Scientists, including an Indian-American researcher, have identified a molecule that can help treat breast cancer, giving hope to patients who have become resistant to traditional therapies.

The first-in-class molecule shuts down oestrogen-sensitive breast cancer in a new way, researchers said.

First-in-class drugs are those that work by a unique mechanism - in this case a molecule that targets a protein on the oestrogen receptor of tumour cells.

The potential drug offers hope for patients whose breast cancer has become resistant to traditional therapies.

"This is a fundamentally different, new class of agents for oestrogen-receptor-positive breast cancer," said Ganesh Raj, professor at the University of Texas Southwestern (UT Southwestern) Simmons Cancer Center.

"Its unique mechanism of action overcomes the limitations of current therapies," Raj said.

All breast cancers are tested to determine if they require oestrogen to grow and about 80 per cent are found to be oestrogen-sensitive, researchers said.

These cancers can often be effectively treated with hormone therapy, such as tamoxifen, but as many as a third of these cancers eventually become resistant, they said.

The new compound is a potential highly effective, next-line treatment for these patients, said Raj.

Traditional hormonal drugs, such as tamoxifen, work by attaching to a molecule called the oestrogen receptor in cancer cells, preventing oestrogen from binding to the receptor, a necessary step for cancer cells to multiply.

However, the oestrogen receptor can mutate and change its shape over time so that the treatment drug no longer fits neatly with the receptor. When this happens, the cancer cells start multiplying again.

"There has been intense interest in developing drugs that block the ability of the oestrogen receptor - the prime target in most breast cancers - from interacting with the co-regulator proteins that cause a tumour's growth," said David Mangelsdorf, professor at UT Southwestern.

"Blocking such "protein-protein interactions" has been a dream of cancer researchers for decades.

The drug works by blocking other molecules - proteins called co-factors - that also must attach to the oestrogen receptor for cancer cells to multiply.

The new molecule, dubbed ERX-11, mimics a peptide, or protein building block.

o far, it

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Ahmedabad (PTI): The ongoing Special Intensive Revision (SIR) of the electoral rolls in Gujarat has revealed that more than 17 lakh deceased voters were still included in the existing voter list across the state, a release by the office of the Chief Electoral Officer (CEO) has stated.

According to the release issued on Thursday, the SIR exercise started in Gujarat on November 4 with booth-level officers (BLOs) distributing enumeration forms in their designated areas.

The campaign will continue till December 11.

"In the last one month, enumeration forms have been distributed to more than five crore voters registered in the 2025 electoral roll. In most of the 33 districts, 100 per cent of the distribution has been completed. Work on digitising the returned forms is currently underway. So far, the digitisation work has been completed in 12 out of 182 assembly constituencies," it said.

These include Dhanera and Tharad of Banaskantha district, Limkheda and Dahod (ST) of Dahod district, Bayad of Aravalli district, Dhoraji, Jasdan and Gondal of Rajkot district, Keshod of Junagadh district, Mehmadabad of Kheda district, Khambhat of Anand district and Jalalpore of Navsari district.

Dang district is at the forefront in this work with 94.35 per cent digitisation of the counting forms, said the release.

"During this exercise, it was revealed that 17 lakh deceased voters were still included in the electoral roll across the state. More than 6.14 lakh voters were found absent from their addresses. It has been noticed that more than 30 lakh voters have permanently migrated," the release said.

BLOs found more than 3.25 lakh voters in the "repeated" category, which means that their names figured at more than one place, the release stated.