation and its potential as a therapeutic target in PDAC. Here, we demonstrate that c-MYC regulates lipid elongation to promote cell transformation, offering a new avenue for therapeutic intervention. Initially, we show the direct regulation of ELOVLs expression by c-MYC in various PDAC mouse models and cell lines, elucidating its upregulation during transformation and tumor progression. Genetic or chemical inhibition of ELOVL6 results in decreased proliferation and migration, accompanied by alterations in fatty acid elongation. These changes in fatty acid composition led to modifications in membrane rigidity, permeability, and thickness, which collectively affect micropinocytosis and macropinocytosis. Importantly, we observe an increase in Abraxane uptake and a synergistic effect when combined with ELOVL6 interference in vitro. In vivo validation demonstrates that ELOVL6 inhibition significantly reduces tumor growth and enhances the response to Abraxane, thereby increasing overall survival. Altogether, these results position ELOVL6 as a promising therapeutic target in the treatment of PDAC ### Competing Interest Statement The authors have declared no competing interest.
#PDAC
Public
victorjavierlo

Excited to join Mastodon! I've embarked on this journey seeking a constructive environment and new opportunities for collaboration. Our lab is deeply engaged in the fight against pancreatic cancer, employing both experimental and computational approaches to unlock new insights and solutions. We're eager to connect with like-minded individuals and groups. We're open to exploring potential collaborations and sharing knowledge. #PDAC #bioinformatics

Public
Thomas Walle

Study from Dana Pe'er and Scott Lowe's labs. Direna Alonso and Cassandra Burdziak show how genetic and environmental events interact to drive tumorigenesis in #PDAC #cancer

Now published: doi.org/10.1126/science.add5327

Lot's of computational innovation in there as well: Quantifying cellular plasticity, a module view on cell cell communication etc.

It was awesome to be part of the team!

Public
TumorBoardTuesday

*From #TumorBoardTuesday archives*

📖A lot of movement in #PancreaticCancer space. Take a look at this November 2021 germline & somatic mut case by @SirohiBhawna & wrap up

Is there something you'd do different?
@MPishvaian @JohnEbbenMDPhD @letswinpc

---
RT @TumorBoardTues
2/8 #TumorBoardTuesday
Thurs Case🎀
11/09/2021
Take🏠:

✅Upfront tx depends on pt- mFFX vs gem/nab-pac
✅Test all #PDAC for germline mut regardless of FH!‼️
✅Scre…
twitter.com/TumorBoardTues/sta

Twitter#TumorBoardTuesday on Twitter“2/8 #TumorBoardTuesday Thurs Case🎀 11/09/2021 Take🏠: ✅Upfront tx depends on pt- mFFX vs gem/nab-pac ✅Test all #PDAC for germline mut regardless of FH!‼️ ✅Screen w annual MRI/EUS in gATM ✅Emerging 💊combos tx ATM-mut ✅#PANCAN req multi-D- role for palliative SBRT, ?IRE”
Public
Thiago Carvalho

"In this work, we explored possibility of using drug-sensitivity data together with basal gene expression data on pancreatic cell lines to predict the combinatorial options available for HDACi and developed bioinformatics screening protocol for predictions of synergistic drug combinations in PDAC. "

#Preprint #PDAC #HDAC

biorxiv.org/content/10.1101/20

bioRxivCorrelating basal gene expression across chemical sensitivity data to screen for novel synergistic interactors of HDAC inhibitors in pancreatic carcinomaPancreatic ductal adenocarcinoma (PDAC) is considered as one of the most aggressive and lethal malignancies. Development of chemoresistance in PDAC is one of the key contributors for the poor survival outcomes of PDAC patients and the major reason for urgent development of novel pharmacological approaches for effective treatment of PDAC. Systematically tailored combination therapy holds the promise for advancing the treatment of PDAC, but number of possible combinations considering all approved drugs and drug candidates is too large to be explored empirically. In respect to the many epigenetic alterations in PDAC, epigenetic drugs including histone deacetylase inhibitors (HDACi) could be seen as a game changers but available data indicates their efficacy only in combined therapy settings. In this work, we explored possibility of using drug-sensitivity data together with basal gene expression data on pancreatic cell lines to predict the combinatorial options available for HDACi and developed bioinformatics screening protocol for predictions of synergistic drug combinations in PDAC. Our results identified sphingolipid signaling pathway with associated downstream effectors as a promising novel target for future development of multi-target therapeutics or combined therapy with HDACi. Through the process of experimental validation of the methodology, we have characterized novel synergism between HDACi and Rho-associated protein kinase (ROCK) inhibitors. ### Competing Interest Statement The authors have declared no competing interest.
Public
Thiago Carvalho

'Pancreatic ductal adenocarcinoma (PDA) remains one of the deadliest major cancers, contrasting a relatively low incidence rate1. The primary reasons for this are related to the difficulty with early detection and a lack of effective therapeutic options. A principal barrier to treatment of pancreatic cancer is the densely fibrotic tumor microenvironment, the high interstitial pressure of which acts to collapse blood vessels and impair the delivery of chemotherapy. This lack of functional vasculature leads to deregulated nutrient availability within the tumor, causing cancer cells to develop numerous metabolic adaptations to allow for proliferation under hypoxic and austere conditions'

#PDAC #CancerMetabolism

nature.com/articles/s43018-022

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