Magnetic resonance imaging tumor regression shrinkage patterns after neoadjuvant chemotherapy in patients with locally advanced breast cancer: Correlation with tumor biological subtypes and pathological response after therapy

Abstract

The objective of this study is to analyze magnetic resonance imaging shrinkage pattern of tumor regression after neoadjuvant chemotherapy and to evaluate its relationship with biological subtypes and pathological response. We reviewed the magnetic resonance imaging studies of 51 patients with single mass-enhancing lesions (performed at time 0 and at the II and last cycles of neoadjuvant chemotherapy). Tumors were classified as Luminal A, Luminal B, HER2+, and Triple Negative based on biological and immunohistochemical analysis after core needle biopsy. We classified shrinkage pattern, based on tumor regression morphology on magnetic resonance imaging at the II cycle, as concentric, nodular, and mixed. We assigned a numeric score (0: none; 1: low; 2: medium; 3: high) to the enhancement intensity decrease. Pathological response on the surgical specimen was classified as complete (grade 5), partial (grades 4-3), and non-response (grades 1-2) according to Miller and Payne system. Fisher test was used to relate shrinkage pattern with biological subtypes and final pathological response. Seventeen patients achieved complete response, 25 partial response, and 9 non-response. A total of 13 lesions showed nodular pattern, 20 concentric, and 18 mixed. We found an association between concentric pattern and HER2+ (p < 0.001) and mixed pattern and Luminal A lesions (p < 0.001). We observed a statistical significant correlation between concentric pattern and complete response (p < 0.001) and between mixed pattern and non-response (p = 0.005). Enhancement intensity decrease 3 was associated with complete response (p < 0.001). Shrinkage pattern and enhancement intensity decrease may serve as early response indicators after neoadjuvant chemotherapy. Shrinkage pattern correlates with tumor biological subtypes.

Association of the genetic variants (‐794 CATT5‐8 and ‐173 G > C) of macrophage migration inhibitory factor (MIF) with higher soluble levels of MIF and TNFα in women with breast cancer

“…In the present study, we have investigated the association of the functional variants of the MIF gene (-173G > C and -794 CATT [5][6][7][8] with the soluble levels of MIF and TNFα in women with BC of western Mexico. BC is a major lethal cancer in female.…”

“…With respect to the functional variant -794 CATT [5][6][7][8] , the Hardy-Weinberg equilibrium in the CS was also performed (P = .99). The distribution of -794CATT [5][6][7][8] MIF polymorphism in women with BC and CS is shown in Table 3. We found no significant differences when comparing the genotypes of women with BC and CS.…”

“…4 The molecular subtypes are classified in Luminal A, Luminal B, HER2, and triple negative (TN). 5,6 BC is a multifactorial disease in which pathogenesis merges several factors like environmental, genetic, and immunologic, where the proinflammatory cytokines highlight. [7][8][9] Migration inhibitory factor is a pleiotropic cytokine that is involved in tumor pathology, 10 because participates promoting inflammation, angiogenesis, and metastasis, 11 besides MIF can regulate innate and adaptive immunity, it constitutively released by many cells including macrophages, B and T cells, dendritic cells, granulocytes, endocrine, endothelial, epithelial cells, 12,13 and also by tumor cells.…”

“…16 The MIF gene is encoded on chromosome 22 (22q11.2) in humans; it consists of 3 exons, 12,17,18 and it is composed of 115 amino acids with a molecular weight of 12.5 kDa, and its active form in the conformation homotrimer. 13,17 There are existing reports that establish functional variants associated with the increased expression the MIF (-173G > C and -794 CATT [5][6][7][8] ). 19 The promoter sequence of MIF has several specific binding sites for different transcription factors that regulate its expression, which include SP1, CREB, NFkB, Pit-1, AP-1, ICBP90, and HIF-1α.…”

“…27 However, it is still unknown if this functional variant of the MIF gene and the soluble levels of MIF and TNFα are associated with BC in the western Mexican population. This study aimed to associate the functional variants of the MIF gene (-173G > C and -94 CATT [5][6][7][8] with the soluble levels of MIF and TNFα in women with BC.…”