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neuralgrndstate.bsky.social
Cancer is a systemic disease. Understanding a systemic disease needs systemic rules: Tumorigenesis is a process of progressive loss of original cell identity and gain of neural stemness, the general stemness that determines tumorigenicity and pluripotency.
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Why is cancer so hard to understand? Perhaps something already wrong in the root, something might cause only confusion. The mysterious mesenchymal state, the enigmatic "EMT," always stands in the spotlight. cellandbioscience.biomedcentral.com/articles/10....

submitted 2 days ago • 0 comments

Numerous studies showed that inhibition of an endogenous oncoprotein, Kras, c-myc, bcat, ezh2... causes decrease in tumorigenicity but also increase in antitumor immunity. (In fact, a typical oncoprotein regulates almost all traits of cancer cells) @cp-cancercell.bsky.social

submitted 2 days ago • 0 comments

Any treatment causes increase in anti-tumor immune response. @cp-cancercell.bsky.social General rule of cancer cell tumorigenicity and immunogenicity. “Tumorigenicity and immunogenicity are inversely correlated and determined by differentiation status of cancer cells“ biorxiv.org/content/10.1...

submitted 2 days ago • 0 comments

General rule of cancer cell tumorigenicity and immunogenicity. “Tumorigenicity and immunogenicity are inversely correlated and determined by differentiation status of cancer cells“ biorxiv.org/content/10.1...

submitted 2 days ago • 0 comments

General rule of cancer cell tumorigenicity and immunogenicity. “Tumorigenicity and immunogenicity are inversely correlated and determined by differentiation status of cancer cells“ biorxiv.org/content/10.1...

submitted 2 days ago • 0 comments

General relationship between cancer promoting genes and cancer cell response to anti-tumor immunity. (Note: major cancer promoting genes are neural stemness/embryonic neural genes, including KRAS, but suppressors are mostly not) biorxiv.org/content/10.1...

submitted 2 days ago • 0 comments

Both mean the same: cancer is process of dedifferentiation into primitive unicellular state, i.e., neural stemness, along a default, reversal route determined by evolution. “Cell dedifferentiation” versus “evolutionary reversal” theories of cancer..." onlinelibrary.wiley.com/doi/epdf/10....

submitted 2 days ago • 0 comments

"HNF4A as suppressors of lineage plasticity and metastasis in colorectal cancer" @nature.com

submitted 7 days ago • 0 comments

Nobody knows what is EMT, but it is stubbornly believed that it explains cancer metastasis. Neural stem/progenitor cells are well known for their migration&cancer cells are characteristic of neural stemness, but people try to avoid mentioning it. @nature.com

submitted 7 days ago • 0 comments

Neural genes are the oldest genes in the animal world, and only they have the power and qualification to promote cancer. Without neural genes, even animals would not exist. But what the hell is the so-called mesenchymal stuff?

submitted 7 days ago • 0 comments

Neural genes are the oldest genes in the animal world, and only they have the power and qualification to promote cancer. Without neural genes, even animals would not exist. But what the hell is the so-called mesenchymal stuff?

submitted 7 days ago • 0 comments

'EMT' and cancer: It is not the undefinable 'EMT' and mesenchymal' but the neural stuff that really matters. @nature.com

submitted 7 days ago • 0 comments

Similarity between cancer cells and a cellular state is not reflected by only a few misinterpreted gene symbols, but includes similarity in different aspects. @nature.com

submitted 7 days ago • 0 comments

It is said that something like rigor, precision, physiological relevance...are the rules to follow in research. How about the basics of EMT, eg E/M cellular states, specific markers, clear evidence, basic rationale of EMT... after >50 y EMT study? @nature.com

submitted 7 days ago • 0 comments

Why the epithelial-mesenchymal transition stuff, which has been studied for >50 years, yet nothing is known about it, is so stubbornly considered to be the answer to cancer metastasis/pasticity? @nature.com

submitted 7 days ago • 0 comments

Epithelial-mesenchymal transition? This is what has been known about it👇 @nature.com ''Lack of basic rationale in epithelial-mesenchymal transition and its related concepts" cellandbioscience.biomedcentral.com/articles/10....

submitted 7 days ago • 0 comments

Why is cancer so hard to understand? Perhaps sth. wrong in the root. Incorrect association between gene/protein symbols and cellular states, and poorly defined concepts like 'EMT' cause only confusion, and cannot be helpful for understanding cancer. @nature.com

submitted 7 days ago • 0 comments

Latest research confirmed that 'tumorigenesis represents progressive loss of original cell identity&gain of neural stemness', which confers cells with tumorigenicity&pluripotency. But the paper considered the effect as result of epithelial-mesenchymal transition. Funny. @nature.com

submitted 7 days ago • 0 comments

Similarity between a cellular state and cancer cells cannot be interpreted by only a few misinterpreted genes, but be interpreted by: @cp-iscience.bsky.social

submitted 8 days ago • 0 comments

Similarity between a cellular state and cancer cells cannot be interpreted by only a few misinterpreted genes, but be interpreted by: @cp-iscience.bsky.social

submitted 8 days ago • 0 comments

'EMT' and cancer: It is not the unknown mesenchymal but the neural stuff that really matters. @cp-iscience.bsky.social

submitted 8 days ago • 0 comments

On what reason it can be expected that wrong associations between gene/protein symbols and cellular states/properties, the undefinable mesenchymal state,..., can be helpful for understanding cancer properly? @cp-iscience.bsky.social

submitted 8 days ago • 0 comments

Mesenchymal state is widely used to explain migration of cancer cells, but nobody knows what is the state. Neural stem/progenitor cells are well known for their single cell migration&cancer cells are characteristic of neural stemness, but people try to avoid mentioning it. @cp-iscience.bsky.social

submitted 8 days ago • 0 comments

Epithelial-mesenchymal transition has been studies for >50 yrs & become 'mainstream concept'. But what is clear about the basics of it? Cellular states? Specific markers? Clear evidence? Basic rationale?... Nothing at all. @cp-iscience.bsky.social cellandbioscience.biomedcentral.com/articles/10....

submitted 8 days ago • 0 comments

Why is cancer so hard to understand? Perhaps sth. wrong in the root. If gene/protein symbols are mistakenly assigned to a cellular state, then no chance to make correct interpretation. Why SLUG, Zeb1/2...must be mesenchymal&what is mes. state? @cp-iscience.bsky.social www.cell.com/action/showP...

submitted 8 days ago • 0 comments

This is what we know about the so-called 'EMT'👇 ''Lack of basic rationale in epithelial-mesenchymal transition and its related concepts" cellandbioscience.biomedcentral.com/articles/10....

submitted 10 days ago • 0 comments

How can the extremely poorly defined 'EMT' stuff really be a little helpful for understanding bioscience? Fake research should be eliminated. But misconceptions play a central role in biomedical study. www.science.org/doi/10.1126/...

submitted 10 days ago • 0 comments

This is what we know about the so-called 'EMT'👇 ''Lack of basic rationale in epithelial-mesenchymal transition and its related concepts" @jclinical-invest.bsky.social cellandbioscience.biomedcentral.com/articles/10....

submitted 14 days ago • 0 comments

Cancer cells share properties incl. migration and regulatory networks with neural stem/progenitor cells, but people avoid mentioning it. Nobody knows what is 'EMT', but it plays a leading role in the spotlight at the center of the stage of biomedical research. @jclinical-invest.bsky.social

submitted 14 days ago • 0 comments

Fake research should be eliminated. How about misconceptions? How can the extremely poorly defined 'EMT' stuff really be helpful for understanding cancer? 'Polybromo 1/vimentin ..., epithelial-mesenchymal transition, and metastasis...' jci.org/articles/vie... @jclinical-invest.bsky.social

submitted 14 days ago • 0 comments

This is what we know about the so-called 'EMT'👇 ''Lack of basic rationale in epithelial-mesenchymal transition and its related concepts" cellandbioscience.biomedcentral.com/articles/10....

submitted 14 days ago • 0 comments

How can the extremely poorly defined 'EMT' stuff really be a little helpful for understanding cancer? Fake research should be eliminated. But misconceptions play a central role in biomedical study. 😂 www.nature.com/articles/s41...

submitted 14 days ago • 0 comments

See the general relation between neural enriched genes and immune related genes, tumorigenicity and immunogenicity of cancer cells @nature.com biorxiv.org/content/10.1...

submitted 14 days ago • 0 comments

Major regulatory relation between genes/proteins in cancer reflects their relation during development. CREM is enriched in neural crest cells, thus it should be low in NK cells. 'CREM is a regulatory checkpoint of CAR and IL-15 signalling in NK cells' @nature.com www.nature.com/articles/s41...

submitted 14 days ago • 0 comments

Loss of tissue-specific or differentiation genes causes dedifferentiation effect and returns cells back to their primitive ground state, i.e., neural stemness, along a default route predetermined by evolution. @nature.com

submitted 14 days ago • 0 comments

Genes on Y chromosome tend to be involved in male sex determination and development. Therefore, loss of Y leads to the loss of tissue-specific or differentiation genes and ultimately, the loss of original cell identity (and gain of neural stemness). @nature.com

submitted 14 days ago • 0 comments

Cancer cells share properties incl. migration and regulatory networks with neural stem/progenitor cells, but people avoid mentioning it. Nobody knows what is 'EMT', but it plays a leading role in the spotlight at the center of the stage of biomedical research. @natrevmcb.nature.com

submitted 14 days ago • 0 comments

4 cells were listed as examples of cell migration, 2 are neural cells, but no mesenchymal cells. Note: neural crest cells are not the so-called mesenchymal stuff. They are just neural crest cells. Without them, no peripheral nervous system, but only mesenchymal stuff left. @natrevmcb.nature.com

submitted 14 days ago • 0 comments

Maybe some well-designed experiments should be done to figure out why a few genes with specific/enriched expression in neural crest cells must be labeled as mesenchymal to explain cell migration.😂😂 @natrevmcb.nature.com

submitted 14 days ago • 0 comments

'EMT..neural crest cells are..mesenchymal...' Astonishing. Migration is the intrinsic property of NCCs, and 'EMT' factors snai1/2/twist are specific/enriched in NCCs&their roles in NCCs are well-known. So, NCCs are mesenchymal because they express genes specific to NCCs. WOW. @natrevmcb.nature.com

submitted 14 days ago • 0 comments

Why the epithelial-mesenchymal transition stuff, which has been studied for >50 years, yet nothing is known about it, is so stubbornly considered to be the answer to cancer metastasis? @natrevmcb.nature.com cellandbioscience.biomedcentral.com/articles/10....

submitted 14 days ago • 0 comments

Neural. It's neural. As generalized before, most cancer promoting genes are embryonic neural/neural stemness genes. Neural stemness is the core of cancer cells. DLAT is enriched in embryonic neural cells. May promote tumorigenesis by promoting neural stemness. @cp-cellmetabolism.bsky.social

submitted 17 days ago • 0 comments

But when increased immunogenicity was observed in cancer cells in response to blocking a same oncoprotein, it was explained by elegant specific molecular mechanisms merely in the context of anti-tumor immunity without considering reduced tumorigenicity. 🧐

submitted 17 days ago • 0 comments

Inhibition of an oncoprotein in cancer cells leads to smaller tumor formation in both immunodeficient&syngeneic mice, meaning reduced tumorigenicity&increased immunogenicity. How are they connected? See Preprint.👇 www.biorxiv.org/content/10.1...

submitted 17 days ago • 0 comments

It's common to see a same oncoprotein, eg c-myc, b-cat, kras,.. regulates different features of cancer cells, eg stemness, metastasis, immune evasion,...via distinct molecular mechanisms. What does this mean? Some discussion in Preprint👇 www.biorxiv.org/content/10.1...

submitted 17 days ago • 0 comments