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全部话题 - 话题: bcl6
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c*2
发帖数: 24
1
来自主题: Biology版 - BCL6 leukemia study appeared in Nature
Just a follow-up on this. In case some of you are interested. I emailed the
author and here is his response.
==
Thanks for your interest and your question. We made the same observation as
you did. Trp53 is represented by multiple probe sets (1438808_at, 1438542_at
, 1459780_at, 1457623_x_at, 1427739_a_at, 1426538_a_at) and only one of them
shows indeed upregulation in Imatinib-treated BCL6-/- leukemia cells (i.e.
the one you can see in Figure S6). Figure S6 shows examples of microarray
probe set... 阅读全帖
c*2
发帖数: 24
2
来自主题: Biology版 - BCL6 leukemia study appeared in Nature
I have been struggling in understanding the results of the supplementary
figure 6 [ http://www.nature.com/nature/journal/v473/n7347/extref/nature09883-s1.pdf ]. The Bcl6 -/- strains was shown to have higher expression of Bcl6 than in the wild type. How could this happen? I kind of think it should be the opposite.
Any clues?
c*2
发帖数: 24
3
来自主题: Biology版 - BCL6 leukemia study appeared in Nature
Hi oranger,
Thanks for the explanation. It is helpful.
I actually downloaded and checked the expression data. Actually there are
two probe sets targeting the Bcl6, one of which as expected has low
expressoin of bcl6 in the mutant strain compared to the wild type.
Interestingly I also noticed that the Trp53 gene has the opposite gene
expression levels as shown in that figure too. It is really confusing.
Thanks.
o*****r
发帖数: 156
4
来自主题: Biology版 - BCL6 leukemia study appeared in Nature
someone has mentioned before that in KO, not the whole gene was completely
deleted.
In most cases, just an exon. So depends on which part of the gene been
probed in microarray,
you might see higher level profile because cells tend to increase the gene
expression level trying to
compromise the KO defect, though not effective.

strains was shown to have higher expression of Bcl6 than in the wild type.
How could this happen? I kind of
think it should be the opposite.
z******o
发帖数: 78
5
前三次化疗用了D美罗华:600mg d1,CTX 1.3g d2,里葆多 40mg d2,长春地辛 5mg
d2,地塞米松 15mg d2-d6,同时予以碱化、水化、止吐、利尿、保护脏器等功能。
治疗效果是PET-CT: 1.口咽部右侧软组织影,胃内异常软组织影,均伴葡萄糖代谢稍增
高。2.肝囊肿,右肾囊肿。FISH(03-21):C-Myc/IgH(-),CCND1/IgH(-),BCL2/IgH(-),
API2/MALT(-),BCL6(-)。骨穿提示:淋巴瘤本次髓象大致缓解。FISH(03-21):C-Myc
/IgH(-),CCND1/IgH(-),BCL2/IgH(-),API2/MALT(-),BCL6(-)。白细胞计数:4.6*
10E9/L,中性粒细胞计数:4.21*10E9/L,血红蛋白:109g/L,血小板计数:132*10E9/L。
最近两次化疗计量增大了,我再问一下我爸要具体的报告。
请问为什么自体干细胞移植不能叫做手术呢?
非常感谢!!!
d******u
发帖数: 178
6
来自主题: Biology版 - 牛人来看看这个图
即使只是truncate部分exon,KO一般会导致mRNA表达不稳定,如果有truncated
protein表达的话,KO是不成功的。
上面情况最可能的解释是:那个probe also detects other Bcl6 family members。查
一查那个probe的序列,然后看看Bcl6 family的同源性。
k*****8
发帖数: 53
7
我在这里代国内的朋友发贴咨询,请各位帮忙。非常感谢!!
一个朋友诊断得了惰性b淋巴细胞侵犯骨髓.治疗无效. 听说美国有药中国还没有开展临
床.想打听下 GA101 和 Bendamustine 这2种药是否能治疗有效.和美国那边有啥办法么
? 另外听说美国和香港有种放射性药物叫Zevalin能否适合使用.
年龄57岁, 红细胞贫血在80g, 骨髓淋巴细胞比率是80% 化疗R+chop 4个疗程,没有明显
效果.医生建议我们观察,说治疗无效.诊断是CD20+ PAX5+ CD3- CD10- BCL6-
MuM1- CD23- CD5- CyclinD1- TdT- ki67 <25% 符合边缘B细胞淋巴瘤侵犯骨髓.
全身没有肿大淋巴结.病变只发生在骨髓. 想咨询下美国医生. 这个病怎么治疗提高生
存期.谢谢啦.
r*********d
发帖数: 42
8
谢谢。
本来以为如果只是Diffuse B lymphoma用R-CHOP方案还能有一些机会。
但后来又是一系列的检查,最后FISH检测结果发现了MYC,BCL2,BCL6同时呈阳性,国内
叫“三打击”,即Triple Hit Lymphoma(THL),非常少见,恶性程度很高,预后也极
其不乐观。
主治医生说干了这么多年,只记得见过三个案列,其中一个检查完就没再来了;另一个
娭毑化疗了一次也再没来了。
月初我爸低剂量CHOP化疗了一次,有些效果,也有些改善。但最近一周又开始恶化,正
在等下周一开始做第二次化疗。。。似乎也只能听天由命了。
i*********0
发帖数: 915
9
来自主题: Biology版 - 牛人来看看这个图
请看看那个bcl6 gene那一行.
为什么ko以后,表达在mRNA水平上会upregulate.
o*****r
发帖数: 156
10
来自主题: Biology版 - BCL6 leukemia study appeared in Nature
I don't know about that.
You could always email the authors for clarification.
s*********y
发帖数: 579
11
好奇。Th17和BCL6/Tfh都是很轰动的发现。和其他实验室同时发现的。
k*****8
发帖数: 53
12
来自主题: Medicalpractice版 - 代人咨询: 惰性b淋巴细胞侵犯骨髓
我在这里代国内的朋友发贴咨询,请各位帮忙。非常感谢!!
一个朋友诊断得了惰性b淋巴细胞侵犯骨髓.治疗无效. 听说美国有药中国还没有开展临
床.想打听下 GA101 和 Bendamustine 这2种药是否能治疗有效.和美国那边有啥办法么
? 另外听说美国和香港有种放射性药物叫Zevalin能否适合使用.
年龄57岁, 红细胞贫血在80g, 骨髓淋巴细胞比率是80% 化疗R+chop 4个疗程,没有明显
效果.医生建议我们观察,说治疗无效.诊断是CD20+ PAX5+ CD3- CD10- BCL6-
MuM1- CD23- CD5- CyclinD1- TdT- ki67 <25% 符合边缘B细胞淋巴瘤侵犯骨髓.
全身没有肿大淋巴结.病变只发生在骨髓. 想咨询下美国医生. 这个病怎么治疗提高生
存期.谢谢啦.
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