Creating Curative Therapies

i joined the stem cell institute over 15

years ago

and it wasn’t just the pleasure of

cutting my salary in half

as i left the for-profit sector but to

work with people like doug melton and

david skadden who are the two scientific

directors of the institute to set up

this new enterprise and what it was is a

virtual research center that spans

harvard the schools of harvard and the

harvard-affiliated hospitals harvard has

a unique footprint in not only this east

coast system but the world and having

eight hospitals affiliated with it and

so the idea here by building this what i

call virtual research center

where we could have a new way of doing r

d we didn’t need to own the assets but

we could have some of the world’s

leading experts and many diseases

work across

these different organizations and

departments and labs and disciplines to

go all the way from bench side signs to

treating patients where else in the

world can you do that so that that was

one of the the appeal the new business

model working with leading experts and

as john alluded to the ability to

actually take a serious go at some of

these diseases and conditions that are

affecting everyone not only some of the

aging issues you heard about from david

sinclair before

but conditions such as diabetes that

doug melton works on spinal cord injury

that my brother suffered from

parkinson’s disease that my

father-in-law

and we all have these stories right and

so far we’ve had no good treatments for

those so what we do we’ve grown that

center to now over 380 faculty across

the different institutions and the whole

point is interdisciplinary inner

organization interlab collaboration to

work on new cell and gene therapies this

is what most of you think about when you

think about stem cell science you think

about how do we fix broken cells i.e you

know the dopaminergic neurons that go in

parkinson’s the

eyelid cells that go on diabetes etc so

this is how do i replace the broken part

theory or fix the

the defective gene which we now can do

much more easily thanks to advanced like

crispr um and other another gene editing

tools but there are also

other mechanisms so stem cell science

has also led us into a whole new way of

thinking about how can we engage

endogenous repair capabilities in other

words how do we stimulate the body’s

internal ability to repair in a way that

it’s either lost because of age or lost

because of accident or disease so that’s

the second point and the third is

because now we’ve developed the tools

and i’ll talk about this a little bit

later where we can create human cells of

interest by mean if you want to study

a motor neuron or heart cell or muscle

cell or fat in a dish we now have the

tools that we can create those cells in

both 2d and three-dimensional systems to

help understand disease mechanism and

seriously change both the economics and

the approaches to drug discovery and

we’ll talk about why so we organized by

disease now that’s unique in an academic

setting because most people are looking

at technical problems but we wanted

people to look at technical problems but

aim them at having an impact on disease

we want the basic research but we don’t

want to be goal directed we also

deliberately set up so that we could

talk across disease categories so for

example that people studying the

autoimmune problem in diabetes where

once and type one diabetes that is where

your immune system attacks your own beta

cells what could they learn from the

cancer program where tumor cells are

really good at avoiding the immune

system that’s the whole issue so how can

they cross-pollinate

how do we also

understand processes that cut across

disease

diseases and organs and

even time such as fibrosis or aging so

think of fibrosis whether it’s

in the heart the kidney the lung the

skeletal muscle as a way where the body

doesn’t repair the way it should

what we can do because we’re people

studying those interact that process

from a molecular cellular level on up in

different organ systems is compare notes

so that we can see what are common

pathways what are common behaviors and

where do they differ so how can we take

you know what we learn in lung fibrosis

and apply it to say liver fibrosis or

vice versa similarly for those of you

who heard david sinclair

uh aging is a process basically of

losing our ability to repair and

regenerate over time

in utero if

a fetus has a skin wound it can heal you

know if there’s an in

intrauterine operation it can heal

scarlessly we

and infants can you know grow a

fingertip back children can grow a

fingertip back we lose that ability over

over time even certain body parts such

as blood skin hair that repair

themselves

every few days during life repair

themselves less and less well over time

why is that true and what can we learn

about the early ability to repair and

apply that to later stages in life

let me fast forward

from 15 years ago to today or actually a

couple weeks ago vertex pharmaceuticals

announced the results from the first

patient in a trial where stem cell

derived beta cell transplant so this is

work coming out of their acquisition of

semi-therapeutics a couple years ago

which itself had been formed five years

before that out of work coming out of

doug melton’s lab and we’re talking

about before so it took well over a

decade in the academic lab to figure out

how to turn an embryonic stem cell or or

pluripotent stem cell into a mature beta

cell in vitro

the startup company then further uh

refined that process and then vertex is

bringing it into the clinic

but what they’re able to do in this

patient and this is a brittle diabetic

an older man who had a type 1 diabetic

who’s been on insulin for 40 years was

hospitalized several times each year

because

is what they call brittle diabetic

because of the condition where his body

would just crash and in the 90 days at

half of their planned dose he was

basically off of insulin and this

remember is a disease that’s multi-genic

there are multiple genes impacting the

disease it’s environmental

and has many causes many different

manifestations but if it but it comes

crashing down on one cell type so gene

therapy isn’t going to fix but if you

can so this is shown at least

conceptually that if you can fix that

cell in question you can potentially

cure the disease potentially

now the next step many of you are going

to say well that’s type 1 diabetes where

your immune system attacks that cell

you’re reading the fine print there you

notice this guy is on immunosuppressive

therapy the next step and this is what

people are working on how do you

encapsulate those cells or gene edit

those cells so that they are invisible

to the immune system or can protect

themselves from the immune system if

some of you were here for uh

john’s conversation with pardesa betty

earlier from the broad in harvard here’s

a paper that she and amy wagers from

harvard led a multi-disciplinary team

working on namely what’s the next stage

in gene therapy many of you have heard

over the last couple of years about car

t therapy for cancer that’s basically

you take cells

the t cells out of the body engineer

them put them back into the body so it’s

essentially gene editing cells for uh

for blood blood-borne cancers there’s

also work where you can um where people

are shown that you can gene correct

blood stem cells such as in sickle cell

anemia that’s in the clinic today

and there have been gene correction

therapies for certain genetic eye

diseases where the local delivery of the

of that gene is is important but the

boss have been cases where patients have

had gene therapy and have had toxic

results because the gene products

accumulate in the liver and have

negative

side effects and

some quite serious

what these labs did together was

essentially create

miniature versions of the gene delivery

vehicle these aav capsids

and could modify them to preferentially

home to a tissue of interest in this

case they’re going after genetic muscle

diseases and they prove the point with

functional recovery in a mouse model

duchenne

muscular dystrophy as well as a very

rare genetic

muscle disease so this is the next wave

of gene therapy is not

gene’s sort of injunctive very

specifically but how do you get it to a

broader system without having the toxic

side effects and to enable potentially

redosing

more broadly

stem cells have opened a whole new

window you heard again david sinclair

talk about aging i won’t talk about

sirtuins here it was clear to me very

painfully a couple of weeks ago when i

ran a half marathon and i ran a lot

slower and it took me longer to recover

than the 20 and 30 year olds

one of the things uh that particulars

research coming in both out of stanford

and harvard has looked a lot at

understanding the differences between

young and old mice and how they repair

or don’t repair over time

one of the avenues that they use to look

at it was what they call parabiotic

mouse models so this image on the left

shows you an old and a young mouse

joined in a way so that they share a

circulatory system and the point of this

is to understand what is it in the blood

if there are if there are factors in the

blood

that enable the old mouse to repair in a

way that they are not because what

they’ve proven if you look on the left

the positive effects on the older mouse

show up in the heart in the brain the

bone and muscle and in different tissue

systems in different ways the converse

is also true where the blood from the

old mouse is negatively affecting the

young mouse the idea is not to give you

know

blood transfers from young people to old

people but what the idea this model has

been used to look at what are the

individual factors and see if we can

tease out from this what is it that’s

driving that repair that regeneration

process and how do we lose that over

time so for example there was a startup

company that spun out of harvard several

years ago called alevian

that

identified a circulating protein in the

animal that is also human protein and

they’re now working their way toward

toward a clinical trial comparably on

the right there’s a recent article

showing the benefits of exercise which

we all know

not only in terms of you know heart

muscle etc but even on indirect effects

such as cognitive function which has

been well documented what this study

showed is that they looked again at

different factors and showed that a

hormone that had been discovered a

decade ago also in a lab in the harvard

system

that is released by the muscles during

exercise if they

created a small peptide version of that

a small protein version of that hormone

they could deliver it systemically they

could replicate the effect of exercise

and they tested that not only in terms

of general effects but also on a an

alzheimer’s mouse model now humans and

mice are very different but the concept

um holds true and so this is leading us

not only to think about conditions like

aging but also leading us to think about

systemic approaches to disease so rather

than thinking about alzheimer’s or

thinking about cardiac can we look at

interventions that have partic

potentially system-wide effects in the

alzheimer’s example maybe untangle us if

you will from the plaques and tangles

debate that sort of wrap treatments of

that disease up in a bit of a quandary

so far

this is all possible because there have

been

major scientific advantages in the last

decade namely uh

yamanaka’s discovery of how to reprogram

cells so can you turn the sands of time

back on individual cells he showed that

you could take an adult cell adult

meaning a mature in this case skin cell

or blood cell and with only four factors

turn that cell back to an embryonic-like

state what they call induced pluripotent

stem cells

then what people can do like the melton

lab spend a lot of time figuring out the

recipe the cookbook for turning that

cell into the cell that’s either impact

you know of interest to the organ or

disease of interest in other words the

forward programming of that into like a

neuron muscle cell uh blood cell

whatever and then you can use that again

either for in vitro experiments under

same disease mechanism or potentially

for cell therapy for example as you know

bayer pharmaceuticals is now

engaged in a parkinson’s clinical study

where they’re making dopaminergic

neurons from ips cells you combine that

with

the

work that jennifer doudna and emmanuel

charpentier received the nobel prize for

in 2020 on crispr and gene editing and

the increasing ability to edit genes

um either

ex vivo

in vitro or ultimately in vivo

combine that with stem cell technology

and open a whole new window for for

curative therapy i mentioned the sickle

cell example before and that’s exactly a

combination of these two technologies

this just shows an optically stimulated

and recorded stimulation of a motor

neuron so what we now have is ability

not only make individual cells in a dish

but the ability to analyze them and

because we can make them we’re using

that reprogramming technology from

people with different genetic

backgrounds we can understand for

example how what the electrical firing

pattern of a motor neuron from a healthy

person is versus say someone with als

that then can be scaled up it’s we used

to think of als as a one disease

category but now we’re realizing there

are actually many different genetic

backgrounds in als there’s actually

another company spun out of the harvard

ecosystem that is specifically doing

that and what they’re doing is not to

replace a motor neurons but to say look

for drugs use this as an in vitro model

in petri dish to look for drugs that can

restore a normal firing pattern and

restore health to those neurons and

hopefully make them live longer and

realize that patients with different

diseases

can treat differently now many of you

said but many diseases aren’t single

cell diseases that they’re

multiple cellular and you’re right cells

do live in 3d environments so the topic

of organoids was mentioned briefly

before

we now can create brain organoids kidney

organoids tumor organoids etc in vitro

to understand how they behave look for

interactions we can combine them with

materials and electronics as you see on

the upper right is a joint project

between someone at the engineering

school and a cardiac developmental

biologist saying how do i integrate nano

electronics into a cardiac organoid in

order to mature heart cells potentially

use them for for cell therapy purposes

and then people have incorporated them

into chips so that what you can do is

then for example in the lung chip we’re

coming out of the vesa institute

at harvest shown how you can take lung

cells put them in a chip flow air and

blood through them and in the covet

example introduce a virus and say how

does a virus impact the lung tissue in

in a living environment again it’s not

the same as a whole body but we now can

study these things with human cells of

interest a human the relevant human

cells that are affected in a

particular disease that’s an ability we

didn’t have a decade ago how do we

repair complex organs that don’t have a

stem cell that can’t repair themselves

the ancient greeks i don’t know if they

knew about stem cells but the myth of

prometheus exists because the liver

repairs itself right

half the liver won’t grow back every

single night that’s asking a little too

much of it um and you don’t want an

eagle cruising around your innards

anyway

however in diseases like the kidney we

found there are no stem cells in the

kidney there was a big argument about

whether there are

but it has a very complex architecture

the bioprinting technologies today are

not going to solve that which means that

hemodialysis as a disease looks today

exactly like it did 70 years ago the bed

frame has changed and the tubing is

probably a little better plastic but the

guy actually looks pretty much the same

it’s an expensive proposition and

transplants don’t save this problem

because in the us only one out of five

people in transplant list gets gets a

transplant so there’s another startup

out of the harvard ecosystem coming out

of mgh aviva medical that’s trying to

work on how do you create a biological

replica of the kidney without

replicating the complexity of the

architecture but taking biologic

material putting cells in the relevant

cells in the relevant channels and

essentially creating a biologic device

that can provide enough kidney function

to get people off of

dialysis and off of transplants

and our purpose in life at hsci was not

to start companies but the science has

accelerated so over the last decade

there have been some 40 companies

started by hsci scientists and more are

happening

some of them you’ve actually heard about

such as moderna i daresay is on some of

your lists

but these are in a range from

drug screening to cell therapy to gene

therapy to mrna a whole range of

technologies but all aimed at this

regeneration and repair one of the

reasons we can do this is because we can

draw on resources like the wet lab

incubator on the business school campus

we live in a town surrounded by other

life science incubators and those

incubators live in an environment

surrounded not only by the venture

capitalists who are deep in life

sciences but by the biotech companies

and by big pharma a decade ago novartis

was the only large pharma had r d here

now essentially all the large pharma

companies have r d either headquarters

or major offices so boston right now in

the particular last decade has really

become the center of gravity in uh in

life sciences but it’s not all about

science so i’ll leave you with this one

cautionary note that stephen johnson

pointed out in his book that he wrote

about major medical interventions and

what’s taken them to succeed as we live

longer and healthier lives and that is

around the social and political and

economic

policies that have to be in place one of

the examples in his book is louis

pasteur it took 50 years from his

discovery of pasteurization to actually

pasteurize milk being on the shelf

that’s not a science problem that’s a

social problem

similarly in walter isaacson’s book

about crispr they centered around

jennifer doudna’s story and crisper cast

9 has now turned into crispr 13 and 14

and crisper phi and g prime editing and

base editing etc so they’ve been huge

advances since but

they won’t be socially useful clinically

use until we can agree on what as we

again increase the capability even

even better and better gene editing

until we agree on what’s a right thing

to do and what’s wrong where are the

lines to draw on gene on what we should

be doing with the technology

that came to the fore a couple years ago

with that case in china where a guy did

in vivo gene editing but that technology

will be driving us down the path and we

need to think programmatically about

what are the right applications of it

and related to that is also what will

health care systems reimburse and how do

we pay for that

because if we can have these gene

correction therapies out there and solve

these problems at scale we also have to

have a way to pay for them in a health

care system that isn’t designed for it

today so i’ll leave you with that

thought because that is a collective

problem it’s not just a science problem

cool things are happening on the science

more is to be done thank you very much

[Applause]

我在 15 多年前加入了干细胞研究所

,我离开营利性部门后不仅能将薪水减半,还能

与像 doug Melton 和 david skadden 这样的人一起工作,

他们是干细胞研究所的两位科学

主管 成立

这个新企业的研究所和它是一个

跨越哈佛的虚拟研究中心

哈佛学院和

哈佛附属医院 哈佛

不仅在这个东海岸系统而且在全世界都有独特的足迹,

并拥有

八家附属医院 有了它,

所以这里的想法是建立这个我

称之为虚拟研究中心

,在那里我们可以有一种新的研发方式,

我们不需要拥有资产,但

我们可以让一些世界

领先的专家和许多疾病一起

工作

这些不同的组织和

部门以及实验室和

学科从板凳侧标一直到

治疗患者,在世界其他地方

你可以做到这一点,所以这是最重要

的之一 e 呼吁

与领先专家合作的新商业模式,

正如约翰所暗示的那样,有能力

真正认真对待其中一些

疾病和状况,这些疾病和状况

不仅影响到

你之前从大卫·辛克莱那里听到的一些老龄化问题,

而且还影响到各种状况 比如糖尿病,道

格·梅尔顿治疗脊髓损伤

,我的兄弟患有

帕金森病,我的

岳父

和我们都有这些故事,

到目前为止,我们还没有很好的治疗方法,

所以我们做什么 该中心已经发展

到现在在不同机构拥有 380 多名教职员工,

重点是跨学科内部

组织实验室间合作,

致力于新的细胞和基因疗法 这

是你们大多数人在

考虑干细胞科学时所

想的 我们是否修复破损的细胞,即您

知道帕金森氏症中的多巴胺能神经元,

糖尿病中的眼睑细胞等,所以

这就是我如何更换 破碎部分

理论或修复

有缺陷的基因,我们现在可以更容易地做到这一点,这

要归功于像

crispr um和其他其他基因编辑

工具这样的先进工具,但也有

其他机制,因此干细胞科学

也将我们带入了一种全新的方式

思考我们如何利用

内源性修复能力,

换句话说,我们如何刺激身体的

内部修复能力,

使其要么因年龄而丧失,要么

因事故或疾病而丧失,所以这

是第二点,第三点是

因为现在 我们已经开发了这些工具

,稍后我会讨论这个问题

,如果你想在一个培养皿中

研究运动神经元、心脏细胞、肌肉

细胞或脂肪,我们可以创建感兴趣的人类细胞,我们现在有

我们可以在二维和三维系统中创建这些细胞的工具,

帮助了解疾病机制并

严重改变经济学和

药物发现的方法,

我们将讨论为什么 所以我们现在按疾病组织,

这在学术环境中是独一无二的,

因为大多数人都

在关注技术问题,但我们希望

人们关注技术问题,但

旨在对疾病产生影响

我们想要基础研究,但我们

不想 以目标为导向,我们还

特意设置了这样的设置,以便我们可以

跨疾病类别进行讨论,

例如,研究

糖尿病中的自身免疫问题的人,其中

曾经和 1 型糖尿病是

您的免疫系统攻击您自己的 β

细胞的地方,他们可以从中学到什么

癌症计划,其中肿瘤细胞

非常擅长避免免疫

系统,这是整个问题,所以

它们如何交叉授粉

我们如何也

了解跨越

疾病和器官

甚至时间的过程,例如纤维化或衰老,所以

想想纤维化是否 它

在心脏 肾脏 肺

骨骼肌 是身体

无法修复的一种方式

我们应该做的事情是因为 我们是

研究

从分子细胞水平到

不同器官系统的相互作用的人,比较笔记,

这样我们就可以看到什么是共同的

途径,什么是共同的行为,

它们在哪里不同,所以我们怎么能让

你知道什么 我们学习肺纤维化

并将其应用于肝纤维化,

反之亦然,对于

那些听过大卫辛克莱的人来说,

老化基本上是一个过程,如果胎儿有皮肤伤口,

随着时间的推移,我们会随着时间的推移

在子宫内失去修复和再生的能力

可以治愈你

知道是否有

宫内手术它可以无

疤痕治愈我们

和婴儿你知道让

指尖长回来吗儿童可以长出

指尖随着时间的推移我们会失去这种能力

即使是某些身体部位,

如血皮毛发,

每一次都能自我修复 生命中的几天,

随着时间的推移,自己的自我修复越来越差,

为什么这是真的?我们能学到什么

关于早期修复能力

并将其应用于后期阶段的能力 生活

让我

从 15 年前快进到今天,或者实际上是

几周前,顶点制药

公司宣布了第一个

患者在干细胞

衍生的 β 细胞移植试验中的结果,所以这

是他们收购

半治疗药物后的工作 几年前

,它本身是在五年前

从道

格·梅尔顿的实验室出来的,我们

之前在谈论过,所以

在学术实验室里花了十多年的时间才弄清楚

如何转化胚胎干细胞 或者或多

能干细胞在体外转化为成熟的β

细胞,

创业公司然后进一步

完善这个过程,然后顶点

将它带入临床,

但他们能够在这个病人身上做些什么

,这是一个脆弱的糖尿病患者

患有 1 型糖尿病

,使用胰岛素 40 年,

每年住院几次,

因为他们称之为脆性糖尿病,

因为他的身体

会 崩溃,在

计划剂量的一半的 90 天内,他

基本上没有使用胰岛素,这

要记住,这是一种多基因疾病,

有多种基因会影响

疾病,它是环境的

,有很多原因,许多不同的

表现,但如果它来了

崩溃在一种细胞类型上,因此基因

疗法无法修复,但如果

可以的话,这至少在

概念上显示,如果你能修复有

问题的细胞,你就有

可能治愈这种疾病,

现在你们中的许多人是

说得好,那是 1 型糖尿病,

你的免疫系统攻击那个细胞

你正在阅读细则,你

注意到这个人下一步正在接受免疫抑制

治疗,这就是

人们正在研究的如何

封装这些细胞或基因 编辑

这些细胞,使它们

对免疫系统不可见,或者

如果

你们中的一些人来这里是为了 uh

john 与 pardesa betty 的谈话,它们可以保护自己免受免疫系统的伤害

早些时候,来自哈佛的

一篇论文,她和

哈佛的艾米赌注领导了一个多学科团队,

研究基因治疗的下一个阶段

是什么,你们中的许多人

在过去几年里听说过

关于癌症的汽车疗法 基本上

你把

细胞从身体里取出来,

然后把它们放回身体里

干细胞,例如

当今临床上的镰状细胞性贫血,

并且已经

对某些遗传性眼病进行了基因校正疗法,

其中

该基因的局部传递很重要,但是

老板已经有患者接受

过基因治疗的案例,并且 有毒性

结果,因为基因产物

在肝脏中积聚并有

负面

副作用,而且

这些实验室一起做的一些相当严重的事情是

必不可少的 可以创建

这些 aav 衣壳的基因传递载体的微型版本,

并可以将它们修改为优先

归巢到感兴趣的组织,在这种

情况下,它们正在治疗遗传性肌肉

疾病,并且它们

通过小鼠模型

杜氏

肌营养不良症的功能恢复证明了这一点 以及一种非常

罕见的遗传性

肌肉疾病,所以这是

下一波基因治疗不是

非常具体的基因禁令,

而是如何在

不产生毒副作用的情况下将其应用于更广泛的系统

并实现

更广泛的潜在再

治疗 细胞打开了一个全新的

窗口你又听到了大卫辛克莱

谈论衰老我不会

在这里谈论sirtuins几周前我很

痛苦地很清楚当我

跑半程马拉松时我跑得慢了很多

比 20 岁和 30 岁的

人恢复得更久 嗯,

斯坦福大学

和哈佛大学的细节研究都在看很多

东西 研究

年轻和年老小鼠之间的差异以及它们如何

随着时间的推移修复或不修复

他们用来观察它的途径之一

是他们所谓的联体

小鼠模型所以左边的这张图片

显示了一个老的和一个年轻的 老鼠

以某种方式加入,以便它们共享一个

循环系统,关键

是要了解血液中是否存在血液

中是否存在

使老老鼠能够以某种

方式进行修复的因素 因为

他们已经证明,如果你看左边

的话,对年长老鼠的积极影响

会出现在大脑的心脏、

骨骼和肌肉以及不同的组织

系统中,以不同的方式出现在旧老鼠

的血液中,反之亦然。

老鼠对年轻老鼠有负面影响

这个想法不是让你

知道

血液从年轻人到老年人的转移,

而是这个模型的想法

是什么,看看

个体因素是什么,看看我们是否可以从中

梳理出 是什么

推动了再生

过程的修复以及随着时间的推移我们如何失去它

,例如,几年前有一家初创

公司从哈佛剥离出来,

名为 alevian

,它

确定了

动物体内的一种循环蛋白质,它也是人类蛋白质

他们现在正

朝着临床试验

的方向努力

有充分的证据

表明,这项研究表明,他们再次研究了

不同的因素,并表明

十年前在哈佛系统的实验室

中也发现了一种激素,如果肌肉产生一种小肽,它会在运动期间由肌肉释放

这种激素的一种小蛋白质版本

他们可以系统地传递它 他们

可以复制运动的效果

他们测试了不仅

在一般效果方面,而且在

阿尔茨海默氏症小鼠模型上,现在人类和

小鼠非常不同,但这个

概念是正确的,所以这

不仅让我们考虑像衰老这样的条件,

而且让我们 考虑

疾病的系统性方法,而

不是考虑阿尔茨海默氏症或

考虑心脏疾病,我们可以看看

在阿尔茨海默氏症的例子中具有特定潜在系统范围影响的干预措施,

如果

你愿意从斑块和缠结

辩论那种包裹治疗中解开我们可能会解开我们 到目前为止,

这种疾病处于困境中

这一切都是可能的,因为

在过去的十年中,有重大的科学优势,

即呃山中

发现了如何重新编程

细胞,所以你能

在他展示的单个细胞上扭转时间的流沙吗?

您可以采用成人细胞成人,

在这种情况下意味着成熟的皮肤细胞

或血细胞,并且只有四个因素

使该细胞变为 回到胚胎样

状态,他们称之为诱导多

能干细胞,

然后人们可以像 Melton 实验室那样做的事情

花费大量时间找出

细胞转化为

细胞的食谱食谱 器官或

感兴趣的疾病,换句话说,将其

向前编程为

神经元肌肉细胞,呃血细胞

,然后您可以再次将

其用于相同疾病机制下的体外实验

或可能

用于细胞治疗,例如您所知道的

拜耳 制药公司现在

正在进行一项帕金森氏症的临床研究

,他们正在

从 ips 细胞中制造多巴胺能神经元

嗯,无论是

在体外体外还是最终在体内,都

将其与干细胞技术相结合

,打开一个全新的窗口 对于

治疗性疗法,我之前提到过镰状

细胞的例子,这正是

这两种技术的结合,

这只是显示了运动神经元的光学刺激

和记录刺激,

所以我们现在拥有的

不仅是在培养皿中制造单个细胞

的能力,而且还有能力 分析它们,

因为我们可以制造它们,所以我们正在使用

来自

具有不同遗传

背景的人的重新编程技术,例如,我们可以理解

来自健康人的运动神经元的电发射模式

是什么,而不是说有 als 的人

可以 扩大规模,我们

过去认为 als 是一种疾病

类别,但现在我们意识到,als

实际上有许多不同的遗传

背景,实际上

还有另一家公司从哈佛

生态系统中分离出来专门做

这件事,他们是什么 做的不是

替换一个运动神经元,而是说

寻找药物,用这个作为体外模型

在培养皿中寻找 可以

恢复正常放电模式并

恢复这些神经元健康的药物,并

有望延长它们的寿命,并

意识到患有不同

疾病的患者

现在可以采用不同的治疗方法,

但许多疾病不是单

细胞疾病,它们是

多细胞疾病 你说

的对 你在右上角看到

的是工程

学院的某个人和心脏发育

生物学家之间的一个联合项目,说我如何将纳米

电子学整合到心脏类器官中,

以使心脏细胞成熟,可能

将它们用于细胞治疗目的

,然后人们就有了 将它们

整合到芯片中,这样你可以做的

就是例如在肺芯片中

在收获时从 vesa 研究所出来,展示了如何将肺

细胞放入芯片中,让空气和

血液流过它们,在令人垂涎的

例子中引入病毒,并说明病毒如何

再次影响生活环境中的肺组织

它与整个身体不同,但我们现在可以

用感兴趣的人类细胞研究这些东西 人类

受特定疾病影响的相关人类细胞 这是

十年前我们没有的能力 我们如何

修复复杂的器官 没有

干细胞无法自我修复

的古希腊人,我不知道他们是否

知道干细胞,但

普罗米修斯的神话存在,因为肝脏可以

自我修复

一半肝脏不会重新长

出来 那个晚上要求的有点

太多了 嗯,你不希望

老鹰在你的内脏周围

游弋,

但是在像肾脏这样的疾病中,我们

发现肾脏中没有干细胞,

关于

是否 这里有,

但它的架构非常复杂

,今天的生物打印技术

无法解决这个问题,这意味着

今天的血液透析作为一种

疾病看起来与 70 年前

完全一样 这

家伙实际上看起来几乎一样,

这是一个昂贵的提议,

移植并不能解决这个问题,

因为在美国

,移植名单中只有五分之一的人得到了

移植,所以哈佛生态系统中的另一家初创公司

来自 mgh aviva Medical 正在尝试

研究如何

在不

复制结构的复杂性的情况下创建肾脏的生物复制品,

而是采用生物

材料将细胞放入相关通道中的相关

细胞中,并从

本质上创建

一种能够提供足够肾脏功能的生物装置

让人们摆脱

透析和移植

,我们在 hsci 的生活目标

不是 苦涩的公司,但科学已经

加速,因此在过去十年中

,有大约 40 家

公司由 hsci 科学家创办,并且正在发生更多的公司

,其中一些你实际上听说过,

比如我敢说 Moderna 在

你的一些名单上,

但这些在 从

药物筛选到细胞疗法到基因

疗法再到 mrna 一系列

技术,但都针对这种

再生和修复

我们可以这样做的原因之一是因为我们可以

利用商学院的湿实验室

孵化器等资源 校园

我们生活在一个被其他生命科学孵化器包围的小镇中,

而这些

孵化器生活在这样一个环境中

现在基本上所有的大型制药

公司都在这里进行了研发,无论是总部

还是主要办事处,所以波士顿现在

在过去十年中已经 真的

成为

生命科学领域的重心,但这不仅仅是关于

科学的,所以我会给你留下一个

警告,斯蒂芬约翰逊

在他的书中指出,他写了

关于重大医疗干预的文章,以及

他们成功的原因 我们的

生活更长寿、更健康,那就是必须实施

的社会、政治和

经济

政策

他书中的一个例子是路易斯·

巴斯德,从他

发现巴氏杀菌到真正

对牛奶进行巴氏杀菌已经上架了 50 年

这不是科学问题,而是

社会问题,

在沃尔特·艾萨克森 (walter isaacson) 的关于crispr 的书中

,他们以

詹妮弗·杜德娜 (jennifer doudna) 的故事为中心,Crisper cast

9 现在变成了crispr 13 和 14,

以及crisper phi 和 g prime editing 和

base editing 等,所以他们一直

自那以后取得了巨大的进步,但

它们不会在临床上对社会有用,

除非我们能就什么达成一致,因为我们

再次将能力提高

得更好, 更好的基因编辑,

直到我们就什么是正确的事情和什么是错误的事情达成一致为止,在

哪里可以利用基因来判断我们

应该如何利用

几年前

在中国出现的那个案例中出现的技术,其中一个人 进行

了体内基因编辑,但该技术

将推动我们走上这条道路,我们

需要以编程方式

思考它的正确应用

以及与之相关的

医疗保健系统将报销什么以及

我们如何为此付费,

因为如果 我们可以有这些基因

校正疗法并

大规模解决这些问题我们还必须

有一种方法在今天

不是为它设计的医疗保健系统中支付它们

所以我会让你有这个

想法因为那 是一个集体

问题 它不仅仅是一个科学问题

很酷的事情正在科学上发生

更多的事情要做 非常感谢你们

[掌声]