Dramatic Recovery of Vision after Trastuzumab Deruxtecan Treatment of HER2-Positive Breast Cancer with Pituitary Metastasis.

In recent years, both the number of patients with breast cancer and those with associated brain metastases (BMs) have increased. Human epidermal growth factor receptor 2 (HER2)-positive breast cancer has a high BM frequency. The prognosis of BM from breast cancer is poor, and establishing effective treatment for this disease is essential. We report a HER2-positive patient with multiple BM and right-eye blindness due to pituitary metastasis. She responded promptly to trastuzumab deruxtecan (T-DXd) in the 5th line of treatment, which shrunk the tumors and restored vision. Although the Graded Prognostic Assessment (GPA) predicted survival of 13 months, the patient recovered well after treatment and continued T-DXd use with no progression, including vision loss at 22 months after treatment initiation. This case demonstrates the successful action of T-DXd in the face of multiple BM and poorly predicted outcomes.

[Locally Advanced Breast Cancer Treated with Mohs' Paste and Neoadjuvant Chemotherapy-A Case Report].

Cutaneous infiltration by breast cancer significantly reduces patient quality of life(QOL)due to bleeding, exudate, and pain. We report a case of combined treatment using Mohs' paste and neoadjuvant chemotherapy for locally advanced breast cancer. Mohs' paste decreased bleeding and exudate from the tumor and neoadjuvant chemotherapy combined with bevacizumab down-staged a large tumor to a volume that permitted mastectomy. Good local control using Mohs' paste and neoadjuvant chemotherapy can improve patient QOL and reduce the physical burden.

Mitogenic activity of tracheal effluents from premature infants with chronic lung disease.

Lung injury alters the expression and release of growth factors that disrupt postnatal pulmonary development in newborns and causes chronic lung disease (CLD). The effect of these factors, released into the airways of newborns with CLD, on cell proliferation and collagen production was characterized in vitro. Human fetal lung fibroblast and alveolar-epithelial-like cell lines (FHs 738Lu and A549, respectively) were exposed to tracheal effluents from infants with CLD (mean gestation, 24.7 +/- 0.9 wk; birth weight, 666 +/- 85 g; postnatal age, 0-62 d). In both cell types, proliferation was assessed by measuring [(3)H]-thymidine uptake; in fibroblasts, collagen production was analyzed by measuring [(3)H]-proline incorporation. The activity of specific growth factors in effluents was determined using anti-growth factor antibodies and the growth factors themselves. Growth factors in tracheal effluents promoted proliferation in a dose-dependent manner and caused up to a 10.2- and 3.1-fold increase in thymidine uptake by fibroblasts and epithelial cells, respectively. Collagen production by fibroblasts increased dose dependently, peaking at 177% of baseline. Antibody against transforming growth factor beta-1 (TGF-beta(1)) inhibited proliferation and the increase in collagen production by 31% (p = 0.01) and 14% (p = 0.045), respectively. Antibody against hepatocyte growth factor (HGF) inhibited proliferation of epithelial cells (25%, p = 0.039). The effects of exogenous TGF-beta(1) on fibroblasts and HGF on epithelial cells resembled those of tracheal effluents. Potent mitogenic and differentiating substances are released into the tracheal effluents of newborns with CLD. TGF-beta(1) may worsen CLD by inducing fibrosis whereas HGF may favor resolution by promoting epithelialization.

Trophic effect of multiple growth factors in amniotic fluid or human milk on cultured human fetal small intestinal cells.

OBJECTIVES: To evaluate the role of growth factors in amniotic fluid and in human milk on gastrointestinal adaptation of the fetus and very low-birth-weight infants, the effects of these fluids and multiple growth factors were investigated in a human fetal small intestinal cell line (FHs 74 Int). METHODS: After FHs 74 Int cells were incubated with amniotic fluid, human milk, or recombinant growth factors, growth-promoting activity was measured by [3H]-thymidine incorporation into cells. RESULTS: Incubating cells with amniotic fluid or human milk promoted growth dose dependently. Genistein almost completely inhibited growth-promoting activity in amniotic fluid P = 0.002), and growth was partially inhibited by antibodies against epidermal growth factor (EGF) (P = 0.047), insulin-like growth factor-1 (IGF-1, P = 0.047), or fibroblast growth factor (FGF, P = 0.014). This activity in human milk was inhibited almost completely by genistein (P < 0.0001) and partially inhibited by antibodies against EGF (P = 0.036), IGF-1 (P = 0.009), FGF (P = 0.004), hepatocyte growth factor (HGF, P = 0.001), or transforming growth factor-alpha (TGF-alpha, P = 0.001). Although recombinant EGF, IGF-1, FGF, HGF, and TGF-alpha elicited a synergistic trophic response on cultured cells, the response was much less than with amniotic fluid or with human milk. CONCLUSION: In aminiotic fluid and in human milk, EGF, IGF-1, FGF, HGF, and TGF-alpha have a strong trophic effect on immature intestinal cells and may be involved in perinatal gastrointestinal adaptation.