Randomized phase 3 efficacy and safety trial of proposed pegfilgrastim biosimilar MYL-1401H in the prophylactic treatment of chemotherapy-induced neutropenia.

Pegfilgrastim is indicated for reducing the duration of neutropenia and incidence of febrile neutropenia in patients receiving cytotoxic chemotherapy. Here, safety and efficacy of MYL-1401H, a proposed pegfilgrastim biosimilar, were investigated as prophylaxis for chemotherapy-induced neutropenia. This was a phase 3, multicenter, randomized, double-blind, parallel-group equivalence trial of MYL-1401H vs European Union-sourced reference pegfilgrastim.

Are aggressive epithelial cancers 'a disease' of Eutherian mammals?

Placental immune editing switches (PIES) have not evolved to prevent or to cause cancer but to make feto-maternal immune tolerance possible, which is at the very core of our placental mammalian ('Eutherian') nature. Aggressive epithelial cancers might be an unfortunate 'side effect' of this highly sophisticated biological nature. Microenvironmental properties in the placenta and decidua are thought to be a key to feto-maternal immune tolerance.

Epigenetic changes found in uterine decidual and placental tissues can also be found in the breast cancer microenvironment of the same unique patient: description and potential interpretations.

Microenvironmental properties are thought to be responsible for feto-maternal tolerance. Speculatively, ectopic expression of placental gene programs might also be related to cancer cells' ability to escape from immune vigilance mechanisms during carcinogenesis and cancer progression. Recently, we published the first human genomic evidence of similar immune related gene expression profiles in both placenta (placenta and decidual tissue) and cancer (both primary and metastatic) in the same patient with lymph-node positive breast carcinoma during pregnancy.

Placental immune editing switch (PIES): learning about immunomodulatory pathways from a unique case report.

The hypothesis of this work is that, in order to escape the natural immune surveillance mechanisms, cancer cells and the surrounding microenvironment might express ectopically genes that are physiologically present in the placenta to mediate fetal immune-tolerance. These natural "placental immune-editing switch" mechanisms (PIES) may represent the result of millions of years of mammalian evolution developed to allow materno-fetal tolerance. Here, we introduce genes of the immune regulatory pathways that are either similarly over- or under-expressed in tumor vs normal tissue.

HER2 blockade in metastatic collecting duct carcinoma (CDC) of the kidney: a case report.

Background: Collecting duct carcinoma of the kidney (CDC) is a rare cancer associated with bad prognosis and, at present, with no specific effective therapies.

Case Report: We report a clinical case with disseminated highgrade CDC presenting with widespread metastasis to both lungs, pelvic bones, axial skeleton, and the central nervous system (posterior fossa, both hemispheres and pituitary-hypothalamic). The primary tumor in the kidney was demonstrated (by fluorescence in situ hybridization and immunohistochemistry with Herceptest (3+ score)) to significantly overexpress HER2.