Morphological Markers of Chromosomal Instability

An unusual presentation of non-specific cystic degeneration of craniofacial fibrous dysplasia: a case report and review of literature

“…In view of the radiographical and intraoperative findings, the absence of any history of trauma, a low probability of dental infection being the cause (as per endodontic and periodontal examinations), absence of evidence of malignant transformation (confirmed by histological findings) [13][14][15], the researchers confirmed that the case involved non-specific cystic degeneration in the CFD site. Postoperative healing was uneventful (Figs.…”

Mitotic abnormalities precede microsatellite instability in lynch syndrome-associated colorectal tumourigenesis

“…Chromosomal instability manifests on tissue level as atypical mitoses which differ morphologically from normal, balanced mitotic figures. 28 An increase in mitotic perimeter directly indicates CIN, as it reflects irregular mitotic division, often resulting in chromosomal rearrangements and potential genetic abnormalities. 29 Here, the mean perimeter of metaphases was higher in LS mucCRC as compared to LS mucADE and increased along with increasing malignancy of the samples ( Fig.…”

“…Since chromosomal instability manifests as atypical mitoses, 28 we reasoned it could be demonstrated by measuring the size of mitoses as previously described by Kesarkar et al. 29 Feulgen staining with light green background stain was used as previously described 12 to visualize nuclear material and mitoses in 4 carcinoma (LS_CAR2, LS_CAR3, LS_CAR4, LS_CAR5), 3 adenoma (LS_ADE9, LS_ADE11, LS_ADE12), and 5 colonic mucosa samples from patients with LS diagnosed either with adenoma (LS_N9, LS_N23) or carcinoma (LS_N5, LS_N6, LS_N7) ( Supplementary Table S1 ).…”

Structural Chromosome Instability: Types, Origins, Consequences, and Therapeutic Opportunities

“…MN are easily identified after DAPI staining and accumulate during cancer genesis and treatment but can also arise due to changes in cellular metabolism during senescence, aging, and the onset of different diseases [ 44 , 45 ]. MNs are considered markers of genotoxic events and CIN [ 46 ], and their presence is very common in most solid tumors, neoplastic lesions, and peripheral lymphocytes of patients that develop cancer [ 47 , 48 ]. Interestingly, although the morphological markers mentioned above (UFBs, bulky chromosome bridges, and acentric fragments) have different origins and resolution mechanisms (see Section 6 below), it seems that all of these aberrations sooner or later may end in the formation of MN, which may explain the widespread presence of MN in tumors and also highlights the tight association among different CIN phenotypes ( Figure 1 ).…”