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CG Ventures

  • CuringGenetics
  • LKB1 STK11
  • PJS
  • Cure
  • Donate
  • CG Ventures
  • Patient Community
  • Get Involved
  • About
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For efficiency, speed, and cost, many sows involve "REPURPOSING FDA APPROVED TREATMENTS"

SOW1 (human phase)

SOW1 (human phase)

SOW1 (human phase)

Ruxolitinib, a Jak 1/2 inhibitor, significantly reduced tumorigenesis in a PJS mouse model. Based on the Inventors' preclinical results, they expect Ruxolitinib to also reduce  tumorigenesis in PJS patients. Other Jak inhibitors such as Itacitinib are also being engaged to reduce or stop polyposis and tumorigenesis.

SOW2 (human phase)

SOW1 (human phase)

SOW1 (human phase)

Rapamycin (Sirolimus), an mTOR inhibitor, is a promising candidate in treatment and prevention of PJS polyps. PJS is caused by mutation of LKB1 gene which leads to increased activity of mTOR pathway. 

SOW3

SOW1 (human phase)

SOW3

 Combo approach. Use the identified FDA approved compounds with Rapa and the mutation in cell lines and or animal models for treatment and repurposing. 


Jack 1/2 inhibitor proof

PJS Animal model proof

Polyps are reduced in Ruxolitinib treated LKB1 knockout mice.

SOW4

SOW4

SOW4

  Gene therapy and editing. 

Repair mutated LKB1/STK11 tumor suppressor gene. 

SOW5

SOW4

SOW4

    Utilize mRNA approach. Intestine delivery pill identified. Develop a vaccine to recognize the mutation and stop formation of polyps. Checkpoint immunotherapy may also be considered as a combo therapy.

SOW6

SOW6

SOW6

  Stem cell therapy. Infuse corrected or donated stem cells to be proliferated as healthy T cells to supplement protein and correct deficiencies. 

SOW7

SOW6

SOW6

  Liquid Biopsy. 

Lessen the burden of ongoing intensive screening and risks for patients. 

research articles and videos

Precision Medicine paving the way for a new era

Precision Medicine paving the way for a new era

Precision Medicine paving the way for a new era

 Over the past few years, a number of products that signal a new era of medical research and development have entered the markets and are on the horizon. 

Molecular Mechanism that underlie LKB1

Precision Medicine paving the way for a new era

Precision Medicine paving the way for a new era

 Germline mutations of the LKB1 tumor suppressor gene result in Peutz–Jeghers Syndrome (PJS) characterized by intestinal hamartomas and increased incidence of epithelial cancers. 

Restoration of silenced PJS gene, LKB1

Precision Medicine paving the way for a new era

Therapeutic opportunities knock when LKB1 inactivated

 

 Germline mutations of the LKB1 tumor suppressor gene lead to Peutz-Jeghers Syndrome (PJS) with a predisposition to cancer.  

Therapeutic opportunities knock when LKB1 inactivated

Therapeutic opportunities knock when LKB1 inactivated

Therapeutic opportunities knock when LKB1 inactivated

 LKB1 is commonly thought of as a tumor suppressor gene because its hereditary mutation is responsible for cancer syndrome, and somatic inactivation of LKB1 is found in non-small cell lung cancer, melanoma, and cervical cancers. 

LKB1 is mutated in PJS and variety of cancers

Therapeutic opportunities knock when LKB1 inactivated

LKB1 is mutated in PJS and variety of cancers

 Increasing evidence has highlighted that deficiency of LKB1 in cancer cells induces extensive metabolic alterations that promote tumorigenesis and development. 

Targeting the LKB1 Tumor Suppressor

Therapeutic opportunities knock when LKB1 inactivated

LKB1 is mutated in PJS and variety of cancers

 Physiologically, LKB1 possesses multiple cellular functions in the regulation of cell bioenergetics metabolism, cell cycle arrest, embryo development, cell polarity, and apoptosis. 

Cancer immunotherapy via dendritic cells

Genome editing with Cas9 corrects mice mutation

Genome editing with Cas9 corrects mice mutation

The molecular identification of human cancer antigens has allowed the development of antigen-specific immunotherapy. 

Genome editing with Cas9 corrects mice mutation

Genome editing with Cas9 corrects mice mutation

Genome editing with Cas9 corrects mice mutation

We demonstrate CRISPR-Cas9-mediated correction of a Fah mutation in hepatocytes in a mouse model of the human disease hereditary tyrosinemia.

LKB1 and PAR-4

Genome editing with Cas9 corrects mice mutation

LKB1 and PAR-4

 The PAR clan of polarity regulating genes was initially discovered in a genetic screen searching for genes involved in asymmetric cell divisions in the Caenorhabditis elegans embryo.  

P53

Autophagy & LKB1

LKB1 and PAR-4

The activation of the p53 pathway by the AMP mimetic AICAR is reduced by inhibitors of the ATM or mTOR kinases.

Autophagy & LKB1

Autophagy & LKB1

Autophagy & LKB1

Does  autophagy take a front seat in lifespan extension? 

Epigenetic changes in pediatric solid tumors

Epigenetic changes in pediatric solid tumors

Epigenetic changes in pediatric solid tumors

 Somatic mutations or deregulated expression of chromatin modifying enzymes are being identified at high frequency. 

LKB1 & Embryonic Stem Cells

Epigenetic changes in pediatric solid tumors

Epigenetic changes in pediatric solid tumors

 Human embryonic stem cells maintained on human amniotic epithelial cells (hESCshAEC) are better preserved in an undifferentiated state and... 

Epigenetics targeting solid tumors

Epigenetic changes in pediatric solid tumors

LKB1 tumor suppressor & Lung Cancer

 Epigenetic therapies may play a prominent role in the future management of solid tumors. 

LKB1 tumor suppressor & Lung Cancer

LKB1 tumor suppressor & Lung Cancer

LKB1 tumor suppressor & Lung Cancer

To stop lung cancer from spreading, researchers target a specific gene. 

By Adam Marcus, PhD

LKB1/STK11 & Lung Cancer

LKB1 tumor suppressor & Lung Cancer

LKB1/STK11 & Lung Cancer

Gene discovery may stop the spread of lung cancer.

By Reuben Shaw, PhD

Precision Medicine

Ability to identify cancerous genes

Ability to identify cancerous genes

Precision medicine when every cancer is personal.

By Adam Marcus, PhD

Ability to identify cancerous genes

Ability to identify cancerous genes

Ability to identify cancerous genes

Research focused on the relative importance of selection of genomic instability. 

By Ian Tomlinson, PhD


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