The Histological Distribution of Blood Group Substances a and B in Man

Szulman, A. E.

doi:10.1084/jem.111.6.785

Cited by 396 publications

(138 citation statements)

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“…We failed to identify either A (0 from 5 group A specimens) or B (0 from 1 group B specimen) BGIs while the H and Y isoantigens were identified in 10 of 12 specimens (see Table II). Szulman (1960Szulman ( ,1962Szulman ( ,1964 but which differs somewhat from those observations made by Gupta et al (1973) who found an increase in BGIs in benign prostatic hypertrophy. In the present study no such increase was found.…”

Section: Resultscontrasting

confidence: 94%

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Are blood group isoantigens lost from malignant prostatic epithelium? Immunohistochemical support for the preservation of the H isoantigen

Vowden¹,

Lowe²,

Lennox³

et al. 1986

Br J Cancer

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Summary Previous studies while demonstrating the presence of blood group isoantigens on normal prostatic epithelium have failed to identify such antigens on malignant prostatic tissue. Using a series of blood group specific monoclonal antibodies directed towards the A, B, H and Y antigens we have reinvestigated blood group isoantigen expression in both benign prostatic hypertrophy and prostatic adenocarcinoma. Results obtained from areas of benign prostatic hypertrophy are in broad agreement with those published however though we were unable to detect either A or B blood group isoantigens Type 2H and Y isoantigens were identified in 10 of the 12 tumours. These findings, while differing from previously reported results, lend support to the suggested connection between ontogenesis, oncogenesis and blood group isoantigen expression and also support the proposed link between Type 2 structures and malignant transformation.

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Section: Resultscontrasting

confidence: 94%

“…The pattern of epithelial A, B and H isoantigen expression during both foetal development and adult life has been described by Szulman (1960Szulman ( ,1962Szulman ( ,1964. These studies have suggested that a relationship exists between blood group isoantigen (BGI) expression and ontogenesis.…”

mentioning

confidence: 99%

Are blood group isoantigens lost from malignant prostatic epithelium? Immunohistochemical support for the preservation of the H isoantigen

Vowden¹,

Lowe²,

Lennox³

et al. 1986

Br J Cancer

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“…Since A/B antigens are not only expressed on RBCs but have a wide tissue distribution, the antihost A/B antibodies produced after minor or bidirectional ABO-incompatible SCT may theoretically bind to and damage the host endothelium, which can potentially trigger GVHD. 20 In support of this hypothesis, it has been shown that patients receiving minor ABO-incompatible BMT had a higher risk of developing GVHD. 9 However, we found no significantly increased risk of developing acute or chronic GVHD in minor or bidirectional ABO-incompatible PBSCT in the present study, and other studies have also not demonstrated this difference.…”

Section: Discussionmentioning

confidence: 93%

Impact of ABO incompatibility on outcome after allogeneic peripheral blood stem cell transplantation

Kim

et al. 2005

Bone Marrow Transplant

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Summary:Few studies have addressed the incidence of graft-versushost disease (GVHD) or survival after ABO-incompatible allogeneic peripheral blood stem cell transplantation (PBSCT). We analyzed the clinical outcome of ABO incompatibility after allogeneic PBSCT. A total of 89 consecutive adult patients with hematological diseases including 49 ABO-identical, 20 major, 15 minor, and five bidirectional ABO-incompatible transplants were enrolled from four medical centers in Korea. No significant difference in engraftment times, graft failure, or transfusion requirements between groups was noted. A clinical diagnosis of severe immune hemolysis or pure red cell aplasia was not made for any patient after transplantation. The incidence of acute or chronic GVHD did not statistically differ between groups. With a median followup duration of 13 months (range, 0.5-61 months), the 3-year overall survival estimates for the ABO-identical, major/bidirectional, and minor group were 44.6.079.0, 43.1711.6, and 43.8713.5%, respectively (P ¼ 0.8652), while the 3-year disease-free survival estimates were 33.877.6, 39.9711.4, and 45.7713.1%, respectively (P ¼ 0.8546). We observed that time to neutrophil, platelet, and red blood cell engraftment, transfusion requirements, incidence of acute or chronic GVHD, relapse, and survival were not influenced by ABO incompatibility after allogeneic PBSCT from HLAmatched sibling donors. Bone Marrow Transplantation (2005) 35, 489-495.

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“…In this regard it is of interest that ABO antigens are not only expressed on RBC but also on endothelial cells as well as on plasma proteins such as the von Willebrand factor. 24 Thus, ABO antigens show a broad distribution throughout body tissues, 25,26 and anti-host A/B antibodies produced after minor or bidirectional ABOincompatible SCT may bind to and damage the host endo-thelium potentially triggering GVHD. In support of this hypothesis, Bacigalupo and colleagues 9 found a higher risk of developing acute GVHD in patients receiving minor ABO-incompatible SCT when compared to ABO-identical SCT.…”

Section: Discussionmentioning

confidence: 99%

Consequences of ABO incompatibility in allogeneic hematopoietic stem cell transplantation

Stüssi

Muntwyler

Passweg

et al. 2002

Bone Marrow Transplant

105

103

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Summary:Aside from causing hemolytic reactions the ABO blood group system does not have an impact on outcome after allogeneic bone marrow or peripheral blood stem cell transplantation (SCT). However, only a few studies have addressed the effect of ABO incompatibility on the incidence of GVHD, time to engraftment, relapse and survival. Therefore, we performed a retrospective twocenter analysis of 562 consecutive patients receiving allogeneic SCT, including 361 ABO-identical, 98 minor, 86 major and 17 bidirectional ABO-incompatible SCT. In multivariate analysis adjusted for potential confounders survival was significantly associated with ABO incompatibility (P = 0.006). Compared to ABO-identical SCT, bidirectional ABO incompatibility increased the risk significantly (RR, 2.8; 95% CI, 1.5-5.1; P = 0.0009), whereas survival of patients with minor (RR, 1.2; 95% CI, 0.9-1.7; P = 0.27), or major ABO-incompatible SCT (RR, 1.3; 95% CI, 0.9-1.8; P = 0.18) was not significantly different. RBC engraftment was delayed in major ABO-incompatible SCT (RR, 0.66; 95% CI, 0.51-0.85; P = 0.001). The incidence of acute GVHD (grade I-IV) was higher in minor ABO-incompatible SCT as compared to ABO identity (RR, 2.8; 95% CI, 1.3-5.9, P = 0.009). This difference was limited to mild GVHD; in moderate-to-severe GVHD (grade II-IV) no significant difference was found among the groups (P = 0.53). The relapse rate was not influenced by ABO incompatibility (P = 0.78). In conclusion, these results suggest that ABO incompatibility represents a risk factor not only for post-transplant hemolysis, but also for survival and the rate of mild GVHD after allogeneic SCT. In contrast to RBC transfusion and solid organ transplantation, approximately one-third of all allogeneic bone marrow or peripheral blood stem cell transplantations (SCT) are performed across the ABO blood group barrier. 1,2 There are three groups of ABO incompatibility: minor ABO incompatibility (eg from an O-type donor to an A-type recipient) is characterized by the ability of donor B lymphocytes to produce anti-recipient isoagglutinins. In clinical practice, preformed anti-host isoagglutinins are removed from the stem cell inoculum by centrifugation prior to transplantation. In contrast, major ABO-incompatible SCT (eg from an A-type donor to an O-type recipient) is characterized by the presence of preformed anti-donor isoagglutinins. In bidirectional ABO incompatibility (eg A-type donor to a B-type recipient), a combination of both the major and minor barrier has to be overcome.It is well known that ABO-incompatible SCT increases the risk of hemolytic reactions in all groups, 3 but it is believed that ABO incompatibility between donor and recipient is of no importance for the overall clinical outcome. [4][5][6][7] Nevertheless, over the past two decades, improvements in GVHD prophylaxis and transplantation technologies have led to a generally lower overall mortality, theoretically unraveling an effect of the ABO system on the outcome of SCT. In particular, there are several lines of ...

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The Histological Distribution of Blood Group Substances a and B in Man

Cited by 396 publications

References 11 publications

Are blood group isoantigens lost from malignant prostatic epithelium? Immunohistochemical support for the preservation of the H isoantigen

Are blood group isoantigens lost from malignant prostatic epithelium? Immunohistochemical support for the preservation of the H isoantigen

Impact of ABO incompatibility on outcome after allogeneic peripheral blood stem cell transplantation

Consequences of ABO incompatibility in allogeneic hematopoietic stem cell transplantation

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