581 research outputs found
Approved CAR T cell therapies
Two autologous chimeric antigen receptor (CAR) T cell therapies (Kymriahβ’ and Yescartaβ’) were recently approved by the FDA. Kymriahβ’ is for the treatment of pediatric patients and young adults with refractory or relapse (R/R) B cell precursor acute ly
Expression of anion exchanger 2 in human gastric cancer
Anion exchanger 2 (AE2), which mediates exchange of Cl-/HCO3- across the plasma membrane, is widely expressed in body tissues. It is most abundantly expressed in stomach and is responsible for the uptake of Cl- ions that are destined to become HCl molecules. Aim: To determine whether AE2 expression was altered in gastric tumors. Methods: We have studied AE2 expression in normal human gastric tissues (n =16) and in gastric tumors (n = 33) using immunohistochemistry and immunofluorescent labeling. Results: In normal gastric tissue positive staining was observed in gastric fundus gland, suggesting parietal cell-related expression of AE2, and AE2 expression was localized in the nuclear membrane and even in cell nuclei. For assay of cancerous gastric tissues, specimens of human gastric cancer arising from the region of the fundus (2 cases), the body (14 cases) and the antrum (17 cases) were randomly selected. Immunohistochemical staining has showed that AE2 was down-regulated in all 14 cancerous gastric body specimens, whereas staining for AE2 in cancerous antrum was less intense and had a diffuse profile. Conclusions: The data suggest that AE2 might be associated with gastric carcinogenesis and the achlorhydria experienced by gastric cancer patients.ΠΠ½ΠΈΠΎΠ½Π½ΡΠΉ ΠΎΠ±ΠΌΠ΅Π½Π½ΠΈΠΊ 2 (ΠΠ2), ΠΊΠΎΡΠΎΡΡΠΉ ΠΎΠΏΠΎΡΡΠ΅Π΄ΡΠ΅Ρ ΠΏΠ΅ΡΠ΅Π½ΠΎΡ Cl-
/HCO3
-
ΡΠ΅ΡΠ΅Π· ΠΏΠ»Π°Π·ΠΌΠ°ΡΠΈΡΠ΅ΡΠΊΡΡ ΠΌΠ΅ΠΌΠ±ΡΠ°Π½Ρ, ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡΡΠ΅ΡΡΡ
ΠΊΠ»Π΅ΡΠΊΠ°ΠΌΠΈ ΡΠ°Π·Π½ΡΡ
ΡΠΊΠ°Π½Π΅ΠΉ. Π‘Π°ΠΌΡΠΉ Π²ΡΡΠΎΠΊΠΈΠΉ ΡΡΠΎΠ²Π΅Π½Ρ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ ΠΠ2 Π² ΠΆΠ΅Π»ΡΠ΄ΠΊΠ΅, ΠΏΠΎΡΠΊΠΎΠ»ΡΠΊΡ ΡΡΠΎΡ Π±Π΅Π»ΠΎΠΊ ΠΎΡΠ²Π΅ΡΠ°Π΅Ρ Π·Π° ΠΏΠΎΠ³Π»ΠΎΡΠ΅Π½ΠΈΠ΅
ΠΈΠΎΠ½ΠΎΠ² Cl-
, ΠΊΠΎΡΠΎΡΡΠ΅ Π²ΠΏΠΎΡΠ»Π΅Π΄ΡΡΠ²ΠΈΠΈ ΠΈΡΠΏΠΎΠ»ΡΠ·ΡΡΡΡΡ Π΄Π»Ρ ΡΠ΅ΠΊΡΠ΅ΡΠΈΠΈ HCl. Π¦Π΅Π»Ρ: ΠΠ·ΡΡΠΈΡΡ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ Π² ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ ΠΠ2 ΠΏΡΠΈ ΡΠ°ΠΊΠ΅
ΠΆΠ΅Π»ΡΠ΄ΠΊΠ°. ΠΠ΅ΡΠΎΠ΄Ρ: ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Π° ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡ ΠΠ2 Π² Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΡΡ
ΡΠΊΠ°Π½ΡΡ
(n = 16) ΠΈ ΠΎΠΏΡΡ
ΠΎΠ»ΡΡ
ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° (n = 33) Ρ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΠ΅ΠΌ
ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ² ΠΈΠΌΠΌΡΠ½ΠΎΠ³ΠΈΡΡΠΎΡ
ΠΈΠΌΠΈΠΈ ΠΈ ΠΈΠΌΠΌΡΠ½ΠΎΡΠ»ΡΠΎΡΠ΅ΡΡΠ΅Π½ΡΠΈΠΈ. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ: Π² Π½Π΅ΡΡΠ°Π½ΡΡΠΎΡΠΌΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° Π² ΡΡΠ½Π΄Π°Π»ΡΠ½ΠΎΠΉ
ΠΆΠ΅Π»Π΅Π·Π΅ Π²ΡΡΠ²Π»ΡΠ»ΠΈ ΡΠΈΠ»ΡΠ½ΡΡ ΠΏΠΎΠ»ΠΎΠΆΠΈΡΠ΅Π»ΡΠ½ΡΡ ΡΠ΅Π°ΠΊΡΠΈΡ, ΡΡΠΎ ΡΠ²ΠΈΠ΄Π΅ΡΠ΅Π»ΡΡΡΠ²ΡΠ΅Ρ ΠΎΠ± ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ ΠΠ2 ΠΏΠ°ΡΠΈΠ΅ΡΠ°Π»ΡΠ½ΡΠΌΠΈ ΠΊΠ»Π΅ΡΠΊΠ°ΠΌΠΈ,
ΠΏΡΠΈΡΠ΅ΠΌ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡ ΠΠ2 Π±ΡΠ»Π° Π»ΠΎΠΊΠ°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°Π½Π° Π² ΡΠ΄Π΅ΡΠ½ΠΎΠΉ ΠΌΠ΅ΠΌΠ±ΡΠ°Π½Π΅ ΠΈ Π² ΡΠ΄ΡΠ΅. Π ΠΎΠΏΡΡ
ΠΎΠ»ΡΡ
ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° (ΡΡΠ½Π΄Π°Π»ΡΠ½ΠΎΠ³ΠΎ ΠΎΡΠ΄Π΅Π»Π° (n =
2), ΡΠ΅Π»Π° (n = 14) ΠΈ Π°Π½ΡΡΠ°Π»ΡΠ½ΠΎΠ³ΠΎ ΠΎΡΠ΄Π΅Π»Π° (n = 17)), ΠΎΡΠΎΠ±ΡΠ°Π½Π½ΡΡ
ΡΠ»ΡΡΠ°ΠΉΠ½ΡΠΌ ΠΎΠ±ΡΠ°Π·ΠΎΠΌ, Π±ΡΠ» ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ Π°Π½Π°Π»ΠΈΠ· ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ ΠΠ2.
ΠΠΌΠΌΡΠ½ΠΎΠ³ΠΈΡΡΠΎΡ
ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΎΠ΅ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ ΠΏΠΎΠΊΠ°Π·Π°Π»ΠΎ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠ΅ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ ΠΠ2 Π²ΠΎ Π²ΡΠ΅Ρ
14 ΡΠ»ΡΡΠ°ΡΡ
ΡΠ°ΠΊΠ° ΡΠ΅Π»Π° ΠΆΠ΅Π»ΡΠ΄ΠΊΠ°. ΠΠΊΡΠ°ΡΠΈΠ²Π°Π½ΠΈΠ΅
ΠΠ2 Π² ΠΎΠ±ΡΠ°Π·ΡΠ°Ρ
ΡΠ°ΠΊΠ° Π°Π½ΡΡΠ°Π»ΡΠ½ΠΎΠ³ΠΎ ΠΎΡΠ΄Π΅Π»Π° ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° Π±ΡΠ»ΠΎ ΠΌΠ΅Π½Π΅Π΅ ΠΈΠ½ΡΠ΅Π½ΡΠΈΠ²Π½ΡΠΌ ΠΈ Π΄ΠΈΡΡΡΠ·Π½ΡΠΌ. ΠΡΠ²ΠΎΠ΄Ρ: ΠΏΠΎΠ»ΡΡΠ΅Π½Π½ΡΠ΅
Π΄Π°Π½Π½ΡΠ΅ ΠΏΠΎΠ·Π²ΠΎΠ»ΡΡΡ ΠΏΡΠ΅Π΄ΠΏΠΎΠ»ΠΎΠΆΠΈΡΡ Π½Π°Π»ΠΈΡΠΈΠ΅ ΡΠ²ΡΠ·ΠΈ ΠΌΠ΅ΠΆΠ΄Ρ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠ΅ΠΉ ΠΠ2 ΠΈ ΡΠ°Π·Π²ΠΈΡΠΈΠ΅ΠΌ ΡΠ°ΠΊΠ° ΠΆΠ΅Π»ΡΠ΄ΠΊΠ°, Π° ΡΠ°ΠΊΠΆΠ΅ Π°Ρ
Π»ΠΎΡΠ³ΠΈΠ΄ΡΠΈΠ΅ΠΉ,
ΠΎΡΠΌΠ΅ΡΠ°Π΅ΠΌΠΎΠΉ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
ΡΠ°ΠΊΠΎΠΌ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ°
Breakthroughs in modern cancer therapy and elusive cardiotoxicity: Critical research-practice gaps, challenges, and insights
To date, five cancer treatment modalities have been defined. The three traditional modalities of cancer treatment are surgery, radiotherapy, and conventional chemotherapy, and the two modern modalities include molecularly targeted therapy (the fourth modality) and immunotherapy (the fifth modality). The cardiotoxicity associated with conventional chemotherapy and radiotherapy is well known. Similar adverse cardiac events are resurging with the fourth modality. Aside from the conventional and newer targeted agents, even the most newly developed, immune-based therapeutic modalities of anticancer treatment (the fifth modality), e.g
Expression site of P2RY12 in residential microglial cells in astrocytomas correlates with M1 and M2 marker expression and tumor grade
The role of resident microglial cells in the pathogenesis and progression of glial tumors is still obscure mainly due to a lack of specific markers. Recently P2RY12, a P2 purinergic receptor, was introduced as a specific marker for microglial cells under normal and pathologic conditions. Here we analyzed the expression of P2RY12 in astrocytomas of various malignancy grades in relation to markers for M1 and M2 macrophage activation profiles by using two web-based glioma datasets and confocal immunohistochemistry to 28 astrocytoma samples grades II-IV. In the gliomas, P2RY12 immunoreactivity delineated CD68 negative cells with otherwise microglial features from CD68 positive tumor associated macrophages (TAMs). The presence of P2RY12 positive cells correlated positively with overall survival. P2RY12 mRNA levels and membrane-bound localization of P2RY12 were inversely correlated with increasing malignancy grade, and the expression site of P2RY12 shifted from cytoplasmic in low-grade gliomas, to nuclear in high-grade tumors. The cytoplasmic expression of P2RY12 was associated with the expression of M1 markers, characteristic of the pro-inflammatory macrophage response. In contrast, the nuclear localization of P2RY12 was predominant in the higher graded tumors and associated with the expression of the M2 marker CD163. We conclude that P2RY12 is a specific marker for resident microglia in glioma and its expression and localization correspond to tumor grade and predominant stage of M1/M2 immune response
Isocitrate dehydrogenase 1R132H mutation in microglia/macrophages in gliomas: Indication of a significant role of microglia/macrophages in glial tumorigenesis
Somatic mutation of Isocitrate dehydrogenase 1 (IDH1) at the locus of R132 (IDH1R132H) occurs in > 70% of WHO grades II-III gliomas and secondary glioblastomas. To date it remains unknown whether the mutation is restricted to glial tumor cells. Microglial cells are the resident macrophages in the central nervous system. Tumor-infiltrating microglial cells/macrophages are major stromal cellular components of malignant gliomas and substantially contribute to the tumor mass. Differential identification of the IDH1 R132H mutant cellular components is of particular importance for understanding of the mutation-associated tumor biology. Here we discovered that a significant portion of CD68+, Iba1+, CX3CR1+ microglial cells/macrophages also harbor the IDH1R132H mutation. The findings provide novel insights for understanding the mutation-associated tumor biology relevant to clinical applications as a predictive and/or prognostic marker or therapeutic target
A study of charged kappa in
Based on events collected by BESII, the decay
is studied. In the invariant mass
spectrum recoiling against the charged , the charged
particle is found as a low mass enhancement. If a Breit-Wigner function of
constant width is used to parameterize the kappa, its pole locates at MeV/. Also in this channel,
the decay is observed for the first time.
Its branching ratio is .Comment: 14 pages, 4 figure
Measurements of the observed cross sections for exclusive light hadrons containing at , 3.650 and 3.6648 GeV
By analyzing the data sets of 17.3, 6.5 and 1.0 pb taken,
respectively, at , 3.650 and 3.6648 GeV with the BES-II
detector at the BEPC collider, we measure the observed cross sections for
, , ,
and at the three energy
points. Based on these cross sections we set the upper limits on the observed
cross sections and the branching fractions for decay into these
final states at 90% C.L..Comment: 7 pages, 2 figure
The pole in
Using a sample of 58 million events recorded in the BESII detector,
the decay is studied. There are conspicuous
and signals. At low mass, a large
broad peak due to the is observed, and its pole position is determined
to be - MeV from the mean of six analyses.
The errors are dominated by the systematic errors.Comment: 15 pages, 6 figures, submitted to PL
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