Gene Therapy - Fixing Single Nucleotide Polymorphisms to cure PGD2 sensitivity

InBeforeTheCure

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@InBeforeTheCure,

Nice post dude. I'll respond later with some studies. Meanwhile have you looked into estrogen action on the hair follicle? As we know castration + estrogen is pretty much the only thing that can sometimes but not always grow back a considerate amount of hair. I like to quote Cotsarelis in this;

Anyway about estrogen, here are two in depth studies; http://press.endocrine.org/doi/full/10.1210/er.2006-0020, http://elib.tiho-hannover.de/dissertations/conradf_ss04.pdf. Curious to your opinion!

I went and cross-referenced the genes mentioned in that first paper with the genes from a paper that looked at gene expression differences between DPCs in balding vs. non-balding scalp.

Here's the list with their abbreviated names:

Code:
[TABLE="width: 128"]
[TR]
[TD="class: xl63, width: 64"]Gene[/TD]
[TD="class: xl63, width: 64"]Level[/TD]
[/TR]
[TR]
[TD]DNPH1[/TD]
[TD="align: right"]10.75[/TD]
[/TR]
[TR]
[TD]CASP4[/TD]
[TD="align: right"]10.38[/TD]
[/TR]
[TR]
[TD]MOG[/TD]
[TD="align: right"]9.23[/TD]
[/TR]
[TR]
[TD]CDKN2B[/TD]
[TD="align: right"]8.38[/TD]
[/TR]
[TR]
[TD]ICAM1[/TD]
[TD="align: right"]6.95[/TD]
[/TR]
[TR]
[TD]PSMA2[/TD]
[TD="align: right"]6.78[/TD]
[/TR]
[TR]
[TD]PMP22[/TD]
[TD="align: right"]6.34[/TD]
[/TR]
[TR]
[TD]PPP1CA[/TD]
[TD="align: right"]6.21[/TD]
[/TR]
[TR]
[TD]TFDP1[/TD]
[TD="align: right"]6.06[/TD]
[/TR]
[TR]
[TD]TPH2[/TD]
[TD="align: right"]5.34[/TD]
[/TR]
[TR]
[TD]TMF1[/TD]
[TD="align: right"]4.89[/TD]
[/TR]
[TR]
[TD]PKD1[/TD]
[TD="align: right"]3.68[/TD]
[/TR]
[TR]
[TD]AKT1[/TD]
[TD="align: right"]3.55[/TD]
[/TR]
[TR]
[TD]PAX5[/TD]
[TD="align: right"]3.45[/TD]
[/TR]
[TR]
[TD]GSTT1[/TD]
[TD="align: right"]3.38[/TD]
[/TR]
[TR]
[TD]DCN[/TD]
[TD="align: right"]2.94[/TD]
[/TR]
[TR]
[TD]SULT1E1[/TD]
[TD="align: right"]2.88[/TD]
[/TR]
[TR]
[TD]ITGAV[/TD]
[TD="align: right"]2.86[/TD]
[/TR]
[TR]
[TD]STAT1[/TD]
[TD="align: right"]2.69[/TD]
[/TR]
[TR]
[TD]CDK10[/TD]
[TD="align: right"]2.51[/TD]
[/TR]
[TR]
[TD]TAF9[/TD]
[TD="align: right"]2.38[/TD]
[/TR]
[TR]
[TD]NTF4[/TD]
[TD="align: right"]2.34[/TD]
[/TR]
[TR]
[TD]CDK5[/TD]
[TD="align: right"]2.27[/TD]
[/TR]
[TR]
[TD]HSPA72[/TD]
[TD="align: right"]2.22[/TD]
[/TR]
[TR]
[TD]PSME2[/TD]
[TD="align: right"]2.19[/TD]
[/TR]
[TR]
[TD]TMSB4X[/TD]
[TD="align: right"]2.02[/TD]
[/TR]
[TR]
[TD]RAD23A[/TD]
[TD="align: right"]1.93[/TD]
[/TR]
[TR]
[TD]MLH1[/TD]
[TD="align: right"]1.81[/TD]
[/TR]
[TR]
[TD]ROBO1[/TD]
[TD="align: right"]1.71[/TD]
[/TR]
[TR]
[TD]PRDX2[/TD]
[TD="align: right"]1.61[/TD]
[/TR]
[TR]
[TD]ZYX[/TD]
[TD="align: right"]1.6[/TD]
[/TR]
[TR]
[TD]MNAT1[/TD]
[TD="align: right"]1.57[/TD]
[/TR]
[TR]
[TD]DNASE2[/TD]
[TD="align: right"]1.52[/TD]
[/TR]
[TR]
[TD]GSS[/TD]
[TD="align: right"]1.51[/TD]
[/TR]
[TR]
[TD]HLA-C[/TD]
[TD="align: right"]1.47[/TD]
[/TR]
[TR]
[TD]DDIT3[/TD]
[TD="align: right"]1.44[/TD]
[/TR]
[TR]
[TD]COMT[/TD]
[TD="align: right"]1.32[/TD]
[/TR]
[TR]
[TD]TIMP2[/TD]
[TD="align: right"]0.8[/TD]
[/TR]
[TR]
[TD]MCL1[/TD]
[TD="align: right"]0.79[/TD]
[/TR]
[TR]
[TD]IL6[/TD]
[TD="align: right"]0.74[/TD]
[/TR]
[TR]
[TD]TYRO3[/TD]
[TD="align: right"]0.69[/TD]
[/TR]
[TR]
[TD]GPX2[/TD]
[TD="align: right"]0.65[/TD]
[/TR]
[TR]
[TD]RHOB[/TD]
[TD="align: right"]0.65[/TD]
[/TR]
[TR]
[TD]VEGFC[/TD]
[TD="align: right"]0.64[/TD]
[/TR]
[TR]
[TD]EZR[/TD]
[TD="align: right"]0.61[/TD]
[/TR]
[TR]
[TD]ACTB[/TD]
[TD="align: right"]0.59[/TD]
[/TR]
[TR]
[TD]NUCB1[/TD]
[TD="align: right"]0.59[/TD]
[/TR]
[TR]
[TD]CDK6[/TD]
[TD="align: right"]0.58[/TD]
[/TR]
[TR]
[TD]MCAM[/TD]
[TD="align: right"]0.57[/TD]
[/TR]
[TR]
[TD]PURA[/TD]
[TD="align: right"]0.57[/TD]
[/TR]
[TR]
[TD]FGR[/TD]
[TD="align: right"]0.56[/TD]
[/TR]
[TR]
[TD]MAPK3[/TD]
[TD="align: right"]0.55[/TD]
[/TR]
[TR]
[TD]MAPKAPK2[/TD]
[TD="align: right"]0.54[/TD]
[/TR]
[TR]
[TD]PTMS[/TD]
[TD="align: right"]0.54[/TD]
[/TR]
[TR]
[TD]ARHGDIA[/TD]
[TD="align: right"]0.51[/TD]
[/TR]
[TR]
[TD]COL4A2[/TD]
[TD="align: right"]0.51[/TD]
[/TR]
[TR]
[TD]CAPN2[/TD]
[TD="align: right"]0.5[/TD]
[/TR]
[TR]
[TD]RAB5A[/TD]
[TD="align: right"]0.49[/TD]
[/TR]
[TR]
[TD]ID2[/TD]
[TD="align: right"]0.48[/TD]
[/TR]
[TR]
[TD]IL4[/TD]
[TD="align: right"]0.48[/TD]
[/TR]
[TR]
[TD]CTGF[/TD]
[TD="align: right"]0.47[/TD]
[/TR]
[TR]
[TD]KRAS[/TD]
[TD="align: right"]0.47[/TD]
[/TR]
[TR]
[TD]MYC[/TD]
[TD="align: right"]0.46[/TD]
[/TR]
[TR]
[TD]MYBL1[/TD]
[TD="align: right"]0.44[/TD]
[/TR]
[TR]
[TD]RBL2[/TD]
[TD="align: right"]0.44[/TD]
[/TR]
[TR]
[TD]TIAM1[/TD]
[TD="align: right"]0.44[/TD]
[/TR]
[TR]
[TD]CCND1[/TD]
[TD="align: right"]0.43[/TD]
[/TR]
[TR]
[TD]CTTN[/TD]
[TD="align: right"]0.43[/TD]
[/TR]
[TR]
[TD]TNFAIP2[/TD]
[TD="align: right"]0.41[/TD]
[/TR]
[TR]
[TD]PSMF1[/TD]
[TD="align: right"]0.37[/TD]
[/TR]
[TR]
[TD]TGFB2[/TD]
[TD="align: right"]0.37[/TD]
[/TR]
[TR]
[TD]BDNF?[/TD]
[TD="align: right"]0.36[/TD]
[/TR]
[TR]
[TD]CDC25B[/TD]
[TD="align: right"]0.36[/TD]
[/TR]
[TR]
[TD]CYP1B1[/TD]
[TD="align: right"]0.34[/TD]
[/TR]
[TR]
[TD]NME1[/TD]
[TD="align: right"]0.34[/TD]
[/TR]
[TR]
[TD]RAF1[/TD]
[TD="align: right"]0.33[/TD]
[/TR]
[TR]
[TD]RARB[/TD]
[TD="align: right"]0.33[/TD]
[/TR]
[TR]
[TD]CDH11[/TD]
[TD="align: right"]0.32[/TD]
[/TR]
[TR]
[TD]CXCL5[/TD]
[TD="align: right"]0.31[/TD]
[/TR]
[TR]
[TD]FLT3[/TD]
[TD="align: right"]0.31[/TD]
[/TR]
[TR]
[TD]RALA[/TD]
[TD="align: right"]0.29[/TD]
[/TR]
[TR]
[TD]PPP3CA[/TD]
[TD="align: right"]0.28[/TD]
[/TR]
[TR]
[TD]GSTA2[/TD]
[TD="align: right"]0.27[/TD]
[/TR]
[TR]
[TD]AXL[/TD]
[TD="align: right"]0.26[/TD]
[/TR]
[TR]
[TD]MARK3[/TD]
[TD="align: right"]0.26[/TD]
[/TR]
[TR]
[TD]FOS[/TD]
[TD="align: right"]0.24[/TD]
[/TR]
[TR]
[TD]NRAS[/TD]
[TD="align: right"]0.24[/TD]
[/TR]
[TR]
[TD]CRABP2[/TD]
[TD="align: right"]0.21[/TD]
[/TR]
[TR]
[TD]ETS1[/TD]
[TD="align: right"]0.21[/TD]
[/TR]
[TR]
[TD]INHBA[/TD]
[TD="align: right"]0.2[/TD]
[/TR]
[TR]
[TD]ELK1[/TD]
[TD="align: right"]0.19[/TD]
[/TR]
[TR]
[TD]PIP5K1A[/TD]
[TD="align: right"]0.18[/TD]
[/TR]
[TR]
[TD]ETV6[/TD]
[TD="align: right"]0.17[/TD]
[/TR]
[TR]
[TD]IGFBP3[/TD]
[TD="align: right"]0.14[/TD]
[/TR]
[TR]
[TD]CCNB1[/TD]
[TD="align: right"]0.13[/TD]
[/TR]
[TR]
[TD]PIP4K2B[/TD]
[TD="align: right"]0.12[/TD]
[/TR]
[TR]
[TD]MPV17[/TD]
[TD="align: right"]0.09[/TD]
[/TR]
[TR]
[TD]SERPINA3[/TD]
[TD="align: right"]0.09[/TD]
[/TR]
[TR]
[TD]CRYZ[/TD]
[TD="align: right"]0.08[/TD]
[/TR]
[TR]
[TD]PIM1[/TD]
[TD="align: right"]0.08[/TD]
[/TR]
[TR]
[TD]NR2F6[/TD]
[TD="align: right"]0.06[/TD]
[/TR]
[TR]
[TD]BMP2[/TD]
[TD="align: right"]0.04[/TD]
[/TR]
[TR]
[TD]NR1D1[/TD]
[TD="align: right"]0.04[/TD]
[/TR]
[TR]
[TD]KSR1[/TD]
[TD="align: right"]0.02[/TD]
[/TR]
[TR]
[TD]EFNA3[/TD]
[TD="align: right"]0.01[/TD]
[/TR]
[TR]
[TD]POLA1[/TD]
[TD="align: right"]0.01[/TD]
[/TR]
[/TABLE]
Genes downregulated in balding DPCs that are upregulated by estrogen: VEGF, c-Fos, Cyclin D1, c-Myc, BMP2
Genes downregulated in balding DPCs that are also downregulated by estrogen: TGFB2, but they say that's in epithelial cells, so NONE really.
Genes upregulated in balding DPCs that are differentially regulated by estrogen: None

Interesting that VEGF, c-Fos, Cyclin D1, c-Myc, and BMP2 are all beta-catenin target genes* (I think). Bcl2 (not a beta-catenin target AFAIK) is also upregulated by estrogen, which protects against oxidative stress-induced apoptosis. Balding DPCs are under oxidative stress, as you know.

* Not exclusively beta-catenin targets, of course.

Swoop said:
Note also that he says mast cells might contribute to hair loss but I'll get into that later. That's why I made a correlation, to me a increase of mast cells might automatically mean enhanced PGD2 levels as they are the biggest source of that.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319975/figure/F4/

I'm no good at interpreting stains, but to me it looks like most of the green Ptgds stained cells don't show any red tryptase staining? But I guess it depends on magnitude of expression as well.
 

Armando Jose

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Do you need more proof than hamilton already gave us? I mean there is real world proof look at castrated men or the pseudo herms that lacked the 5-ar 2 enzyme that finasteride was based off of. Do lots of women grow beards and back hair where your from? Androgens fit the hole perfectly as to why men go bald as they get older because hormone levels naturally change. Yes there is a ton more related to it and many many questions still to answer, but the theory fits. There is nothing to prove for me so believe it or dont. Doesnt matter to me if someone wants to think the world is flat.

Me too .... Anyone can have its own opinion....

Do you think that Hamilton ideas are a dogma? I think that it could be better a second apinion or trial.... Did you read the full publications of Hamilton? Androgen's knowledege in these years were scarcy..

And you can not forget that the important androgens for scalp hair is made in yhe same pilosebaceous unit.....

Did you noticed that chidrens before puberty have sebum in its hair? If yes,. you can agree with me that actual theory have great problems.

Cheers.

BTW In my country live great "damiseles", most of them without beards ;)
 

Dench57

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Me too .... Anyone can have its own opinion....

Do you think that Hamilton ideas are a dogma? I think that it could be better a second apinion or trial.... Did you read the full publications of Hamilton? Androgen's knowledege in these years were scarcy..

And you can not forget that the important androgens for scalp hair is made in yhe same pilosebaceous unit.....

Did you noticed that chidrens before puberty have sebum in its hair? If yes,. you can agree with me that actual theory have great problems.

Cheers.

BTW In my country live great "damiseles", more of them without beards ;)

You really love that sebum theory huh
 

InBeforeTheCure

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Really nice info gathering and analysis on your part, thank you so much for your contribution to this discussion.

In regards to beta catenin, i found this helpful video that talks about the Wnt pathways, including beta catenin: https://youtu.be/o6Bbm4Tczfc

Interesting that beta catenin is so linked/instrumental in cancer/cell proliferation, though it makes sense since hairloss obviously requires cell proliferation/trigger.

Thanks. The video mentions BMP and Shh as well and their roles in development, and there's an intricate system of cross-talk between the Wnt, BMP, and Shh pathways that controls stem cell lineages in hair follicles with every cycle. If the balance and timing of these signals isn't right, the HF can fail to develop properly.
 

Rockinlove

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I'd concur. Knowing how Big Pharma functions; they are not seeking out a cure but a treatment that would garner them a steady stream of income for a lifetime. A cure defeats that purpose; profit. They are not in it for the science or philantrophy.


It's not that scientists can't do it, what always bothered me is why they DON'T do it. Not enough funding. It won't make them
rich...There's so many scams making money out there. A scientist has to be logical minded. It would seem like if there were any
possibility they would go for it?
 

InBeforeTheCure

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Gents - what do you make of this:
"Many of these genes required for hair follicle homeostasis are significantly under expressed in Androgenetic Alopecia but not in SA compared to normal scalp tissue (Table 1 and Figure S1). Our data (Table 1 & Figure S1) showed that the Androgen Receptor (AR) is up regulated in Androgenetic Alopecia, but not in SA. Previous studies [4] have shown that genetic variability in AR is a prerequisite for the development of early-onset Androgenetic Alopecia. A novel Androgenetic Alopecia susceptibility locus has been identified at 17q21.31 [5]. In our dataset, the DEAD box polypeptide 5 (DDX5), a transcriptional regulator of AR [6] is down regulated in Androgenetic Alopecia and maps to this locus."


It is an excerpt from this study (which perhaps you are already familiar with):
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4164265/

It clearly defines AR up regulation as the issue (which is what you all were also indicating), but it also points out that DDX5, which is supposed to regulate AR gene is itself down regulated. Could it be that the downregulation of DDX5 is a key component causing the up regulation of AR which in turn causes the issues we all face?

DDX5 is also known to be essential in initiating adipogenesis (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4670549/)

Will continue digging further to see what other pieces connect to this puzzle...

DDX5 does a lot of things. It's also a co-activator for p53, for example. It's interesting that they find DDX5 is downregulated in Androgenetic Alopecia though, because DDX5 is actually one of the most upregulated genes in balding DPCs when exposed to 100 nM DHT. Maybe it's underexpressed in the epithelial follicle though, who knows? It's also overexpressed in prostate cancer, not underexpressed.

"Previous studies [4] have shown that genetic variability in AR is a prerequisite for the development of early-onset Androgenetic Alopecia. A novel Androgenetic Alopecia susceptibility locus has been identified at 17q21.31 [5]. In our dataset, the DEAD box polypeptide 5 (DDX5), a transcriptional regulator of AR [6] is down regulated in Androgenetic Alopecia and maps to this locus."


DDX5 is something like 20 megabases away from the susceptibility gene, which seems to be MAPT (tau) actually.
 

abcdefg

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DDX5 does a lot of things. It's also a co-activator for p53, for example. It's interesting that they find DDX5 is downregulated in Androgenetic Alopecia though, because DDX5 is actually one of the most upregulated genes in balding DPCs when exposed to 100 nM DHT. Maybe it's underexpressed in the epithelial follicle though, who knows? It's also overexpressed in prostate cancer, not underexpressed.

"Previous studies [4] have shown that genetic variability in AR is a prerequisite for the development of early-onset Androgenetic Alopecia. A novel Androgenetic Alopecia susceptibility locus has been identified at 17q21.31 [5]. In our dataset, the DEAD box polypeptide 5 (DDX5), a transcriptional regulator of AR [6] is down regulated in Androgenetic Alopecia and maps to this locus."


DDX5 is something like 20 megabases away from the susceptibility gene, which seems to be MAPT (tau) actually.

I think we need inbeforethecure working in a lab somewhere. This guy knows more about this stuff than half the researchers probably do.
 

Omega2327

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@Swoop and @InBeforeTheCure since you guys seem to be the most knowledgeable and respected on this forum, what year do you think the cure will actually come? I'm assuming you both believe in Tsuji the most.
 

InBeforeTheCure

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I think we need inbeforethecure working in a lab somewhere. This guy knows more about this stuff than half the researchers probably do.

I'm no good in the lab man. I couldn't even make aspirin back in freshman chemistry lab without impurities. ;)

BTW, in regard to the post you quoted...When I ran a quick and dirty scoring algorithm for genes near M.P.B-associated SNPs, it was CRHR1 (a receptor for corticotropin-releasing hormone) and not MAPT that scored highest in that region of Chromosome 17. So I would say that CRHR1 is the most likely causative gene there.

@Swoop and @InBeforeTheCure since you guys seem to be the most knowledgeable and respected on this forum, what year do you think the cure will actually come? I'm assuming you both believe in Tsuji the most.

AFAIK Tsuji is planning on a release in the early 2020's. This depends on everything going well of course.
 

Omega2327

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I'm no good in the lab man. I couldn't even make aspirin back in freshman chemistry lab without impurities. ;)

BTW, in regard to the post you quoted...When I ran a quick and dirty scoring algorithm for genes near M.P.B-associated SNPs, it was CRHR1 (a receptor for corticotropin-releasing hormone) and not MAPT that scored highest in that region of Chromosome 17. So I would say that CRHR1 is the most likely causative gene there.



AFAIK Tsuji is planning on a release in the early 2020's. This depends on everything going well of course.
Yes I definitely know of the 2020 timeline but many people are skeptical so I suppose it was more of a question asking if you truly believe they will succeed in commercialization by 2020/2021 or if you think there will likely be delays and something like 2025 is more reasonable, etc.
 

Trichosan

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Yes I definitely know of the 2020 timeline but many people are skeptical so I suppose it was more of a question asking if you truly believe they will succeed in commercialization by 2020/2021 or if you think there will likely be delays and something like 2025 is more reasonable, etc.

Wait! Don't answer yet, let me get the shotgun in my mouth first.
 

Kevand

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DDX5 does a lot of things. It's also a co-activator for p53, for example. It's interesting that they find DDX5 is downregulated in Androgenetic Alopecia though, because DDX5 is actually one of the most upregulated genes in balding DPCs when exposed to 100 nM DHT. Maybe it's underexpressed in the epithelial follicle though, who knows? It's also overexpressed in prostate cancer, not underexpressed.

"Previous studies [4] have shown that genetic variability in AR is a prerequisite for the development of early-onset Androgenetic Alopecia. A novel Androgenetic Alopecia susceptibility locus has been identified at 17q21.31 [5]. In our dataset, the DEAD box polypeptide 5 (DDX5), a transcriptional regulator of AR [6] is down regulated in Androgenetic Alopecia and maps to this locus."


DDX5 is something like 20 megabases away from the susceptibility gene, which seems to be MAPT (tau) actually.

Completely off topic but: Do you or maybe swoop have a theory on how minodoxil works? Does it have any potential effect on the hair miniaturization process? And do you think NSAID would help on the miniaturization process?
 

InBeforeTheCure

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Completely off topic but: Do you or maybe swoop have a theory on how minodoxil works?

Off the top of my head:

- increases ERK and Akt activity
- stabilizes beta-catenin, probably through Akt
- increases Bcl2/Bax ratio (anti-apoptotic)
- increases VEGF production; therefore, promotes angiogenesis around the hair follicle
- decreases Androgen Receptor activity
- increases PGE1 and/or PGE2 synthesis
- increases intracellular calcium concentration, which is involved in keratinocyte differentiation

Does it have any potential effect on the hair miniaturization process?

In the short term, yes. In the long term, not necessarily.

And do you think NSAID would help on the miniaturization process?

No, except in rare cases.
 

Omega2327

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Off the top of my head:

- increases ERK and Akt activity
- stabilizes beta-catenin, probably through Akt
- increases Bcl2/Bax ratio (anti-apoptotic)
- increases VEGF production; therefore, promotes angiogenesis around the hair follicle
- decreases Androgen Receptor activity
- increases PGE1 and/or PGE2 synthesis
- increases intracellular calcium concentration, which is involved in keratinocyte differentiation



In the short term, yes. In the long term, not necessarily.



No, except in rare cases.
Didn't respond to my query :)
 

InBeforeTheCure

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Yes I definitely know of the 2020 timeline but many people are skeptical so I suppose it was more of a question asking if you truly believe they will succeed in commercialization by 2020/2021 or if you think there will likely be delays and something like 2025 is more reasonable, etc.

Hold on, let me consult my magic 8 ball.

"Will Tsuji succeed in commercialization by 2020/2021?"



Damn. Tough luck.
 

bridgeburn

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BTW, in regard to the post you quoted...When I ran a quick and dirty scoring algorithm for genes near M.P.B-associated SNPs, it was CRHR1 (a receptor for corticotropin-releasing hormone) and not MAPT that scored highest in that region of Chromosome 17. So I would say that CRHR1 is the most likely causative gene there.



AFAIK Tsuji is planning on a release in the early 2020's. This depends on everything going well of course.
do you know if reducing that hormone itself would be beneficial? i read it's involved in stress response so could there be any truth in stress being bad for hair?
 

Balding curse

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Off the top of my head:

- increases ERK and Akt activity
- stabilizes beta-catenin, probably through Akt
- increases Bcl2/Bax ratio (anti-apoptotic)
- increases VEGF production; therefore, promotes angiogenesis around the hair follicle
- decreases Androgen Receptor activity
- increases PGE1 and/or PGE2 synthesis
- increases intracellular calcium concentration, which is involved in keratinocyte differentiation

You should make your own lab man, most of these pathways are linked to cancer and one of them is linked to prostate cancer and autoimmune diseases
does increasing everyone of them individually will make a better regrowth?
 
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