News
US benefits provider launches genetic testing division
The new addition is hoped to to democratise access to genomic information
The US family-building benefits provider Kindbody has launched its in-house genetic testing division.
Kindlabs will offer a genetic testing platform, from wet lab chemistry to software and bioinformatics, hoped to provide medical-grade genetic tests at price points to help to democratise access to genomic information.
The addition of the new division will incorporate genomics into the company’s end-to-end model, with the aim to deliver a “continuum of care” to patients.
Kindlabs will operate its reference laboratory in Secaucus, New Jersey, under the leadership of Dr Amber Cooper, Kindbody’s chief medical officer of genomics and laboratory sciences, and Manuel Viotti, vice president of preimplantation genetic testing and clinical laboratory director.
“Under the visionary leadership of Dr Viotti, our dedicated scientific team has made significant strides in advancing genomic sequencing analysis for the benefit of patients,” said Cooper.
“Dr Viotti’s instrumental role in spearheading the development of Kindlabs has positioned Kindbody as leaders in the industry. Together, our team is revolutionising genomic analysis, delivering valuable improvements that positively impact patients’ lives.”
Dr Angeline Beltsos, CEO, clinical, at Kindbody, said: “At the heart of Kindbody’s mission is to help build healthy families for our patients.
“The addition of Kindlabs combines industry-leading technology and expertise, and stringent quality standards, to optimise our patients’ chances of achieving a successful pregnancy and bringing home a healthy baby.”
Kindbody says its clinically-managed programme covers the full-spectrum of reproductive health, including both female and male fertility, as well as a full continuum of reproductive care including physical, mental, and emotional support.
The company owns and operates 32 clinics throughout the US, including in California, Texas, Michigan, New York and Wisconsin.
Diagnosis
Lung cancer drug shows breast cancer potential
Ovarian cancer cells quickly activate survival responses after PARP inhibitor treatment, and a lung cancer drug could help block this, research suggests.
PARP inhibitors are a common treatment for ovarian cancer, particularly in tumours with faulty DNA repair. They stop cancer cells fixing DNA damage, which leads to cell death, but many tumours later stop responding.
Researchers identified a way cancer cells may survive PARP inhibitor treatment from the outset, pointing to a potential way to block that response. A Mayo Clinic team found ovarian cancer cells rapidly switch on a pro-survival programme after exposure to PARP inhibitors. A key driver is FRA1, a transcription factor (a protein that turns genes on and off) that helps cancer cells adapt and avoid death.
The team then tested whether brigatinib, a drug approved for certain lung cancers, could block this response and boost the effect of PARP inhibitors. Brigatinib was chosen because it inhibits multiple signalling pathways involved in cancer cell survival.
In laboratory studies, combining brigatinib with a PARP inhibitor was more effective than either treatment alone. Notably, the effect was seen in cancer cells but not normal cells, suggesting a more targeted approach.
Brigatinib also appeared to act in an unexpected way. Rather than working through the usual DNA repair routes, it shut down two signalling molecules, FAK and EPHA2, that aggressive ovarian cancer cells rely on. FAK and EPHA2 are proteins that relay survival signals inside cells. Blocking both at once weakened the cells’ ability to adapt and resist treatment, making them more vulnerable to PARP inhibitors.
Tumours with higher levels of FAK and EPHA2 responded better to the drug combination. Other data link high levels of these molecules to more aggressive disease, pointing to potential benefit in harder-to-treat cases.
Arun Kanakkanthara, an oncology investigator at Mayo Clinic and a senior author of the study, said: “This work shows that drug resistance does not always emerge slowly over time; cancer cells can activate survival programmes very early after treatment begins.”
John Weroha, a medical oncologist at Mayo Clinic and a senior author of the study, said: “From a clinical perspective, resistance remains one of the biggest challenges in treating ovarian cancer. By combining mechanistic insights from Dr Kanakkanthara’s laboratory with my clinical experience, this preclinical work supports the strategy of targeting resistance early, before it has a chance to take hold. This strategy could improve patient outcomes.”
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