ATCC Announces First Isogenic Cell Line Produced by the CRISPR/Cas9 Technology

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ATCC Announces First Isogenic Cell Line Produced by the CRISPR/Cas9 Technology

January 28, 2016 by sjwilliamspa

ATCC Announces First Isogenic Cell Line Produced by the CRISPR/Cas9 Technology

Reporter: Stephen J. Williams, PhD.

EML4-ALK Isogenic Cells — New!

ATCC is proud to announce its first product developed using CRISPR/Cas9 technology, the EML4-ALK Fusion-A549 Isogenic Cell Line Human (ATCC^® CCL-185IG™). This cell line was derived from the parental A549 (ATCC^® CCL-185™) non-small cell lung cancer cell line. EML4-ALK Fusion-A549 Isogenic Cell Line has been intensively validated on the genome, transcript, and protein level, and is otherwise identical to the parental line. This isogenic cell line is more sensitive to ALK inhibitor crizotinib when compared to A549, and serves as a vital model to study cell signaling pathways in cancer as well as in drug screening when used side-by-side with A549 cells.

Further your lung cancer research with the EML4-ALK Fusion-A549 Isogenic Cell Line Human ATCC^® CCL-185IG™ derived from A549 ATCC ^® CCL-185™ today!

Lung Cancer

Lung cancers are classified by type: small cell lung carcinoma (SCLC) and non-small cell lung carcinoma (NSCLC). SCLCs are associated with smoking and metastasize very early. By contrast, non-smokers usually present with NSCLC, which are further subdivided into squamous cell carcinomas, adenocarcinomas, and large cell carcinomas. Since both SCLC and NSCLC are usually diagnosed after the disease has spread beyond the primary site, the overall survival rates for lung cancers are poor. To breathe new life into your lung cancer research, ATCC provides numerous lung cancer cell lines, a new gene-edited isogenic NSCLC cell line, human primary cells, and h-TERT-immortalized cell lines. And to increase the throughput of your lung cancer experiments, ATCC has lung cancer cell lines organized into tumor cell panels.

Find out more about ATCC Lung Cancer Resources.

Physiologically Relevant Controls

All experiments should include physiologically relevant controls. ATCC provides both primary and hTERT-immortalized bronchial epithelial cells and small airway cells that may be used side-by-side with NSCLC or SCLC cells as normal controls. The primary and hTERT-immortalized cells may also be used to create 3D cell culture models to better represent an in vivo environment, ex vivo.

Browse the ATCC Primary Cells and hTERT Immortalized Cells to find physiological models relevant for your research needs.

Add new dimension to your research, read our application note Human Bronchial/Tracheal Epithelial Cells: Improving Functional Studies to find out how primary bronchial epithelial cells differentiate into mature airway tissue using a 3-D Air-Liquid Culture Interface model.

Posted in Cancer - General, Cancer and Current Therapeutics, CANCER BIOLOGY & Innovations in Cancer Therapy | Tagged ATCC, CRISPR-Cas9, Lung cancer | 2 Comments

2 Responses

on January 30, 2016 at 7:18 PM | Reply 2012pharmaceutical

This is very insightful. There is no doubt that there is the bias you refer to. 42 years ago, when I was postdocing in biochemistry/enzymology before completing my residency in pathology, I knew that there were very influential mambers of the faculty, who also had large programs, and attracted exceptional students. My mentor, it was said (although he was a great writer), could draft a project on toilet paper and call the NIH. It can’t be true, but it was a time in our history preceding a great explosion. It is bizarre for me to read now about eNOS and iNOS, and about CaMKII-á, â, ã, ä – isoenzymes. They were overlooked during the search for the genome, so intermediary metabolism took a back seat. But the work on protein conformation, and on the mechanism of action of enzymes and ligand and coenzyme was just out there, and became more important with the research on signaling pathways. The work on the mechanism of pyridine nucleotide isoenzymes preceded the work by Burton Sobel on the MB isoenzyme in heart. The Vietnam War cut into the funding, and it has actually declined linearly since.

A few years later, I was an Associate Professor at a new Medical School and I submitted a proposal that was reviewed by the Chairman of Pharmacology, who was a former Director of NSF. He thought it was good enough. I was a pathologist and it went to a Biochemistry Review Committee. It was approved, but not funded. The verdict was that I would not be able to carry out the studies needed, and they would have approached it differently. A thousand young investigators are out there now with similar letters. I was told that the Department Chairmen have to build up their faculty. It’s harder now than then. So I filed for and received 3 patents based on my work at the suggestion of my brother-in-law. When I took it to Boehringer-Mannheim, they were actually clueless.

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on January 30, 2016 at 9:37 PM | Reply sjwilliamspa

This is very insightful. There is no doubt that there is the bias you refer to. 42 years ago, when I was postdocing in biochemistry/enzymology before completing my residency in pathology, I knew that there were very influential mambers of the faculty, who also had large programs, and attracted exceptional students. My mentor, it was said (although he was a great writer), could draft a project on toilet paper and call the NIH. It can’t be true, but it was a time in our history preceding a great explosion. It is bizarre for me to read now about eNOS and iNOS, and about CaMKII-á, â, ã, ä – isoenzymes. They were overlooked during the search for the genome, so intermediary metabolism took a back seat. But the work on protein conformation, and on the mechanism of action of enzymes and ligand and coenzyme was just out there, and became more important with the research on signaling pathways. The work on the mechanism of pyridine nucleotide isoenzymes preceded the work by Burton Sobel on the MB isoenzyme in heart. The Vietnam War cut into the funding, and it has actually declined linearly since.

A few years later, I was an Associate Professor at a new Medical School and I submitted a proposal that was reviewed by the Chairman of Pharmacology, who was a former Director of NSF. He thought it was good enough. I was a pathologist and it went to a Biochemistry Review Committee. It was approved, but not funded. The verdict was that I would not be able to carry out the studies needed, and they would have approached it differently. A thousand young investigators are out there now with similar letters. I was told that the Department Chairmen have to build up their faculty. It’s harder now than then. So I filed for and received 3 patents based on my work at the suggestion of my brother-in-law. When I took it to Boehringer-Mannheim, they were actually clueless.

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