Tự học Tiếng Anh chuyên ngành sinh học thông qua dịch tài liệu.

[Ho Huu Tho]

#21.8
<link rel="File-List" href="file://localhost/Users/hohuutho/Library/Caches/TemporaryItems/msoclip/0/clip_filelist.xml"> <!--[if gte mso 9]><xml> <o:OfficeDocumentSettings> <o:AllowPNG/> </o:OfficeDocumentSettings> </xml><![endif]--><!--[if gte mso 9]><xml> <w:WordDocument> <w:Zoom>0</w:Zoom> <w:TrackMoves>false</w:TrackMoves> <w:TrackFormatting/> <wunctuationKerning/> <wrawingGridHorizontalSpacing>18 pt</wrawingGridHorizontalSpacing> <wrawingGridVerticalSpacing>18 pt</wrawingGridVerticalSpacing> <wisplayHorizontalDrawingGridEvery>0</wisplayHorizontalDrawingGridEvery> <wisplayVerticalDrawingGridEvery>0</wisplayVerticalDrawingGridEvery> <w:ValidateAgainstSchemas/> <w:SaveIfXMLInvalid>false</w:SaveIfXMLInvalid> <w:IgnoreMixedContent>false</w:IgnoreMixedContent> <w:AlwaysShowPlaceholderText>false</w:AlwaysShowPlaceholderText> <w:Compatibility> <w:BreakWrappedTables/> <wontGrowAutofit/> <wontAutofitConstrainedTables/> <wontVertAlignInTxbx/> </w:Compatibility> </w:WordDocument> </xml><![endif]--><!--[if gte mso 9]><xml> <w:LatentStyles DefLockedState="false" LatentStyleCount="276"> </w:LatentStyles> </xml><![endif]--> <style> <!-- /* Font Definitions */ @font-face {font-family:Arial; panose-1:2 11 6 4 2 2 2 2 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:Cambria; panose-1:2 4 5 3 5 4 6 3 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:JansonText-Roman; panose-1:0 0 0 0 0 0 0 0 0 0; mso-font-alt:Cambria; mso-font-charset:77; mso-generic-font-family:auto; mso-font-formatther; mso-font-pitch:auto; mso-font-signature:3 0 0 0 1 0;} /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-parent:""; margin-top:0cm; margin-right:0cm; margin-bottom:10.0pt; margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:Cambria; mso-fareast-theme-font:minor-latin; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:"Times New Roman"; mso-bidi-theme-font:minor-bidi;} @page Section1 {size:595.0pt 842.0pt; margin:72.0pt 90.0pt 72.0pt 90.0pt; mso-header-margin:35.4pt; mso-footer-margin:35.4pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> </style> <!--[if gte mso 10]> <style> /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-parent:""; mso-padding-alt:0cm 5.4pt 0cm 5.4pt; mso-para-margin-top:0cm; mso-para-margin-right:0cm; mso-para-margin-bottom:10.0pt; mso-para-margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin;} </style> <![endif]--> <!--StartFragment--> Oncogenic cancers can also start when proto-oncogenes are placed near antibody genes, which are highly expressed during infection. In Burkitt’s lymphoma, which causes a large tumor to form in the lymph glands near the jaw, infection with Epstein-Barr virus in B cells places a protooncogene on chromosome 8 next to an antibody gene on chromosome 14. The cancer cells of these patients have the telltale chromosomal exchange.<o></o>

Các ung thư gây ra bởi gen sinh ung thư cũng có thể khởi phát khi các gen tiền ung thư được xếp gần các gen của kháng thể, đó là những gen được biểu hiện mạnh trong quá trình nhiễm trùng. Trong ung thư lympho Burkitt, một bệnh ung thư hình thành khối u lớn tại các tuyến bạch huyết cạnh quai hàm, nhiễm vi rút Epstein-Barr trong các tế bào B khiến gen tiền ung thư trên nhiễm sắc thể số 8 được xếp cạnh một gen kháng thể trên nhiễm sắc thể số 14. Các tế bào ung thư của những bệnh nhân này có sự trao đổi nhiễm sắc thể mang tính chỉ điểm.

 

[Ho Huu Tho]

#21.9
<link rel="File-List" href="file://localhost/Users/hohuutho/Library/Caches/TemporaryItems/msoclip/0/clip_filelist.xml"> <!--[if gte mso 9]><xml> <o:OfficeDocumentSettings> <o:AllowPNG/> </o:OfficeDocumentSettings> </xml><![endif]--><!--[if gte mso 9]><xml> <w:WordDocument> <w:Zoom>0</w:Zoom> <w:TrackMoves>false</w:TrackMoves> <w:TrackFormatting/> <wunctuationKerning/> <wrawingGridHorizontalSpacing>18 pt</wrawingGridHorizontalSpacing> <wrawingGridVerticalSpacing>18 pt</wrawingGridVerticalSpacing> <wisplayHorizontalDrawingGridEvery>0</wisplayHorizontalDrawingGridEvery> <wisplayVerticalDrawingGridEvery>0</wisplayVerticalDrawingGridEvery> <w:ValidateAgainstSchemas/> <w:SaveIfXMLInvalid>false</w:SaveIfXMLInvalid> <w:IgnoreMixedContent>false</w:IgnoreMixedContent> <w:AlwaysShowPlaceholderText>false</w:AlwaysShowPlaceholderText> <w:Compatibility> <w:BreakWrappedTables/> <wontGrowAutofit/> <wontAutofitConstrainedTables/> <wontVertAlignInTxbx/> </w:Compatibility> </w:WordDocument> </xml><![endif]--><!--[if gte mso 9]><xml> <w:LatentStyles DefLockedState="false" LatentStyleCount="276"> </w:LatentStyles> </xml><![endif]--> <style> <!-- /* Font Definitions */ @font-face {font-family:Arial; panose-1:2 11 6 4 2 2 2 2 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:Cambria; panose-1:2 4 5 3 5 4 6 3 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:JansonText-Roman; panose-1:0 0 0 0 0 0 0 0 0 0; mso-font-alt:Cambria; mso-font-charset:77; mso-generic-font-family:auto; mso-font-formatther; mso-font-pitch:auto; mso-font-signature:3 0 0 0 1 0;} /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-parent:""; margin-top:0cm; margin-right:0cm; margin-bottom:10.0pt; margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:Cambria; mso-fareast-theme-font:minor-latin; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:"Times New Roman"; mso-bidi-theme-font:minor-bidi;} @page Section1 {size:595.0pt 842.0pt; margin:72.0pt 90.0pt 72.0pt 90.0pt; mso-header-margin:35.4pt; mso-footer-margin:35.4pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> </style> <!--[if gte mso 10]> <style> /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-parent:""; mso-padding-alt:0cm 5.4pt 0cm 5.4pt; mso-para-margin-top:0cm; mso-para-margin-right:0cm; mso-para-margin-bottom:10.0pt; mso-para-margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin;} </style> <![endif]--> <!--StartFragment--> Chronic Myeloid Leukemia and the BCR-ABL Fusion Gene<o></o>
Sometimes a proto-oncogene that has been moved next to a highly expressed gene is transcribed and translated with the second gene. The result is called a fusion protein, which then causes cancer. Discovery of the first cancercausing fusion protein was a milestone in medical history, and has recently received renewed attention because of development of a highly effective drug treatment. This fusion protein forms in people with a tiny, unusual chromosome, named the Philadelphia chromosome, who also have chronic myeloid leukemia (CML). The errant chromosome forms from a translocation of the tip of chromosome 9 to the minuscule chromosome 22, and transfer of a bit of chromosome 22 material to chromosome 9.<o></o>
<!--EndFragment-->

 

[Ho Huu Tho]

#21.9
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Sometimes a proto-oncogene that has been moved next to a highly expressed gene is transcribed and translated with the second gene. The result is called a fusion protein, which then causes cancer. Discovery of the first cancercausing fusion protein was a milestone in medical history, and has recently received renewed attention because of development of a highly effective drug treatment. This fusion protein forms in people with a tiny, unusual chromosome, named the Philadelphia chromosome, who also have chronic myeloid leukemia (CML). The errant chromosome forms from a translocation of the tip of chromosome 9 to the minuscule chromosome 22, and transfer of a bit of chromosome 22 material to chromosome 9.<o></o>

Bệnh bạch cầu tủy mạn và gen tiếp hợp BCR-ABL
Đôi khi gen tiền ung thư được chuyển đến gần gen có mức độ biểu hiện cao lại được phiên mã và dịch mã cùng với gen thứ hai này. Sản phẩm tạo thành có tên gọi là protein tiếp hợp và có tác dụng gây ra ung thư. Việc khám phá ra protein tiếp hợp đầu tiên gây ung thư là một sự kiện quan trọng trong lịch sử y học và gần đây lại thu hút nhiều sự chú ý do sự phát triển thuốc điều trị có hiệu quả cao. Protein tiếp hợp này tạo ra trong người đó một nhiễm sắc thể nhỏ xíu bất thường có tên gọi là nhiễm sắc thể Philadelphia và cũng là người mắc bệnh bạch cầu tủy mạn (CML). Nhiễm sắc thể dị thường hình thành do sự chuyển đoạn của đầu mút nhiễm sắc thể số 9 và nhiễm sắc thể nhỏ xíu số 22, và chuyển một phần nhỏ vật chất của nhiễm sắc thể số 22 sang nhiễm sắc thể số 9.

 

[Ho Huu Tho]

#21.10
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mso-bidi-theme-font:minor-bidi;} @page Section1 {size:595.0pt 842.0pt; margin:72.0pt 90.0pt 72.0pt 90.0pt; mso-header-margin:35.4pt; mso-footer-margin:35.4pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> </style> <!--[if gte mso 10]> <style> /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-parent:""; mso-padding-alt:0cm 5.4pt 0cm 5.4pt; mso-para-margin-top:0cm; mso-para-margin-right:0cm; mso-para-margin-bottom:10.0pt; mso-para-margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin;} </style> <![endif]--> <!--StartFragment--> Researchers discovered the Philadelphia chromosome in 1958, when two men were hospitalized in that city complaining of chronic fatigue. Each man’s blood had far too many white blood cells, which led to the diagnosis of leukemia. Their blood samples were sent to two young investigators at the University of Pennsylvania, assistant professor Peter Nowell and graduate student David Hungerford, who detected the small, unusual chromosome. At that time, cancer was not considered to be a genetic disorder, and so the apparent association of leukemia with a chromosomal abnormality was a surprise. With time, cases accumulated, and the link strengthened.<o></o>
<!--EndFragment-->

 

[Ho Huu Tho]

#21.10
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mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-parent:""; mso-padding-alt:0cm 5.4pt 0cm 5.4pt; mso-para-margin-top:0cm; mso-para-margin-right:0cm; mso-para-margin-bottom:10.0pt; mso-para-margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin;} </style> <![endif]--> <!--StartFragment--> <link rel="File-List" href="file://localhost/Users/hohuutho/Library/Caches/TemporaryItems/msoclip/0/clip_filelist.xml"> <!--[if gte mso 9]><xml> <o:OfficeDocumentSettings> <o:AllowPNG/> </o:OfficeDocumentSettings> </xml><![endif]--><!--[if gte mso 9]><xml> <w:WordDocument> <w:Zoom>0</w:Zoom> <w:TrackMoves>false</w:TrackMoves> <w:TrackFormatting/> <wunctuationKerning/> <wrawingGridHorizontalSpacing>18 pt</wrawingGridHorizontalSpacing> <wrawingGridVerticalSpacing>18 pt</wrawingGridVerticalSpacing> <wisplayHorizontalDrawingGridEvery>0</wisplayHorizontalDrawingGridEvery> <wisplayVerticalDrawingGridEvery>0</wisplayVerticalDrawingGridEvery> <w:ValidateAgainstSchemas/> <w:SaveIfXMLInvalid>false</w:SaveIfXMLInvalid> <w:IgnoreMixedContent>false</w:IgnoreMixedContent> <w:AlwaysShowPlaceholderText>false</w:AlwaysShowPlaceholderText> <w:Compatibility> <w:BreakWrappedTables/> <wontGrowAutofit/> <wontAutofitConstrainedTables/> <wontVertAlignInTxbx/> </w:Compatibility> </w:WordDocument> </xml><![endif]--><!--[if gte mso 9]><xml> <w:LatentStyles DefLockedState="false" LatentStyleCount="276"> </w:LatentStyles> </xml><![endif]--> <style> <!-- /* Font Definitions */ @font-face {font-family:Arial; panose-1:2 11 6 4 2 2 2 2 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:Cambria; panose-1:2 4 5 3 5 4 6 3 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:JansonText-Roman; panose-1:0 0 0 0 0 0 0 0 0 0; mso-font-alt:Cambria; mso-font-charset:77; mso-generic-font-family:auto; mso-font-formatther; mso-font-pitch:auto; mso-font-signature:3 0 0 0 1 0;} /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-parent:""; margin-top:0cm; margin-right:0cm; margin-bottom:10.0pt; margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:Cambria; mso-fareast-theme-font:minor-latin; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:"Times New Roman"; mso-bidi-theme-font:minor-bidi;} @page Section1 {size:595.0pt 842.0pt; margin:72.0pt 90.0pt 72.0pt 90.0pt; mso-header-margin:35.4pt; mso-footer-margin:35.4pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> </style> <!--[if gte mso 10]> <style> /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-parent:""; mso-padding-alt:0cm 5.4pt 0cm 5.4pt; mso-para-margin-top:0cm; mso-para-margin-right:0cm; mso-para-margin-bottom:10.0pt; mso-para-margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin;} </style> <![endif]--> <!--StartFragment--> Researchers discovered the Philadelphia chromosome in 1958, when two men were hospitalized in that city complaining of chronic fatigue. Each man’s blood had far too many white blood cells, which led to the diagnosis of leukemia. Their blood samples were sent to two young investigators at the University of Pennsylvania, assistant professor Peter Nowell and graduate student David Hungerford, who detected the small, unusual chromosome. At that time, cancer was not considered to be a genetic disorder, and so the apparent association of leukemia with a chromosomal abnormality was a surprise. With time, cases accumulated, and the link strengthened.<o></o>

Các nhà khoa học khám phá ra nhiễm sắc thể Philadelphia vào năm 1958, khi có hai người đàn ông phải nhập viện trong thành phố đó và phàn nàn là bị mệt mỏi trường diễn. Máu của mỗi người đàn ông có quá nhiều tế bào bạch cầu và điều này đã đưa đến chẩn đoán là bệnh bạch cầu. Mẫu máu của họ được gửi đến hai nhà nghiên cứu trẻ ở đại học Pennsylvania là trợ lý giáo sư Peter Nowell và sinh viên sau đại học David Hungerford, là người đã phát hiện ra nhiễm sắc thể nhỏ và bất thường này. Vào thời gian đó, ung thư không được coi là bệnh liên quan đến di truyền và bởi vậy mối liên hệ rõ ràng giữa bệnh bạch cầu với bất thường nhiễm sắc thể là một điều ngạc nhiên. Theo thời gian thì số ca bệnh tăng lên và mối liên quan này được củng cố.

 

[Ho Huu Tho]

#21.11
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mso-bidi-theme-font:minor-bidi;} @page Section1 {size:595.0pt 842.0pt; margin:72.0pt 90.0pt 72.0pt 90.0pt; mso-header-margin:35.4pt; mso-footer-margin:35.4pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> </style> <!--[if gte mso 10]> <style> /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-parent:""; mso-padding-alt:0cm 5.4pt 0cm 5.4pt; mso-para-margin-top:0cm; mso-para-margin-right:0cm; mso-para-margin-bottom:10.0pt; mso-para-margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin;} </style> <![endif]--> <!--StartFragment--> By 1972, chromosome banding technology made it possible to describe the nature of the material that makes up the Philadelphia chromosome, and to infer its origin. Janet Rowley at the University of Chicago identified the translocation between chromosomes 9 and 22 that produces the tiny Philadelphia chromosome. By 1984, other researchers discovered the genes that are juxtaposed in the translocation. One gene from chromosome 9 is called the Abelson oncogene (ABL), and the other gene, from chromosome 22, is called the breakpoint cluster region (BCR).<o></o>
<!--EndFragment--> <o></o>
<!--EndFragment-->

 

[Ho Huu Tho]

#21.11
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panose-1:2 11 6 4 2 2 2 2 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:Cambria; panose-1:2 4 5 3 5 4 6 3 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:JansonText-Roman; panose-1:0 0 0 0 0 0 0 0 0 0; mso-font-alt:Cambria; mso-font-charset:77; mso-generic-font-family:auto; mso-font-formatther; mso-font-pitch:auto; mso-font-signature:3 0 0 0 1 0;} /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-parent:""; margin-top:0cm; margin-right:0cm; margin-bottom:10.0pt; margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:Cambria; mso-fareast-theme-font:minor-latin; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:"Times New Roman"; mso-bidi-theme-font:minor-bidi;} @page Section1 {size:595.0pt 842.0pt; margin:72.0pt 90.0pt 72.0pt 90.0pt; mso-header-margin:35.4pt; mso-footer-margin:35.4pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> </style> <!--[if gte mso 10]> <style> /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-parent:""; mso-padding-alt:0cm 5.4pt 0cm 5.4pt; mso-para-margin-top:0cm; mso-para-margin-right:0cm; mso-para-margin-bottom:10.0pt; mso-para-margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin;} </style> <![endif]--> <!--StartFragment--> By 1972, chromosome banding technology made it possible to describe the nature of the material that makes up the Philadelphia chromosome, and to infer its origin. Janet Rowley at the University of Chicago identified the translocation between chromosomes 9 and 22 that produces the tiny Philadelphia chromosome. By 1984, other researchers discovered the genes that are juxtaposed in the translocation. One gene from chromosome 9 is called the Abelson oncogene (ABL), and the other gene, from chromosome 22, is called the breakpoint cluster region (BCR).<o></o>

Đến năm 1972, kỹ thuật nhuộm băng nhiễm sắc thể giúp người ta có thể mô tả thực chất vật liệu cấu thành nhiễm sắc thể Philadelphia và luận đoán về nguồn gốc của nó. Janet Rowley ở Đại học Chicago xác định sự chuyển đoạn giữa nhiễm sắc thể số 9 và số 22 để tạo thành nhiễm sắc thể nhỏ xíu Philadelphia. Đến năm 1984, các nhà khoa học khác đã khám phá ra các gen được xếp cạnh nhau trong chuyển đoạn. Một gen trên nhiễm sắc thể số 9 có tên gọi là gen sinh ung thư Abelson (ABL) và gen còn lại từ nhiễm sắc thể số 22 có tên gọi là breakpoint cluster region (BCR).

 

[Ho Huu Tho]

#21.12
<link rel="File-List" href="file://localhost/Users/hohuutho/Library/Caches/TemporaryItems/msoclip/0/clip_filelist.xml"> <!--[if gte mso 9]><xml> <o:OfficeDocumentSettings> <o:AllowPNG/> </o:OfficeDocumentSettings> </xml><![endif]--><!--[if gte mso 9]><xml> <w:WordDocument> <w:Zoom>0</w:Zoom> <w:TrackMoves>false</w:TrackMoves> <w:TrackFormatting/> <wunctuationKerning/> <wrawingGridHorizontalSpacing>18 pt</wrawingGridHorizontalSpacing> <wrawingGridVerticalSpacing>18 pt</wrawingGridVerticalSpacing> <wisplayHorizontalDrawingGridEvery>0</wisplayHorizontalDrawingGridEvery> <wisplayVerticalDrawingGridEvery>0</wisplayVerticalDrawingGridEvery> <w:ValidateAgainstSchemas/> <w:SaveIfXMLInvalid>false</w:SaveIfXMLInvalid> <w:IgnoreMixedContent>false</w:IgnoreMixedContent> <w:AlwaysShowPlaceholderText>false</w:AlwaysShowPlaceholderText> <w:Compatibility> <w:BreakWrappedTables/> <wontGrowAutofit/> <wontAutofitConstrainedTables/> <wontVertAlignInTxbx/> </w:Compatibility> </w:WordDocument> </xml><![endif]--><!--[if gte mso 9]><xml> <w:LatentStyles DefLockedState="false" LatentStyleCount="276"> </w:LatentStyles> </xml><![endif]--> <style> <!-- /* Font Definitions */ @font-face {font-family:Arial; panose-1:2 11 6 4 2 2 2 2 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:Cambria; panose-1:2 4 5 3 5 4 6 3 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:JansonText-Roman; panose-1:0 0 0 0 0 0 0 0 0 0; mso-font-alt:Cambria; mso-font-charset:77; mso-generic-font-family:auto; mso-font-formatther; mso-font-pitch:auto; mso-font-signature:3 0 0 0 1 0;} /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-parent:""; margin-top:0cm; margin-right:0cm; margin-bottom:10.0pt; margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:Cambria; mso-fareast-theme-font:minor-latin; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:"Times New Roman"; mso-bidi-theme-font:minor-bidi;} @page Section1 {size:595.0pt 842.0pt; margin:72.0pt 90.0pt 72.0pt 90.0pt; mso-header-margin:35.4pt; mso-footer-margin:35.4pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> </style> <!--[if gte mso 10]> <style> /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-parent:""; mso-padding-alt:0cm 5.4pt 0cm 5.4pt; mso-para-margin-top:0cm; mso-para-margin-right:0cm; mso-para-margin-bottom:10.0pt; mso-para-margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin;} </style> <![endif]--> <!--StartFragment--> <o> </o>Because the translocation is reciprocal, swapping parts of two chromosomes, two different fusion genes form called BCR-ABL and ABL-BCR. The BCR-ABL fusion gene is part of the Philadelphia chromosome, and this is the one that causes CML. The encoded fusion protein, called the BCR-ABL oncoprotein, is a form of the enzyme tyrosine kinase, which is the normal product of the ABL gene. The cancer-causing form of tyrosine kinase is active for too long, which somehow turns on a cascade of signals that ultimately results in deregulated cell division and cancer. Further evidence that implicates the BCR-ABL oncoprotein in causing CML is that mice genetically modified to harbor the fusion gene develop leukemia. (The other translocated chromosome, which is mostly chromosome 9 material, includes the ABL-BCR fusion gene, which is not known by itself to affect health.)<o></o>
<!--EndFragment-->

 

[Ho Huu Tho]

#21.12
<link rel="File-List" href="file://localhost/Users/hohuutho/Library/Caches/TemporaryItems/msoclip/0/clip_filelist.xml"> <!--[if gte mso 9]><xml> <o:OfficeDocumentSettings> <o:AllowPNG/> </o:OfficeDocumentSettings> </xml><![endif]--><!--[if gte mso 9]><xml> <w:WordDocument> <w:Zoom>0</w:Zoom> <w:TrackMoves>false</w:TrackMoves> <w:TrackFormatting/> <wunctuationKerning/> <wrawingGridHorizontalSpacing>18 pt</wrawingGridHorizontalSpacing> <wrawingGridVerticalSpacing>18 pt</wrawingGridVerticalSpacing> <wisplayHorizontalDrawingGridEvery>0</wisplayHorizontalDrawingGridEvery> <wisplayVerticalDrawingGridEvery>0</wisplayVerticalDrawingGridEvery> <w:ValidateAgainstSchemas/> <w:SaveIfXMLInvalid>false</w:SaveIfXMLInvalid> <w:IgnoreMixedContent>false</w:IgnoreMixedContent> <w:AlwaysShowPlaceholderText>false</w:AlwaysShowPlaceholderText> <w:Compatibility> <w:BreakWrappedTables/> <wontGrowAutofit/> <wontAutofitConstrainedTables/> <wontVertAlignInTxbx/> </w:Compatibility> </w:WordDocument> </xml><![endif]--><!--[if gte mso 9]><xml> <w:LatentStyles DefLockedState="false" LatentStyleCount="276"> </w:LatentStyles> </xml><![endif]--> <style> <!-- /* Font Definitions */ @font-face {font-family:Arial; panose-1:2 11 6 4 2 2 2 2 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:Cambria; panose-1:2 4 5 3 5 4 6 3 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:JansonText-Roman; panose-1:0 0 0 0 0 0 0 0 0 0; mso-font-alt:Cambria; mso-font-charset:77; mso-generic-font-family:auto; mso-font-formatther; mso-font-pitch:auto; mso-font-signature:3 0 0 0 1 0;} /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-parent:""; margin-top:0cm; margin-right:0cm; margin-bottom:10.0pt; margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:Cambria; mso-fareast-theme-font:minor-latin; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:"Times New Roman"; mso-bidi-theme-font:minor-bidi;} @page Section1 {size:595.0pt 842.0pt; margin:72.0pt 90.0pt 72.0pt 90.0pt; mso-header-margin:35.4pt; mso-footer-margin:35.4pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> </style> <!--[if gte mso 10]> <style> /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-parent:""; mso-padding-alt:0cm 5.4pt 0cm 5.4pt; mso-para-margin-top:0cm; mso-para-margin-right:0cm; mso-para-margin-bottom:10.0pt; mso-para-margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin;} </style> <![endif]--> <!--StartFragment--> Because the translocation is reciprocal, swapping parts of two chromosomes, two different fusion genes form called BCR-ABL and ABL-BCR. The BCR-ABL fusion gene is part of the Philadelphia chromosome, and this is the one that causes CML. The encoded fusion protein, called the BCR-ABL oncoprotein, is a form of the enzyme tyrosine kinase, which is the normal product of the ABL gene. The cancer-causing form of tyrosine kinase is active for too long, which somehow turns on a cascade of signals that ultimately results in deregulated cell division and cancer. Further evidence that implicates the BCR-ABL oncoprotein in causing CML is that mice genetically modified to harbor the fusion gene develop leukemia. (The other translocated chromosome, which is mostly chromosome 9 material, includes the ABL-BCR fusion gene, which is not known by itself to affect health.)

Do sự chuyển đoạn có tính giao hoán, nghĩa là hoán đổi các phần của hai nhiễm sắc thể, nên có hai gen tiếp hợp khác nhau được tạo thành có tên gọi là BCR-ABL và ABL-BCR. Gen tiếp hợp BCR-ABL là một phần của nhiễm sắc thể Philadelphia và đây là một nguyên nhân gây ra bệnh CML. Protein tiếp hợp được mã hóa có tên gọi là protein sinh ung thư BCR-ABL, một dạng enzym tyrosin kinase, nó là sản phẩm bình thường của gen ABL. Dạng gây ra ung thư của tyrosin kinase ở trạng thái hoạt hóa trong thời gian quá dài, điều đó bằng cách này hay cách khác khởi động dây chuyền các tín hiệu để cuối cùng dẫn đến sự phân bào không kiểm soát được và ung thư. Bằng chứng sâu hơn cho thấy protein sinh ung thư BCR-ABL tham gia gây bệnh CML là những con chuột nhắt biến đổi gen có chứa gen tiếp hợp đã bị bệnh bạch cầu. (Nhiễm sắc thể bị chuyển đoạn khác chủ yếu là vật liệu của nhiễm sắc thể số 9, chứa gen tiếp hợp ABL-BCR, người ta chưa biết tự nó có ảnh hưởng đến sức khỏe hay không.)

Để tiện theo dõi, mời các bạn xem Trang chủ của topic

 

[Ho Huu Tho]

#21.13
<link rel="File-List" href="file://localhost/Users/hohuutho/Library/Caches/TemporaryItems/msoclip/0/clip_filelist.xml"> <!--[if gte mso 9]><xml> <o:OfficeDocumentSettings> <o:AllowPNG/> </o:OfficeDocumentSettings> </xml><![endif]--><!--[if gte mso 9]><xml> <w:WordDocument> <w:Zoom>0</w:Zoom> <w:TrackMoves>false</w:TrackMoves> <w:TrackFormatting/> <wunctuationKerning/> <wrawingGridHorizontalSpacing>18 pt</wrawingGridHorizontalSpacing> <wrawingGridVerticalSpacing>18 pt</wrawingGridVerticalSpacing> <wisplayHorizontalDrawingGridEvery>0</wisplayHorizontalDrawingGridEvery> <wisplayVerticalDrawingGridEvery>0</wisplayVerticalDrawingGridEvery> <w:ValidateAgainstSchemas/> <w:SaveIfXMLInvalid>false</w:SaveIfXMLInvalid> <w:IgnoreMixedContent>false</w:IgnoreMixedContent> <w:AlwaysShowPlaceholderText>false</w:AlwaysShowPlaceholderText> <w:Compatibility> <w:BreakWrappedTables/> <wontGrowAutofit/> <wontAutofitConstrainedTables/> <wontVertAlignInTxbx/> </w:Compatibility> </w:WordDocument> </xml><![endif]--><!--[if gte mso 9]><xml> <w:LatentStyles DefLockedState="false" LatentStyleCount="276"> </w:LatentStyles> </xml><![endif]--> <style> <!-- /* Font Definitions */ @font-face {font-family:Arial; panose-1:2 11 6 4 2 2 2 2 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:Cambria; panose-1:2 4 5 3 5 4 6 3 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:JansonText-Roman; panose-1:0 0 0 0 0 0 0 0 0 0; mso-font-alt:Cambria; mso-font-charset:77; mso-generic-font-family:auto; mso-font-formatther; mso-font-pitch:auto; mso-font-signature:3 0 0 0 1 0;} /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-parent:""; margin-top:0cm; margin-right:0cm; margin-bottom:10.0pt; margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:Cambria; mso-fareast-theme-font:minor-latin; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:"Times New Roman"; mso-bidi-theme-font:minor-bidi;} @page Section1 {size:595.0pt 842.0pt; margin:72.0pt 90.0pt 72.0pt 90.0pt; mso-header-margin:35.4pt; mso-footer-margin:35.4pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> </style> <!--[if gte mso 10]> <style> /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-parent:""; mso-padding-alt:0cm 5.4pt 0cm 5.4pt; mso-para-margin-top:0cm; mso-para-margin-right:0cm; mso-para-margin-bottom:10.0pt; mso-para-margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin;} </style> <![endif]--> <!--StartFragment--> <link rel="File-List" href="file://localhost/Users/hohuutho/Library/Caches/TemporaryItems/msoclip/0/clip_filelist.xml"> <!--[if gte mso 9]><xml> <o:OfficeDocumentSettings> <o:AllowPNG/> </o:OfficeDocumentSettings> </xml><![endif]--><!--[if gte mso 9]><xml> <w:WordDocument> <w:Zoom>0</w:Zoom> <w:TrackMoves>false</w:TrackMoves> <w:TrackFormatting/> <wunctuationKerning/> <wrawingGridHorizontalSpacing>18 pt</wrawingGridHorizontalSpacing> <wrawingGridVerticalSpacing>18 pt</wrawingGridVerticalSpacing> <wisplayHorizontalDrawingGridEvery>0</wisplayHorizontalDrawingGridEvery> <wisplayVerticalDrawingGridEvery>0</wisplayVerticalDrawingGridEvery> <w:ValidateAgainstSchemas/> <w:SaveIfXMLInvalid>false</w:SaveIfXMLInvalid> <w:IgnoreMixedContent>false</w:IgnoreMixedContent> <w:AlwaysShowPlaceholderText>false</w:AlwaysShowPlaceholderText> <w:Compatibility> <w:BreakWrappedTables/> <wontGrowAutofit/> <wontAutofitConstrainedTables/> <wontVertAlignInTxbx/> </w:Compatibility> </w:WordDocument> </xml><![endif]--><!--[if gte mso 9]><xml> <w:LatentStyles DefLockedState="false" LatentStyleCount="276"> </w:LatentStyles> </xml><![endif]--> <style> <!-- /* Font Definitions */ @font-face {font-family:Arial; panose-1:2 11 6 4 2 2 2 2 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:Cambria; panose-1:2 4 5 3 5 4 6 3 2 4; mso-font-charset:0; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 0 0 0 1 0;} @font-face {font-family:JansonText-Roman; panose-1:0 0 0 0 0 0 0 0 0 0; mso-font-alt:Cambria; mso-font-charset:77; mso-generic-font-family:auto; mso-font-formatther; mso-font-pitch:auto; mso-font-signature:3 0 0 0 1 0;} /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-parent:""; margin-top:0cm; margin-right:0cm; margin-bottom:10.0pt; margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:Cambria; mso-fareast-theme-font:minor-latin; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:"Times New Roman"; mso-bidi-theme-font:minor-bidi;} @page Section1 {size:595.0pt 842.0pt; margin:72.0pt 90.0pt 72.0pt 90.0pt; mso-header-margin:35.4pt; mso-footer-margin:35.4pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> </style> <!--[if gte mso 10]> <style> /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-parent:""; mso-padding-alt:0cm 5.4pt 0cm 5.4pt; mso-para-margin-top:0cm; mso-para-margin-right:0cm; mso-para-margin-bottom:10.0pt; mso-para-margin-left:0cm; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-ascii-font-family:Cambria; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Cambria; mso-hansi-theme-font:minor-latin;} </style> <![endif]--> <!--StartFragment--> The discovery that a fusion oncoprotein sets into motion the cellular changes that cause CML has led directly to a new and very promising treatment. The new drug is called signal transduction inhibitor 571, or STI571. (Existing treatment is the immune system biochemical interferon alfa, but it does not help most patients.) In 1990, Brian J. Druker, now at the Oregon Health Sciences University in Portland, proposed to a major pharmaceutical company that he design a small molecule that would lock onto the aberrant tyrosine kinase and squelch its overactivity. He knew that the tyrosine kinase must bind ATP to begin the signal cascade that causes cancer. So he synthesized the small molecule in a shape that enabled it to nestle into the pocket where ATP binds. This, he hoped, would block the signal cascade and stop the cancer.

Để tiện theo dõi, mời các bạn xem Trang chủ của topic
<!--EndFragment-->

 

[Ho Huu Tho]

#21.13
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The new drug is called signal transduction inhibitor 571, or STI571. (Existing treatment is the immune system biochemical interferon alfa, but it does not help most patients.) In 1990, Brian J. Druker, now at the Oregon Health Sciences University in Portland, proposed to a major pharmaceutical company that he design a small molecule that would lock onto the aberrant tyrosine kinase and squelch its overactivity. He knew that the tyrosine kinase must bind ATP to begin the signal cascade that causes cancer. So he synthesized the small molecule in a shape that enabled it to nestle into the pocket where ATP binds. This, he hoped, would block the signal cascade and stop the cancer.<o></o>

Khám phá về việc protein sinh ung thư loại tiếp hợp vận hành những biến đổi của tế bào để gây ra bệnh CML đã trực tiếp dẫn tới một phương pháp điều trị mới và rất triển vọng. Thuốc mới có tên gọi là yếu tố ức chế dòng tín hiệu 571 hay STI571 (Phương pháp điều trị lúc đó là interferon alfa của hệ thống miễn dịch nhưng đó không phải là biện pháp có hiệu quả với đa số bệnh nhân). Năm 1990, Brian J.Drucker, hiện làm việc tại Đại học Y khoa Oregon ở Porland, đã đề xuất với một công ty dược lớn là ông ấy thiết kế một phân tử nhỏ có thể khoá tyrosin kinase bất thường và ngăn chặn sự hoạt hoá quá mức của nó. Ông ấy biết rằng tyrosin kinase phải gắn với ATP để bắt đầu dây chuyền tín hiệu và gây ra ung thư. Bởi thế, ông ấy tổng hợp một phân tử nhỏ có hình dạng sao cho có thể chui vào cái hốc là chỗ mà ATP gắn. Ông ấy hy vọng là điều này có thể sẽ khoá dây chuyền tín hiệu và ngăn chặn bệnh ung thư.

 

[Ho Huu Tho]

#21.14
Following the usual drug discovery trajectory, Druker and his coworkers demonstrated that the molecule indeed halts the cancer in cell culture, and in mice. By 1998, STI571 was ready for phase I clinical trials, which are set up to determine safety at different dosages. In the study, 83 patients for whom interferon had not worked received doses ranging from 25 to 1000 milligrams per day (each participant received the same dose each day). Of the 54 participants who received 300 milligrams or more daily, 53 had their blood counts return to normal, and 29 of them had significantly fewer cells that had the telltale Philadelphia chromosome. In 7 participants, the unusual chromosome disappeared completely.

 

[Ho Huu Tho]

#21.14
Following the usual drug discovery trajectory, Druker and his coworkers demonstrated that the molecule indeed halts the cancer in cell culture, and in mice. By 1998, STI571 was ready for phase I clinical trials, which are set up to determine safety at different dosages. In the study, 83 patients for whom interferon had not worked received doses ranging from 25 to 1000 milligrams per day (each participant received the same dose each day). Of the 54 participants who received 300 milligrams or more daily, 53 had their blood counts return to normal, and 29 of them had significantly fewer cells that had the telltale Philadelphia chromosome. In 7 participants, the unusual chromosome disappeared completely.

Tuân thủ quy trình bình thường của nghiên cứu khám phá thuốc điều trị, Druker và cộng sự đã chứng minh được là phân tử đó thực sự kìm hãm tế bào ung thư trong môi trường nuôi cấy tế bào và trên chuột. Đến năm 1998, STI571 đã sẵn sàng cho thử nghiệm lâm sàng pha I, là pha được thiết kế để xác định tính an toàn của thuốc ở các liều khác nhau. Trong nghiên cứu đó, 83 bệnh nhân mà interferon không có tác dụng được dùng các liều từ 25 cho tới 1000 miligram mỗi ngày (mỗi người tham gia dùng liều giống nhau mỗi ngày). Trong số 54 người tham gia sử dụng liều từ 300 miligram trở lên mỗi ngày, 53 người có số lượng tế bào máu trở về bình thường và 29 người trong số đó giảm đáng kể số tế bào chứa nhiễm sắc thể Philadelphia chỉ điểm. Có 7 người nhiễm sắc thể bất thường biến mất hoàn toàn.

 

[Ho Huu Tho]

#21.15
The new drug appears to have many benefits. Side effects are minimal; the drug is taken by mouth, unlike interferon, which must be injected; response is evident by four weeks; and perhaps most important, it helps people who did not respond to the conventional treatment.

Chronic myeloid leukemia is in many ways a landmark in cancer biology. It was the first type of leukemia to be recognized, in the 1840s, and was the subject of the first chromosome-cancer link. CML was also the type of cancer that led to identification of the first oncogene fusion protein. Finally, a highly effective new treatment is in development, based on understanding the molecular events that underlie the disease. SEE ALSO Cancer; Cell Cycle; Chromosome Aberrations; Chromosome, Eukaryotic; Clinical Trials; Genetic Diseases; Mitosis; Mutation

 

[Ho Huu Tho]

#21.15
The new drug appears to have many benefits. Side effects are minimal; the drug is taken by mouth, unlike interferon, which must be injected; response is evident by four weeks; and perhaps most important, it helps people who did not respond to the conventional treatment.

Chronic myeloid leukemia is in many ways a landmark in cancer biology. It was the first type of leukemia to be recognized, in the 1840s, and was the subject of the first chromosome-cancer link. CML was also the type of cancer that led to identification of the first oncogene fusion protein. Finally, a highly effective new treatment is in development, based on understanding the molecular events that underlie the disease. SEE ALSO Cancer; Cell Cycle; Chromosome Aberrations; Chromosome, Eukaryotic; Clinical Trials; Genetic Diseases; Mitosis; Mutation

Thuốc mới có vẻ mang lại nhiều lợi ích. Tác dụng phụ rất ít; thuốc được dùng bằng đường uống, không như interferon bắt buộc phải tiêm; đáp ứng với thuốc rõ ràng trong vòng 4 tuần và có lẽ quan trọng nhất là nó phát huy tác dụng với những người không đáp ứng với phương pháp điều trị kinh điển.

Bệnh bạch cầu tuỷ mạn là bước ngoặt trong sinh học ung thư trên nhiều khía cạnh. Nó là loại bệnh bạch cầu được biết đến đầu tiên (năm 1840) và là chủ đề về mối liên hệ nhiễm sắc thể - ung thư được biết đến đầu tiên. CML cũng là loại ung thư đã dẫn đến việc xác định protein tiếp hợp của gen sinh ung thư đầu tiên. Cuối cùng, một phương pháp điều trị mới có hiệu quả cao đang được phát triển, dựa trên hiểu biết về các sự kiện phân tử cốt lõi của bệnh lý. Xem thêm: Ung thư, Chu trình tế bào, Bất thường nhiễm sắc thể, Nhiễm sắc thể, Sinh vật nhân chuẩn, Thử nghiệm lâm sàng, Bệnh di truyền, Nguyên phân, Đột biến.

 

[Ho Huu Tho]

#22. Phát tín hiệu và truyền tin

#22.1
Signaling and Signal Transduction
All cells are able to sense and respond to substances present in their external environments. For example, motile bacteria will move toward a source of sugar but away from a toxic chemical such as phenol. Cells are not only able to sense chemical substances in their environments, but also such things as heat and cold. Sudden exposure to elevated temperatures results in the synthesis of a set of proteins that protect the cell from heat damage.

 

[Ho Huu Tho]

#22.1
Signaling and Signal Transduction
All cells are able to sense and respond to substances present in their external environments. For example, motile bacteria will move toward a source of sugar but away from a toxic chemical such as phenol. Cells are not only able to sense chemical substances in their environments, but also such things as heat and cold. Sudden exposure to elevated temperatures results in the synthesis of a set of proteins that protect the cell from heat damage.

Phát tín hiệu và truyền tin
Mọi tế bào đều có khả năng cảm nhận và phản ứng lại các chất xuất hiện trong môi trường bên ngoài của chúng. Ví dụ, các vi khuẩn động sẽ di chuyển đến nơi có đường nhưng di chuyển tránh xa khỏi hóa chất độc hại chẳng hạn như phenol. Các tế bào không chỉ có khả năng cảm nhận được các chất hóa học trong môi trường của chúng mà còn có thể cảm nhận cả những thứ khác chẳng hạn như nóng và lạnh. Sự phơi nhiễm đột ngột với nhiệt độ cao sẽ dẫn đến việc tổng hợp một tập hợp các protein để bảo vệ tế bào không bị phá hủy bởi nhiệt độ.

 

[Ho Huu Tho]

#22.2
The ability to respond to external stimuli enhances a cell’s chance of survival, but in addition, especially in multicellular organisms, responding to external stimuli can be part of a cell’s moment-to-moment function. For example, nerve impulses are transmitted through the body by the action of extracellular signaling molecules called neurotransmitters. Insulin, a hormone circulating in the bloodstream, promotes the absorption of sugar into a variety of cell types. Neurotransmitters and hormones are two important examples of extracellular signaling molecules released by one cell to influence another.

 

[Ho Huu Tho]

#22.2
The ability to respond to external stimuli enhances a cell’s chance of survival, but in addition, especially in multicellular organisms, responding to external stimuli can be part of a cell’s moment-to-moment function. For example, nerve impulses are transmitted through the body by the action of extracellular signaling molecules called neurotransmitters. Insulin, a hormone circulating in the bloodstream, promotes the absorption of sugar into a variety of cell types. Neurotransmitters and hormones are two important examples of extracellular signaling molecules released by one cell to influence another.

Khả năng đáp ứng lại các kích thích bên ngoài làm tăng cơ hội sống sót của tế bào, nhưng bên cạnh đó, đặc biệt là ở các sinh vật đa bào, đáp ứng lại các kích thích bên ngoài có thể còn là một bộ phận tạo nên chức năng chớp nhoáng (???) của tế bào. Ví dụ, các xung thần kinh được truyền đi khắp cơ thể nhờ vào hoạt động của các phân tử tín hiệu ngoại bào có tên gọi là chất trung gian dẫn truyền thần kinh. Inuslin, một hoóc môn tuần hoàn trong dòng máu, thúc đẩy sự hấp thu đường của một loạt các loại tế bào. Chất trung gian dẫn truyền thần kinh và các hoóc môn là hai ví dụ quan trọng về các phân tử tín hiệu ngoại bào được giải phóng bởi một tế bào để tác động lên tế bào khác.

Để tiện theo dõi, mời các bạn xem Trang chủ của topic
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[Ho Huu Tho]

#22.3
Extracellular signaling molecules exert their effects on a cell by binding to cellular receptors. In some cases these are inside the cell, and the signaling molecule must pass through the membrane to bind with the receptor. In most cases, however, the receptor spans the plasma membrane and the signal remains outside the cell. A membrane receptor is ideally positioned to sense signals on the outside and transmit them to the cell’s interior. The binding of a signaling molecule to its receptor activates the receptor, setting off a chain of events, much like a row of falling dominoes, called a signal transduction cascade. Activation of the receptor transmits the signal (but not the signaling molecule) to the first in a series of enzymes inside the cell, which in turn activates others, until the ultimate enzyme (or enzymes) is reached that causes the final response.

The different kinds of signal transduction pathways that exist are discussed below, followed by a more detailed description of a few of those that are the best understood, and that are ubiquitous throughout the animal kingdom.

Để tiện theo dõi, mời các bạn xem Trang chủ của topic
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