相关实验视频
Updated: Jun 28, 2025

05:39
Spontaneous Murine Model of Anaplastic Thyroid Cancer
Published on: February 3, 2023
1.6K
无塑性和差异化甲状腺癌:从差异化甲状腺癌的高度转变的遗传证据
Haiyan Gu1, Jingnan Wang2, Wenwen Ran1
1Department of Pathology, The Affiliated Hospital of Qingdao University, Qingdao, PR China.
The journal of pathology. Clinical research
|April 11, 2024
概括
无塑性和差异化甲状腺癌 (ATC/PDTC) 与差异化甲状腺癌 (DTC) 有共同的遗传联系,这表明它们起源于DTC. 积极的DTC亚型经常存在TERT促进子突变.
科学领域:
- 在瘤学瘤学.
- 遗传学 是一个遗传学.
- 病理学 病理学 病理学
背景情况:
- 无塑性甲状腺癌 (ATC) 和差异化甲状腺癌 (PDTC) 代表了先进的,侵略性的甲状腺癌.
- ATC,PDTC和共存的分化甲状腺癌 (DTC) 之间的遗传关系仍未得到充分研究.
- 了解这些关系对于推进甲状腺癌诊断和治疗至关重要.
研究的目的:
- 研究ATC和PDTC的临床病理特征和遗传特征.
- 探索晚期甲状腺癌 (ATC/PDTC) 和它们的差异化对应物 (DTC) 之间的遗传关系.
- 确定侵袭性甲状腺癌的起源和潜在的前体损伤.
主要方法:
- 分析了57个ATC和PDTC样本,其中33个具有并发DTC组件或历史.
- 对于BRAF V600E,p53和PD-L1表达的免疫组织化学.
- 对TERT促进体和RAS突变进行桑格测序.
- 在ALK和RET重组中进行光现场杂交 (FISH).
主要成果:
- 在ATC和PDTC的同时存在的DTC组件中,它们表现出类似的基因变异.
- 激进的DTC亚型经常存在TERT促进子突变.
- 与DTC相比,ATC的p53和PD-L1表达显著更高,PAX-8和TTF-1表达更低.
结论:
- ATC和PDTC可能源于差异化甲状腺癌 (DTC).
- 共享的遗传特征支持一个共同的发育路径.
- 在ATC中不同的分子标记突出显示了潜在的治疗点.
相关概念视频
Tumor Progression
6.3K
Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
6.3K
Cancers Originate from Somatic Mutations in a Single Cell
11.9K
Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
11.9K
Cancer-Critical Genes I: Proto-oncogenes
8.8K
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
8.8K
Metastasis
5.5K
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
5.5K
Mutagenicity and Carcinogenicity
1.3K
Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
1.3K
Adaptive Mechanisms in Cancer Cells
5.7K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.7K

