Biocept to Present at the 103rd AACR Annual Meeting on New Analytic Methods for Circulating Tumor Cell Analysis, Including SelectorTM, Ultra-Sensitive Mutation Detection Technology

SAN DIEGO–(BUSINESS WIRE)–Apr 2, 2012 – Biocept, Inc., a privately-held, CLIA certified laboratory testing company focused on detection and analysis of circulating tumor cells (CTCs) in cancer patients, announced that it will be presenting three posters at the 103rd Annual Meeting of the American Association for Cancer Research, being held in Chicago March 31 – April 4. The presentations will cover the company’s ultra-sensitive mutation detection technology, SelectorTM, which is being applied to CTC analysis and other clinical and research applications where nucleic acid analysis requires exceptional sensitivity and specificity, as well as biomarker analysis in CTCs related to breast and prostate cancer.

The Selector presentation, entitled “The CEE-Selector Assay: A Tool for the Identification of Rare Allele Variants” (Alexiadis, V., et al) will take place on Tuesday, April 3rd, from 8:00 am to 12:00 pm (Abstract #3198). Selector is a proprietary, highly sensitive mutation detection technology that offers unprecedented sensitivity and specificity. It is able to detect rare mutations in complex wild-type genomic backgrounds with a ratio of greater than 1 in 10,000. It was developed at Biocept, initially for analysis of mutations in rare CTCs, and will be utilized in the company’s future tests, including OncoCEE-LUTM for non-small cell lung cancer and OncoCEE-CRTM for colorectal cancer. Additionally, Biocept has recently demonstrated broader utility for the technology, including detection of mutations in cell-free circulating DNA (cfcDNA) in the plasma of cancer patients. For example, it was able to identify the tyrosine kinase inhibitor resistance mutation T790M in the EGFR gene in lung cancer patients, where ratios of mutant to wild-type gene ranged down to 0.004%. Dr. Lyle Arnold, CSO and Sr. Vice President, R&D at Biocept, commented, “The sensitivity and precision of this technology will enable completely new analyses. We expect to be able to detect and track the rise of a clonal group of cancer cells harboring a specific mutation even before it becomes clinically significant, allowing treatment at a very early stage.”

A second presentation is entitled “Estrogen Receptor and Progesterone Receptor Immunochemistry Staining in Circulating Tumor Cells as Compared to Primary Tumor or Metastatic Biopsy” (Mayer, JA, et al), which will take place on Tuesday, April 3rd, from 1:00 pm to 5:00 pm (Abstract #4568) and will cover a study performed in collaboration with researchers at Columbia University Medical Center demonstrating high concordance of hormone status in breast cancer patients between CTCs and tumor tissue by staining with fluorescently labeled antibodies. The third poster, entitled “Increased Detection of Circulating Prostate Epithelial Tumor Cells on Microfluidic Channels Using Enhanced Staining and Automated Scanning” (Pircher, TJ, et al), addresses technology developed by the company to detect cytokeratin negative CTCs with a new staining technique called CEE-EnhancedTM as well as with anti-PSA antibodies, and to automate the detection of these cells with scanning technology and microscopy, and will take place on Monday, April 2nd, from 1:00 pm to 5:00 pm (Abstract #2390). These abstracts reflect technology that is being added to Biocept’s platform and test products to enhance CTC capture, detection and analysis.

Biocept’s first CTC test, OncoCEE-BRTM for breast cancer, is now available through Biocept and its commercialization partner, Clarient, Inc., a GE Healthcare Company. The test includes CTC enumeration and determination of HER2 status by fluorescence in situ hybridization (FISH) from a blood sample. Determination of estrogen receptor (ER) and progesterone receptor (PR) status by immunocytochemical staining will be added to the test later this year, and early next year, respectively. OncoCEE-BR is the first commercially available CTC test to include analysis of a specific, treatment-associated biomarker (HER2).

About Biocept, Inc.

Biocept, Inc., headquartered in San Diego, California, is an advanced laboratory services company specializing in the capture, isolation, detection and analysis of Circulating Tumor Cells (CTCs). Biocept’s mission is to enhance the lives of cancer patients through the development of innovative diagnostic products and services. Biocept utilizes patented and innovative technologies to deliver clinically relevant and actionable information to physicians that enable better patient care. This includes clinical assessments of CTCs, both prognostic and predictive, which may provide physicians with important information for the treatment of their patients with cancer.

Contact: Biocept, Inc.
Michael Dunn
1 858 320-8200
Web site: http://www.biocept.com/

Posted: April 2012

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Cancer gene mutation more complex than previously thought -study

LONDON (Reuters) – Taking a sample or biopsy from just one part of a tumour might not give a full picture of its genetic diversity and may explain why doctors, despite using genetically targeted drugs, are often unable to save patients whose cancer has spread, scientists said.

A study by British researchers found there are more genetic differences than similarities between biopsies taken from separate areas of the same tumour, and yet further gene differences in samples taken from secondary tumours.

That might help explain why, despite recent development of a wave of highly targeted drugs designed to tackle cancers of specific genetic types, the prognosis remains poor for many patients with so-called solid-tumour disease like breast, lung, or kidney cancer that has spread to others parts of the body.

But the researchers, whose study was partly funded by charity Cancer Research UK and published in the New England Journal of Medicine, said it also pointed to a way forward.

The team carried out the first ever genome-wide analysis of the genetic changes or faults in different regions of the same tumour.

They looked at four patients with cancer in their kidneys, taking samples from different regions of the primary tumour and also from other organs where the tumour had spread.

They found that the majority of gene faults, around two-thirds, were not the same in one sample as in another, even when the biopsies were taken from the same tumour.

Samples taken from secondary tumours – which are a result of the disease spreading to other parts of the body – had yet more different genetic faults, suggesting that basing treatment decisions on just one primary tumour sample is not sufficient.

“We’ve known for some time that tumours are a patchwork of faults, but this is the first time we’ve been able to use cutting-edge genome sequencing technology to map out the genetic landscape of a tumour in such exquisite detail,” said Charles Swanton, of University College London’s cancer institute, who led the study and presented its results at a briefing in London on Tuesday.

He said they had uncovered “an extraordinary amount of diversity” at a genetic level both within tumours and within a single patient, with more differences between biopsies from the same tumour than similarities.

“The next step will be to understand what’s driving this diversity in different cancers and identify key driver mutations that are common throughout all parts of a tumour,” Swanton said.

PERSONALISED MEDICINE

Genetic profiling of patients and their tumours has become more common in cancer treatment in wealthy countries as drug companies develop new generations of so-called “personalised medicines” that target cancers with specific genetic features.

Roche’s blockbuster breast cancer drug Herceptin is designed to treat only women who make too much of the HER2 protein, for example, while Novartis’s Afinitor targets mTOR, a protein that acts as an important regulator of tumour cell division, blood vessel growth and cell metabolism.

James Larkin, an oncologist at London’s Royal Marsden Hospital who also worked on the study, said the findings suggest the reality of personalised cancer treatment is far more complex than previously thought.

“The molecular changes that drive the growth of the cancer once it has spread may be different from those that drive the growth of the primary tumour,” he said.

The researchers compared genetic faults in various tumour samples taken from the four patients.

They found 118 different mutations – 40 of which were “ubiquitous mutations” found in all biopsies, 53 “shared mutations” that were found in most but not all biopsies, and 25 “private mutations” only found in a single sample.

By analysing where the shared mutations were in relation to the whole tumour, the researchers were able to trace the origins of certain subtypes of cancer cells back to what they called key “driver mutations.” This allowed them to create a map of how the pattern of faults might have evolved over time.

Swanton likened the findings to a tree, in which the trunk is the primary tumour and the branches the secondary tumours from the cancer’s spread.

While he stressed the results would need to be replicated with larger numbers of patients and in different types of cancer, he said these early indications showed “the importance of targeting common mutations found in the trunk of the tree as opposed to those found in the branches.”

“It may also explain why surgery to remove the primary kidney tumour can improve survival,” he added, since cutting out a tumour reduces the risk that cells resistant to drug treatment could go on to re-grow the tumour or spread elsewhere.

(Reporting by Kate Kelland; Editing by Ben Hirschler and Alessandra Rizzo)

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