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PubMed1997

Induction of BCL2 family member MCL1 as an early response to DNA damage.

When ML-1 human myeloid leukemia cells are exposed to DNA damaging agents, they exhibit dramatic changes in the expression of a variety of gene products. This includes an increase in p53 (wild-type), a decrease in BCL2, a p53-dependent increase in the BCL2 family member BAX, and increases in Growth Arrest and DNA Damage-inducible (GADD) genes such as GADD45; these changes occur as early events in a sequence that culminates in DNA damage-induced apoptosis. DNA damaging agents have now been tested for effects on expression of another BCL2 family member, MCL1, a gene expressed during ML-1 cell differentiation. Expression of MCL1 was found to increase upon exposure of ML-1 cells to various types of DNA damaging agents, including ionizing radiation, ultraviolet radiation, and alkylating drugs. The increase in MCL1 occurred rapidly and was transient, levels of the MCL1 mRNA being elevated within 4 h and having returned to near baseline within 24 h. An increase in the Mcl1 protein was also seen, with the maximal increase occurring at an intermediate dose of IR (5 Gray) and lesser increases occurring at either lower or higher doses. The increase in expression of MCL1 was further studied using a panel of human cell lines that includes cells containing or not containing alterations in p53 as well as cells sensitive or insensitive to the apoptosis-inducing effects of DNA damage. The DNA damage-induced increase in MCL1 mRNA did not depend upon p53 as it was seen in cells lacking functional p53. However, the increase did depend upon susceptibility to apoptosis as it was not seen in cells insensitive to apoptosis-induction by DNA damaging agents. These findings demonstrate that cytotoxic DNA damage causes an increase in the expression of MCL1 along with increases in GADD45 and BAX and a decrease in BCL2. Furthermore, while the increase in GADD45 is seen both in cells that undergo growth arrest and in cells that undergo apoptosis in response to DNA damage, alterations in the profile of expression of BCL2 family members occur exclusively in cells that undergo the apoptotic response, with some family members increasing through p53-dependent (BAX) and others through p53-independent (MCL1) pathways. Overall, expression MCL1 can increase during the induction of cell death as well as during the induction of differentiation.

Cell Survival↗

PubMed1998

Molecular features of a new human lymphoma cell line carrying both BCL2 and BCL6 gene rearrangements.

Chromosomal translocations and/or their molecular equivalents involving the BCL6 gene on 3q27 band have been suggested to be involved in the development of non-Hodgkin's lymphoma of B-cell type (B-NHL). The rearrangement of BCL6 sometimes coexists with other translocations specific to B-NHL. Here, we report a novel B-cell lymphoma cell line, YM, established from a patient with diffuse large cell lymphoma. The YM cells expressed B-cell-associated antigens in addition to mu delta/kappa monoclonal immunoglobulin. Southern blot analysis of DNA from YM cells demonstrated rearrangement of the BCL2 gene within the 5' flanking region (5'-BCL2). Polymerase chain reaction (PCR) using primer pairs for the BCL2 exons 1 and 2, and for the constant region of the immunoglobulin kappa light chain gene (IGkappa) revealed PCR products encompassing the 5'-BCL2/IGkappa fusion, indicating that the YM cells had a t(2;18)(p11;q21) translocation. The BCL6 gene was rearranged at a point within the first intron, and cloning of the rearranged BCL6 revealed unidentified sequences juxtaposed to the 5' side of the gene. The isolated clones were mapped to 16p11.2 by high resolution fluorescence in situ chromosomal hybridization. Thus, the YM cells carried a 3q27 translocation involving 16p11.2 as a partner. Chromosome painting of metaphase spreads confirmed that the YM cells had both t(2;18) and t(3;16). Northern blot analysis using a fragment immediately adjacent to the breakpoint on 16p11.2 revealed transcriptional activity within this locus. The YM cells expressed abundant transcripts with aberrant sizes from BCL2 and BCL6, indicating deregulated overexpression of the two genes resulting from the t(2;18) and t(3;16). The YM cell line will therefore be useful to study whether BCL2 and BCL6 genes collaborate in the pathogenesis of B-NHL.

Base Sequence↗

PubMed2001

Cell cycle control in cellular homeostasis during the immune response: interactions between TH1, TH2 cytokines, and Bcl2 and p53 molecules.

Cytokine regulation of lymphocyte survival may play an important role in the control of the cell cycle during the immune response both in health and disease. Expression of the Bcl2 gene promotes cell survival by countering apoptosis stimuli. The p53 protein has been implicated in the control of the cell cycle, in the synthesis and repair of DNA and in programmed cell death. TH1 and TH2 cytokines exert a mutual cross-regulation on the precursors of TH1- or TH2-type effector cells which are important mediators in directing the immune system towards the appropriate response. TH1 and TH2 cytokines have also been implicated in the modulation of the expression of cell cycle regulator genes. Therefore, the study of the relationships between TH1 and TH2 cytokines and Bcl2 and p53 molecules in healthy subjects could lead to a better understanding of the physiological regulation of the immune response and identify markers for prognostic and diagnostic indices and biotherapeutic treatment. We determined the serum levels of cytokines (IL2, IFN gamma, IL4, IL10, IL5, IL6, IL1 beta, TNF alpha, IL8), soluble receptors (sIL2R, sIL6R), Bcl2-protein and p53-antibody in a group of healthy subjects. Multivariate statistical analyses were used to study the cytokine network relationships with Bcl2-protein and p53-antibody, as they allow a simultaneous evaluation of all variables which reflects the physiological situation. Our overall results suggest that relationships exist between TH1 and TH2 cytokines and the Bcl2-protein and p53-antibody in physiological conditions. This information could now be used in experimental studies to create diagnostic and prognostic indices for the monitoring of health and disease.

Adult↗

PubMed2002

BCL2 antisense reduces prostate cancer cell survival following irradiation.

Irradiation of the prostate, delivered as external beam radiation therapy (EBRT), is currently one of the few treatment options for localized prostate cancer. While it is relatively effective, the failure rate still remains unacceptably high with a 5-year biochemical failure rate of 10-40%. Utilizing genetically engineered LNCaP prostate cancer sublines that either overexpress Bcl2 (LNCaP/S22-d) or have down-regulated Bcl2 (LNCaP/AS17-f) we investigated the influence of this antiapoptotic protein on clonogenic survival following radiation. The radiation dose response curves (2-8 Gy) for the sublines differed significantly from the parental LNCaP (LNCaP/S22d: p < 0.001 and LNCaP/AS17-f: p = 0.008). The relative survival of the sublines revealed increased survival in the Bcl2 overexpressing cells, and decreased survival in the Bcl2 down-regulated cells. These data suggest a potentially important therapeutic approach for enhancing radiosensitivity in prostate tumors via antisense oligonucleotide or other drug therapies that down-regulate Bcl2. Strategies such as these likely hold the promise of enhancing the efficacy of EBRT by decreasing tumor cell survival, reducing the incidence of tumor recurrence and improving patient outcome.

Cell Survival↗

PubMed2005

Muscle-specific BCL2 expression ameliorates muscle disease in laminin {alpha}2-deficient, but not in dystrophin-deficient, mice.

To examine the role of apoptosis in neuromuscular disease progression, we have determined whether pathogenesis in dystrophin-deficient (mdx) and laminin alpha2-deficient (Lama2-null) mice is ameliorated by overexpression of the anti-apoptosis protein BCL2 in diseased muscles. The mdx mice are a model for the human disease, Duchenne muscular dystrophy (DMD), and the Lama2-null mice are a model for human congenital muscular dystrophy type 1A (MDC1A). For these studies, we generated transgenic mice that overexpressed human BCL2 under control of muscle-specific MyoD or MRF4 promoter fragments. We then used cross-breeding to introduce the transgenes into diseased mdx or Lama2-null mice. In mdx mice, we found that overexpression of BCL2 failed to produce any significant differences in muscle pathology. In contrast, in the Lama2-null mice, we found that muscle-specific expression of BCL2 led to a several-fold increase in lifespan and an increased growth rate. Thus, BCL2-mediated apoptosis appears to play a significant role in pathogenesis of laminin alpha2 deficiency, but not of dystrophin deficiency, suggesting that therapies designed to ameliorate disease by inhibition of apoptosis are more likely to succeed in MDC1A than in DMD.

Animals↗

PubMed2006

Molecular cytogenetic evidence of t(14;18)(IGH;BCL2) in a substantial proportion of primary cutaneous follicle center lymphomas.

In contrast to nodal follicular lymphoma, limited data exist on genetic changes in primary cutaneous follicular lymphoma (primary cutaneous follicle center lymphoma according to WHO-EORTC). The detection rate of the BCL2 rearrangement, representing the characteristic t(14;18)(q32;q21) underlying follicular lymphoma, by polymerase chain reaction (PCR) has been reported to vary over a wide range (0%-41%), and only a few cases have been studied by molecular cytogenetic techniques such as fluorescence in situ hybridization (FISH). In this study, 27 primary cutaneous follicle center lymphomas were analyzed by FISH and the results compared with those obtained by PCR. FISH demonstrated translocations affecting the immunoglobulin heavy chain locus (IGH) in 14 of 27 cases (52%): a t(14;18)(q32;q21) involving BCL2 was found in 11 cases (41%), a t(3;14)(q27;q32) affecting BCL6 in 2 cases (7%), and in 1 case the partner gene of IGH could not be identified. Interestingly, PCR did not detect BCL2 rearrangement in any case. These data suggest that the t(14;18)(q32;q21) frequently occurs in primary cutaneous follicular lymphoma. The reason(s) why BCL2 rearrangements escape the detection by PCR is (are) not clear but could be due to BCL2 mutations, breakpoints outside the amplified DNA, or a high load of somatic mutations.

Adult↗

PubMed1992

Detection of rearrangements of the BCL2 major breakpoint region in follicular lymphomas. Correlation of polymerase chain reaction results with Southern blot analysis.

The translocation t(14;18)(q32;q21) occurs in 70% of follicular lymphomas and places the BCL2 proto-oncogene, normally located at 18q21, under the control of the immunoglobulin heavy chain (IgH) gene at 14q32. Its detection by the polymerase chain reaction (PCR), made possible by the close clustering of most of the BCL2 breakpoints in the major breakpoint region (MBR) of the gene, has numerous clinical applications. Since the PCR covers shorter lengths of DNA than Southern blotting, PCR-based tests may be more susceptible to microheterogeneity in breakpoint location. There have been no published studies of the impact of breakpoint microheterogeneity on the detection rate of this translocation by PCR. We studied 30 follicular lymphomas with the t(14;18), in which a BCL2 MBR rearrangement had previously been demonstrated and mapped by conventional Southern blotting, by PCR with the commonly used IgH and BCL2 MBR primers. Twenty-five cases (83%) had a junction fragment demonstrable by PCR. All three cases in which the MBR rearrangement mapped outside of the 4.3-kb HindIII fragment containing the MBR, as determined by Southern blotting, were negative by PCR. In addition, two cases with rearrangements within the HindIII fragment were also negative. All negative results were repeated at least once and were confirmed to be true negatives by actin PCR. Our results suggest that negative PCR results in this setting are attributable to small variations in BCL2 MBR breakpoint location and cannot be interpreted without the corresponding conventional Southern blotting data. With this caveat in mind, PCR analysis for the t(14;18) remains an extremely useful technique, especially in the follow-up and monitoring for minimal residual disease in previously characterized cases of follicular lymphoma.

Base Sequence↗

PubMed1997

PCR analysis of IgH and BCL2 gene rearrangement in the diagnosis of follicular lymphoma in lymph node fine-needle aspiration. A critical appraisal.

In order to improve the cytomorphologic diagnosis of malignant lymphoma on lymph node fine-needle aspiration (FNA), and to make a confident discrimination between low-grade follicular non-Hodgkin's lymphoma (NHL) and lymphoid hyperplasia, polymerase chain reaction (PCR) analysis was performed of the Ig CDR3 region and BCL2 breakpoint region in 25 nonselected cases of malignant lymphoma (17 NHL and 8 Hodgkin's disease [HD]) with histologic control, and 22 cases of lymph nodal hyperplasia with histologic and/or clinical control. Among lymphomas, IgH monoclonality was detected in 7 (77%) of 9 NHLs and BCL2 rearrangement in 3 (17.6%) of 17 NHLs, all of which were follicular centroblastic-centrocytic (FCBCC). Three BCL2/JH negative FCBCC cases were monoclonal for CDR3. Neither IgH monoclonality nor BCL2 rearrangement were found in HD. Among cytologically diagnosed lymphoid hyperplasias, one IgH polyclonal case was considered false-negative, being histologically diagnosed as lymphoplasmacytic NHL on the subsequent excisional biopsy. Another 4 cases (2 BCL2 rearranged and 2 monoclonal for IgH) were considered false-positive on the basis of histologic features or clinical control. These data indicate that the combined PCR analysis of IgH and BCL2 rearrangements can confirm a cytologic diagnosis of lymphoma in FNAs while, due to the occurrence of both false-positive and false-negative results, it is of limited value in the distinction between follicular lymphoma and lymphoid hyperplasia without morphologic or clinical support.

Biopsy, Needle↗

PubMed1990

Complementation by BCL2 and C-HA-RAS oncogenes in malignant transformation of rat embryo fibroblasts.

The BCL2 (B cell lymphoma/leukemia-2) and C-HA-RAS oncogenes encode membrane-associated proteins of 26 and 21 kilodaltons, respectively. Although RAS proteins have long been known for their ability to bind and hydrolyze GTP, recent investigations suggest that BCL2 encodes a novel GTP-binding protein (S. Haldar, C. Beatty, Y. Tsujimoto, and C. M. Croce, Nature [London] 342:195-198, 1989). Cotransfection of BCL2 and HA-RAS oncogenes resulted in morphological transformation of early-passage rodent fibroblasts, rendering these cells tumorigenic in animals and enabling them to grow in semisolid medium. In contrast, cotransfection of BCL2 with oncogenes that encode nuclear proteins (E1A and C-MYC) did not produce malignant transformation, whereas HA-RAS did complement with these genes. These findings suggest that proteins encoded by oncogenes such as BCL2 and HA-RAS, although having similar subcellular locations and perhaps similar biochemical properties, can regulate distinct complementary pathways involved in cellular transformation.

Animals↗

PubMed1996

Functional dissection of the human Bcl2 protein: sequence requirements for inhibition of apoptosis.

Overexpression of the cytoplasmic oncoprotein Bcl2 blocks programmed cell death (apoptosis) in many cellular systems. To map the sequences in Bcl2 that are necessary for its activity, we created a library of deletion-scanning mutants of this 239-amino-acid protein and tested their abilities to block staurosporine-induced fibroblast apoptosis, using a novel transient-transfection assay. Phenotypes of informative mutants were then confirmed by assaying for inhibition of steroid-induced apoptosis in stably transfected T-lymphoid cells. In accordance with earlier results, we found that Bcl2 activity was only partially reduced after deletion of the hydrophobic tail that normally anchors it in cytoplasmic membranes. Essential sequences were found in the remainder of the protein and appeared to be organized in at least two discrete functional domains. The larger, more C-terminal region (within residues 90 to 203) encompassed, but extended beyond, two oligopeptide motifs called BH1 and BH2, which are known to mediate dimerization of Bcl2 and related proteins. The second, more N-terminal regions (within residues 6 to 31) was not required for protein dimerization in vivo, but its deletion imparted a dominant negative phenotype, yielding mutants that promoted rather than inhibited apoptotic death. Residues 30 to 91 were not absolutely required for function; by deleting most of this region along with the hydrophobic tail, we derived a 155-residue mini-Bcl2 that retains significant ability to inhibit apoptosis.

Apoptosis↗

PubMed2005

Positional and functional characterisation of apoptosis related genes belonging to the BCL2 family in sheep.

Apoptosis is a process whereby cells die in a controlled manner and it is involved in animal development, tissue homeostasis and a variety of diseases. The B-cell lymphoma 2 family proteins are central regulators of intracellular apoptotic signalling cascades. This work describes the isolation of cDNA and genomic fragments from five sheep BCL2 related genes: BCL2, BCL2L1, BCL2L2, BAX and MCL1. Transcript sequences showed a high homology with BCL2 related genes from other species. Three cattle BAC probes containing the homologous BCL2, BCL2L1 and BCL2L2 genes were identified and used for comparative FISH mapping in sheep. BCL2 was localised in OAR23q27, BCL2L1 in OAR13q22 and BCL2L2 in OAR7q15-->q21. Intron polymorphisms were used for linkage mapping of BAX and MCL1, which were mapped on OAR14 and OAR1 respectively. Moreover, a BCL2L1 pseudogene was also identified and linkage mapped on OAR2. The expression of these genes was analysed in mammary gland, ovary, intestine and brain which are target tissues for sheep pathological processes where apoptosis is involved.

Animals↗

PubMed2005

Medium from irradiated cells induces dose-dependent mitochondrial changes and BCL2 responses in unirradiated human keratinocytes.

Exposure of unirradiated human keratinocytes to irradiated cell conditioned medium (ICCM) is known to cause a cascade of events that leads to reproductive death and apoptosis. This study investigates the effect of ICCM on clonogenic survival, mitochondrial mass and BCL2 expression in unirradiated keratinocytes. Exposure to 5 mGy, 0.5 Gy and 5 Gy ICCM resulted in a significant decrease in clonogenic survival. Human keratinocytes incubated with ICCM containing an antioxidant, N-acetylcysteine, showed no significant decrease in clonogenic survival. HPV-G cells incubated with ICCM containing a caspase 9 inhibitor showed no significant decrease in clonogenic survival when the ICCM dose was < or =0.5 Gy. A significant increase in mitochondrial mass per cell was observed after exposure to 5 mGy and 0.5 Gy ICCM. A change in the distribution of the mitochondria from a diffuse cytoplasmic distribution to a more densely concentrated perinuclear distribution was also observed at these doses. No significant increase in mitochondrial mass or change in distribution of the mitochondria was found for 5 Gy ICCM. Low BCL2 expression was observed in HPV-G cells exposed to 5 mGy or 0.5 Gy ICCM, whereas a large significant increase in BCL2 expression was observed in cells exposed to 5 Gy ICCM. This study has shown that low-dose irradiation can cause cells to produce medium-borne signals that can cause mitochondrial changes and the induction of BCL2 expression in unirradiated HPV-G cells. The dose dependence of the mitochondrial changes and BCL2 expression suggests that the mechanisms may be aimed at control of response to radiation at the population level through signaling pathways.

Bystander Effect↗

PubMed2006

Posttranslational modifications of Bcl2 family members--a potential therapeutic target for human malignancy.

Apoptosis is a process that can occur normally, such as during tissue remodeling, embryogenesis or abnormally during certain pathologies, such as cancer. The identification of the Bcl2 as well as IAP family members has suggested that excessive inhibition of apoptosis may constitute a common feature of all known human cancers-the ability to influence their onset, progression and outcome. Bcl2 family proteins are frequently regulated by phosphorylation that affects their activity and conformation. The structural analysis of antiapoptotic members of Bcl2 family has contributed to a better understanding of the functional domains including the discovery of an unstructured "loop region" (LR) near the N-terminus exposed to the cytoplasm. The antiapoptotic members of Bcl2 family such as Bcl2/Bcl-xL/Mcl-1 are phosphorylated on specific serine/threonine residues within this unstructured loop in response to diverse stimuli including treatment with chemotherapeutic taxanes, survival factor addition or chemopreventive agents. In most instances, such phosphorylation has been associated with the loss of their biological function. The chemoresistant tumors overexpress Bcl2/Bcl-xL/Mcl-1. To this end, the apoptosis yielding effect due to phosphorylation of antiapoptotic Bcl2 family members is quite interesting. Phosphorylation-dephosphorylation pathway of these antiapoptotic proteins should be an ideal molecular target for therapy of subpopulation of cancer in which these death repressors are essential prognostic markers. Thus, further gaining the knowledge on the mechanism of inactivation of Bcl2/Bcl-xL/Mcl-1 by phosphorylation might be of paramount importance to therapy for human malignancies in which overexpression of these antiapoptotic proteins plays an essential role.

Alanine↗

PubMed1999

Bcl2 and Bax expression in naevi and melanomas and their relation to ploidy status and proliferation.

Twenty-five naevi, 53 primary melanomas, 36 melanoma metastases were stained immunohistochemically for the presence of Bcl2, Bax and Ki-67 antigen in order to define the relation between apoptosis regulators and proliferative activity. Additionally, ploidy status and S-phase were measured. Bax demonstrated a tendency to increase and Bcl2 was decreasing along with melanoma progression. In the group of euploid cases Bcl2 showed a strong significant correlation with Bax expression (p = 0.0001) and both Bcl2 and Bax correlated with Ki-67 expression and S-phase. In the group of aneuploid cases only the correlation Bcl2-Ki-67 was preserved. Others did not reach the level of statistical significance.

Adolescent↗

PubMedDate not supplied

Bcl2, p53 and clinical outcome in a series of 138 operable breast cancer patients.

Medical oncologists are increasingly interested in identifying reliable prognostic factors for breast cancer in order to distinguish subsets of breast cancer patients and to optimize therapeutic approaches. Among them, the p53 tumor suppressor gene and bcl2 protein continue to be extensively studied, but their role remains to be defined. Moreover the mechanism of action by which they affect cell kinetics has to be clarified, particularly with respect to the balance between cell proliferation and apoptosis. We studied 138 operable breast cancer patients in order to verify the relationships of p53 and bcl2 proteins with better known clinicopathological features and their impact on the clinical outcomes of relapse-free survival (RFS) and overall survival (OS). Our data indicated a significant relationship between bcl2 expression and steroid receptor positive status, wild-type p53 and low proliferative index. Mutant p53 accumulation was found to be related to the absence of steroid receptors and high proliferation. Both were significant markers of better prognosis in univariate analysis. Multivariate analysis confirmed the favorable impact of bcl2 on both RFS and OS. On the contrary, we failed to observe any prognostic role for p53 status. We describe herein an independent favorable prognostic impact for patients with positive bcl2 expression that appears to be worthy of larger confirmatory study. On the contrary, our series seems to confirm the decreasing prognostic relevance of p53 in clinical practice.

Aged↗

PubMedDate not supplied

BCL2 and BAX expression in hyperplastic and dysplastic rectal polyps.

BACKGROUND/AIMS: Members of the gene family that includes BCL2 and BAX are functionally antagonists in the apoptosis process and they have been observed in normal and neoplastic tissues. The aim of this study is to investigate the combined effects of BCL2 and BAX protein in normal mucosa, dysplastic and hyperplastic polyps of the rectum. METHODOLOGY: We studied BCL2 and BAX protein expression in 40 cases of adenomatous polyps all located in the rectum, with different dysplastic gradings, and the mean time in 10 cases of normal rectal mucosa. RESULTS: BCL2 expression was found more frequently in hyperplastic and in low dysplastic polyps with moderate and strong positivity compared to moderate and severe dysplasia. BAX expression was found in normal mucosa in hyperplastic and dysplastic polyps, the immunoreactivity was prevalently moderate and strong. CONCLUSIONS: These preliminary data suggest that BCL2 and BAX confirm a probably different role in apoptosis. Nevertheless, it is important to know the relation between the molecular pathways of apoptosis, the defective mismatch repair and the tumor suppressor genes associated with an increased mutation rate in cancerogenesis of the colorectum.

Adenoma↗

PubMed2001

bcl2, p53 and bax in thyroid tumors and their relation to apoptosis.

Twenty five thyroid tumors were investigated by immunohistochemistry for the presence of apoptosis, expression of p53, bax and bcl2. In nine adenomas (average age 40) the rate of p53 positive cells was 5.7%, while it was 13.3% for bax and 41.7% for bcl2 in the tumor cells. In six follicular carcinomas (average age 56) p53 positivity was obtained for 71.1%, while bax and bcl2 positivity constituted 3.4% and 2.5%, respectively. In ten papillary adenocarcinomas (average age 42) p53 was positive in 39.6%, but bax and bcl2 were positive in 3.4% and 3% of the tumor cells, respectively. Almost no signs of spontaneous apoptosis were found in any of the cases. Determination of p53, bax and bcl2 ratio in thyroid tumors may contribute to the differentiation between follicular adenomas and carcinomas.

Adenocarcinoma, Follicular↗

PubMed2001

BCL2 and BAX mRNA concentration profile in fibrillary astrocytoma.

A high level of the BCL2 protein and the lack of apoptosis promoting protein BAX are beginning to be treated as markers of cellular resistance to anti-neoplastic drugs. The object of the study were specimens from stereotactic biopsy of Astrocytoma fibrillare in the central brain area, inaccessible to conventional surgery. The cytological preparations have been evaluated with histopathological and immunohistochemical methods in order to determine the origin of the tumour and assess cell proliferation activity. The molecular analysis conducted in order to determine the sensitivity of the tumour to radio- or chemotherapy included the determination of the number of mRNA BCL2 alpha and beta molecules and of BAX in 1 microg total RNA obtained from microscope slides. A higher expression of BAX than of BCL2-alpha is a prognosis for a positive result of chemo- or radiotherapy. A trace number of mRNA BCL2-beta molecules and a smaller number of mRNA BCL2-alpha molecules than mRNA BAX is a good prognosis for therapy.

Astrocytoma↗