Identification of M-induced molecular mechanisms underlying chemoresistance processes
Organisation/Company Dipartimento di Medicina Molecolare- Sapienza università di Roma Research Field Medical sciences » Medicine Researcher Profile Recognised Researcher (R2) Leading Researcher (R4) First Stage Researcher (R1) Established Researcher (R3) Application Deadline 23 Nov 2026 - 23:59 (UTC) Country Italy Type of Contract To be defined Job Status Not Applicable Is the job funded through the EU Research Framework Programme? Not funded by a EU programme Is the Job related to staff position within a Research Infrastructure? No
Offer Description
Triple-negative breast cancer (TNBC) is a highly aggressive tumor subtype, characterized by early onset, high metastatic capacity, and a high recurrence rate, representing a significant clinical challenge. Currently, platinum-based chemotherapy and PARP inhibitors (indicated in tumors with BRCA1/2 gene mutations)
are the mainstay of systemic treatment aimed at inducing DNA damage and replicative stress. However, a significant proportion of patients show primary or acquired resistance to such treatments. In this context, the MAML1 protein emerges as a potential key regulator of tumor progression. Preliminary data indicate that MAML1 may support cell survival and proliferation under conditions of carboplatin- or olaparib-induced therapeutic stress, promoting DNA damage repair mechanisms.
- Italy
Eligibility of fellows: country/ies of residence:
- EUROPE
Eligibility of fellows: nationality/ies:
- EUROPE
Selection process
Qualifications and interview. See detail in the call
Offer Description
Triple-negative breast cancer (TNBC) is a highly aggressive tumor subtype, characterized by early onset, high metastatic capacity, and a high recurrence rate, representing a significant clinical challenge. Currently, platinum-based chemotherapy and PARP inhibitors (indicated in tumors with BRCA1/2 gene mutations)
are the mainstay of systemic treatment aimed at inducing DNA damage and replicative stress. However, a significant proportion of patients show primary or acquired resistance to such treatments. In this context, the MAML1 protein emerges as a potential key regulator of tumor progression. Preliminary data indicate that MAML1 may support cell survival and proliferation under conditions of carboplatin- or olaparib-induced therapeutic stress, promoting DNA damage repair mechanisms.
- Italy
Eligibility of fellows: country/ies of residence:
- EUROPE
Eligibility of fellows: nationality/ies:
- EUROPE
Selection process
Qualifications and interview. See detail in the call