Full tumor triplets were available for four patients undergoing NACT; whereas primary carcinomas from these patients demonstrated BRCA1 LOH, the retention of the wild-type allele was detected in all four post-NACT residual tumors.
A simultaneous detection of germline and somatic mutations in ovarian cancer (OC) using tumor materials is considered to be cost-effective for <i>BRCA1/2</i> testing.
More than 80% of women with a breast cancer associated with a breast cancer type 1 (BRCA1) mutation develop a TNBC. microRNAs (miRNAs) play critical roles in diverse biological processes and are aberrantly expressed in several human neoplasms including breast cancer, where they function as actors of tumor onset, behavior, and progression.
Whether germline BRCA1/BRCA2 mutation status is independently associated with central nervous system (CNS) relapse, controlling for tumor subtype, is unknown.
The highest CPA was found in breast cancer patients with a hereditary predisposition bearing BRCA1 gene mutations, and the lowest activity was found in patients who had a tumour surgically removed and before adjuvant therapy.
With the approval of the poly (ADP-ribose) polymerase (PARP) inhibitor olaparib for newly diagnosed, breast cancer gene <i>(BRCA)1/2</i> mutated, ovarian cancer women, the assessment of <i>BRCA1/2</i> tumour status will be shortly required at the time of diagnosis.
Consistent with earlier studies, TP53 mutations were present in the majority (96.6%) of the tumors studied, and mutations in BRCA1/2 that affect DNA repair were also detected frequently in 20.5% of the tumors.
In mouse mammary tumors, we showed that Procr<sup>+</sup> cells are enriched for cancer stem cells (CSCs) in Wnt1 basal-like tumors, but not in Brca1 basal-like tumors or PyVT luminal tumors.
Because BRCA1 is highly expressed in neuronal progenitor cells during early development<sup>4</sup> and MYC is less efficient than MYCN in recruiting BRCA1, our findings indicate that a cell-lineage-specific stress response enables MYCN-driven tumours to cope with deregulated RNAPII function.
A total of 29/61 (48%) <i>BRCA1/2</i>-associated patients relapsed as a single local tumor; this was lower in sporadic cancer patients (38/134 (28%); p=0.01).
Investigators are building on these results by designing novel clinical trials for patients with BRCA1/2-deficient tumors and/or triple-negative breast cancer.
New therapeutic approaches are being developed that target BC patients with germline mutations in either <i>BRCA1, BRCA2</i> as well as <i>BRCAness,</i> a condition in which tumors have molecular similarity to BRCA-mutated tumors.
We carried out WGS on 78 paired germline and tumour DNA samples from individuals carrying pathogenic variants in BRCA1 (n = 26) or BRCA2 (n = 22) or from non-carriers (non-BRCA1/2; n = 30).
Finally, a mouse-optimized PEG~SN-38 showed remarkable antitumor activity in BRCA1-deficient MX-1 xenografts; a single dose gave tumor regression, suppression, and shrinkage of massive tumors.
This has lend clues to supervene the risk of GTD patients towards BRCA1 associated diseases and unveil novel therapeutic for GTD, a plant derived naphthoquinone, PB, already reported as selectively cytotoxic against BRCA1 defective tumors.
To better understand the correlation between BRCA1/2 mutations and the immune phenotype in prostate cancer, we characterized the immune infiltrate of eight BRCA2-mutated tumors in comparison with eight BRCA1/2 wild-type patients by T-cell receptor sequencing and immunohistochemistry for CD45, CD4, CD8, FOXP3, and CD163.
BRCA1/2 mutation carriers were younger (P < 0.001) with more often negative HER-2 expression (P = 0.01) and tumor size over 2 cm (P = 0.04) than non-carriers.
Thus, AhR represents an attractive target to inhibit redox homeostasis and modulate the tumor promoting microenvironment of basal-like and BRCA1-associated BC.
Xenografts of NaAsIII‑preconditioned MCF7 cells (MCF7NaAsIII) into the mammary fat pads of nude mice produced a larger tumor volume compared to tumors from control MCF7 cells and were more refractory to TAM in association with the reduced expression of BRCA1 and ERα, CpG hypermethylation of estrogen receptor 1 (ESR1) and BRCA1, and the increased expression of FOLR1.