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Welcome to the Cantor Lab website, where we share our research projects, ideas, photos, and stories.

We focus on DNA replication and its response to replication stress and how dysregulated in hereditary breast/ovarian cancer and the rare cancer syndrome Fanconi Anemia (FA) that manifests in children.

Featured Articles:

Replication gaps underlie BRCA-deficiency and therapy response. Nicholas J. Panzarino, John Krais, Min Peng, Michelle Mosqueda, Sumeet Nayak, Samuel Bond, Jennifer Calvo, Ke Cong, Mihir Doshi, Matt Bere, Jianhong Ou, Bin Deng, Lihua Julie Zhu, Neil Johnson, Sharon B. Cantor. bioRxiv 781955. 

PARPi synthetic lethality derives from replication-associated single-stranded DNA gaps. Ke Cong, Arne Nedergaard Kousholt, Min Peng, Nicholas J. Panzarino, Wei Ting Chelsea Lee, Sumeet Nayak, John Krais, Jennifer Calvo, Matt Bere, Eli Rothenberg, Neil Johnson, Jos Jonkers, Sharon B. Cantor. bioRxiv 781989

Inhibition of the translesion synthesis polymerase REV1 exploits replication gaps as a cancer vulnerability. Sumeet Nayak, Jennifer A. Calvo, Ke Cong, Min Peng, Emily Berthiaume, Jessica Jackson, Angela M. Zaino, Alessandro Vindigni, M. Kyle Hadden and Sharon B. Cantor. Science Advances.         Article showcased at Science in Boston!


What's wrong with Fanconia anemia cells?
Fanconi anemia (FA) patients have distinct manifestations and severity of diseases (ranging from congenital abnormalities, bone marrow failure, and cancer). However, cells from FA patients share an inability to recover from replication stress. A key question Is what is wrong and can FA cell defects be suppressed to improve the health of FA patients.

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How do DNA repair defective cancers become resistant to chemotherapy?
Hereditary cancers with BRCA mutations and defects in DNA repair are initially sensitive to chemotherapies such as cisplatin, which induces DNA damage.  However, cisplatin resistance can develop.  One mechanism of resistance includes secondary mutations that reinstate the function of the BRCA gene in DNA repair.  Recently, we found another way resistance occurs. Featured in UMassMed Now


Does the hereditary breast/ovarian cancer gene, FANCJ, prevent or cause cancer?

Over 250 mutations occur in the hereditary breast and ovarian cancer gene, FANCJ (also known as BRIP1/BACH1).  However, it is not known how or if a disease-associated DNA mutation alters FANCJ function. Moreover, some helicase domain mutations inactivate its DNA unwinding activity while others over-activate it.  Further suggesting that too much FANCJ activity could be oncogenic, FANCJ is also amplified in some cancers.  Thus, for effective cancer therapy, It will be critical to determine how FANCJ clinical mutations are pathogenic.

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News and Events
February 2021: Congrats Jen Calvo paper accepted at Molecular Cancer Research!
January 2021: Welcome new postdocs; SiddhantPandurang Bhoir and Jenna Whalen
January 2021: Congratulations to Sumeet and Jen on TLS review out this month!

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