Pneumatic tourniquet

A method for the contemporaneous, heterogeneously-oriented metabolic modification and/or modulation of the biochemical activity of multiple target molecules;

• wherein any combination of target molecules is selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif;
• and
• wherein said method is comprised of the administration of the sulfur-containing, amino acid-specific small molecules of the present invention in an amount sufficient to provide a therapeutic benefit to a subject suffering from one or more types of cellular metabolic anomalies or other pathophysiological conditions where there is evidence of the biochemical activities of said multiple target molecules being abnormal and the cellular metabolic modification and/or modulation of the target molecule(s) is used to treat said subject suffering from one or more cellular metabolic anomalies or other pathophysiological conditions.

A method for quantitatively ascertaining:

• (i) the level of expression of DNA, mRNA, or protein, and/or (ii) the abnormal biochemical activities of any combination of multiple target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif, in cells which have been isolated from a subject suffering from one or more types of cellular metabolic anomalies or other pathophysiological conditions where there is evidence of:
• (i) elevated levels of expression;
• and/or (ii) abnormal biochemical activities of any combination of said multiple target molecules;
• wherein said method for quantitatively ascertaining:
• (i) the level of expression of DNA, mRNA, or protein, and/or (ii) the abnormal biochemical activities of any combination of said multiple target molecules is selected from the group consisting of:
• (a) fluorescence in situ hybridization (FISH), nucleic acid microarray analysis, immunohistochemistry (IHC), radioimmunoassay (RIA), quantitative immunofluorescence and/or automated quantitative analysis (e.g., Genoptix's AQUA);
• (b) ELISA approaches including, but not limited to, high-throughput ELISA, InCell ELISAs, or quantitative western analyses (e.g., Licor and related systems), and related ELISA methodologies, and flow cytometry-based analyses (e.g., Affymetrix's Luminex assay and related approaches);
• (c) PCR coupled with MS approaches including, but not limited to, MALDI-TOF MS (e.g., Sequenom's MassARRAY system and related approaches);
• (d) mass spectroscopy based methods including, but not limited to, NanoLC coupled with ESI-MS (e.g., Bruker Daltonics/Eksigent Technologies system and related approaches), LC-MS, LC-MS/MS, and other MS systems designed to generate accurate-mass, high-resolution data on heterogeneous samples;
• and (e) isoelectric focusing, agarose/polyacrylamide gel electrophoresis, Southern blotting, Western blotting, Northern blotting, enzyme/substrate activity assay, X-ray crystallography, and other related analytic methodologies.

A contemporaneous, heterogeneously-oriented method to metabolically modify and/or modulate the intracellular environment of cancer cells in a subject suffering from one or more types of cancer such that the intracellular environment of said cancer cells is made more amenable to the pharmacological activity of the one or more chemotherapeutic, cytotoxic, or cytostatic agent(s) administered to treat the subject's cancer;

• wherein said method is comprised of the administration of an amount of the sulfur-containing, amino acid-specific small molecules of the present invention sufficient to metabolically modify and/or modulate the intracellular environment of cancer cells in said subject suffering from one or more types of cancer;
• and
• wherein said cancer exhibits evidence of:
• (i) abnormal biochemical activity and/or (ii) abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif.

A contemporaneous, heterogeneously-oriented method to metabolically modify and/or modulate the intracellular environment of cells in a subject suffering from one or more types of non-cancerous, cellular metabolic anomalies or other pathophysiological conditions such that the intracellular environment of said cells is made more amenable to the pharmacological activity of one or more medicinal agent(s) administered to treat the subject's non-cancerous, cellular metabolic anomalies or other pathophysiological conditions;

• wherein said method is comprised of the administration of an amount of the sulfur-containing, amino acid-specific small molecules of the present invention sufficient to metabolically modify and/or modulate the intracellular environment of cells in said subject suffering from one or more types of non-cancerous, cellular metabolic anomalies or other pathophysiological conditions;
• and
• wherein said non-cancerous, cellular metabolic anomalies or other pathophysiological conditions exhibit evidence of:
• (i) abnormal biochemical activity and/or (ii) abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif.

A method for quantitatively ascertaining:

• (i) the level of expression of DNA, mRNA, or protein, and/or (ii) the abnormal biochemical activities of any combination of multiple target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif, in cells which have been isolated from a subject suffering from one or more types of cancer or one or more types of non-cancerous, cellular metabolic anomalies or other pathophysiological conditions where there is evidence of:
• (i) abnormal levels of expression;
• and/or (ii) abnormal biochemical activities of any combination of said multiple target molecules;
• wherein said method for quantitatively ascertaining:
• (i) the abnormal level of expression of DNA, mRNA, or protein, and/or (ii) the abnormal biochemical activities of any combination of said multiple target molecules is selected from the group consisting of:
• (a) fluorescence in situ hybridization (FISH), nucleic acid microarray analysis, immunohistochemistry (IHC), radioimmunoassay (RIA), quantitative immunofluorescence and/or automated quantitative analysis (e.g., Genoptix's AQUA);
• (b) ELISA approaches including, but not limited to, high-throughput ELISA, InCell ELISAs, or quantitative western analyses (e.g., Licor and related systems), and related ELISA methodologies, and flow cytometry-based analyses (e.g., Affymetrix's Luminex assay and related approaches);
• (c) PCR coupled with MS approaches including, but not limited to, MALDI-TOF MS (e.g., Sequenom's MassARRAY system and related approaches);
• (d) mass spectroscopy based methods including, but not limited to, NanoLC coupled with ESI-MS (e.g., Bruker Daltonics/Eksigent Technologies system and related approaches), LC-MS, LC-MS/MS, and other MS systems designed to generate accurate-mass, high-resolution data on heterogeneous samples;
• and (e) isoelectric focusing, agarose/polyacrylamide gel electrophoresis, Southern blotting, Western blotting, Northern blotting, enzyme/substrate activity assay, X-ray crystallography, and other related analytic methodologies.

A contemporaneous, heterogeneously-oriented method for treating a subject suffering from one or more types of cancer where a contemporaneous, heterogeneously-oriented, multiple targeted, molecular-directed treatment regimen is pharmacologically-effective in overcoming cellular metabolic resistance to treatment in a subject with one or more types of cancer;

• wherein such cellular metabolic resistance to treatment is associated with the cancer cells exhibiting evidence of:
• (i) abnormal biochemical activity and/or (ii) abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif;
• and wherein said method is comprised of the administration of an amount of the sulfur-containing, amino acid-specific small molecules of the present invention sufficient to overcome the cellular metabolic resistance to treatment in said subject with one or more types of cancer.

A contemporaneous, heterogeneously-oriented method for treating a subject suffering from one or more types of cellular metabolic anomalies or other pathophysiological conditions where a contemporaneous, heterogeneously-oriented multiple targeted, molecular-directed treatment regimen is pharmacologically-effective in overcoming cellular metabolic resistance to treatment in a subject with one or more types of cellular metabolic anomalies or other pathophysiological conditions;

• wherein such cellular metabolic resistance to treatment is associated with exhibiting evidence of:
• (i) abnormal biochemical activity and/or (ii) abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif;
• and wherein said method is comprised of the administration of an amount of the sulfur-containing, amino acid-specific small molecules of the present invention sufficient to overcome the cellular metabolic resistance to treatment in said subject with one or more types of cellular metabolic anomalies or other pathophysiological conditions.

A method for quantitatively ascertaining:

• (i) the level of expression of DNA, mRNA, or protein, and/or (ii) the abnormal biochemical activities of any combination of multiple target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif, in cells which have been isolated from a subject suffering from one or more types of cancer or one or more types of non-cancerous, cellular metabolic anomalies or other pathophysiological conditions where there is evidence of:
• (i) abnormal levels of expression;
• and/or (ii) abnormal biochemical activities of any combination of said multiple target molecules;
• wherein said method for quantitatively ascertaining:
• (i) the level of expression of DNA, mRNA, or protein, and/or (ii) the abnormal biochemical activities of any combination of said multiple target molecules is selected from the group consisting of:
• (a) fluorescence in situ hybridization (FISH), nucleic acid microarray analysis, immunohistochemistry (IHC), radioimmunoassay (RIA), quantitative immunofluorescence and/or automated quantitative analysis (e.g., Genoptix's AQUA);
• (b) ELISA approaches including, but not limited to, high-throughput ELISA, InCell ELISAs, or quantitative western analyses (e.g., Licor and related systems), and related ELISA methodologies, and flow cytometry-based analyses (e.g., Affymetrix's Luminex assay and related approaches);
• (c) PCR coupled with MS approaches including, but not limited to, MALDI-TOF MS (e.g., Sequenom's MassARRAY system and related approaches);
• (d) mass spectroscopy based methods including, but not limited to, NanoLC coupled with ESI-MS (e.g., Bruker Daltonics/Eksigent Technologies system and related approaches), LC-MS, LC-MS/MS, and other MS systems designed to generate accurate-mass, high-resolution data on heterogeneous samples;
• and (e) isoelectric focusing, agarose/polyacrylamide gel electrophoresis, Southern blotting, Western blotting, Northern blotting, enzyme/substrate activity assay, X-ray crystallography, and other related analytic methodologies.

A method to determine the dosage of the sulfur-containing, amino acid-specific small molecules of the present invention required to be administered to provide the maximal therapeutic benefit to a subject with one or more types of cancer that exhibit evidence of:

• (i) abnormal biochemical activity and/or (ii) abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif;
• wherein said method is comprised of quantitatively determining:
• (i) the abnormal biochemical activity and/or (ii) the abnormal expression of any combination of said target molecules and then using the results obtained to select the amount of the sulfur-containing, amino acid-specific small molecules of the present invention to administer to provide a therapeutic benefit to said subject in need thereof;
• and
• wherein said method for quantitatively ascertaining the amount of the sulfur-containing, amino acid-specific small molecules of the present invention required to be administered to provide the maximal therapeutic benefit to a subject with one or more types of cancer that exhibit evidence of:
• (i) abnormal biochemical activity and/or (ii) abnormal expression of any combination of target molecules is selected from the group consisting of:
• (a) fluorescence in situ hybridization (FISH), nucleic acid microarray analysis, immunohistochemistry (IHC), radioimmunoassay (RIA), quantitative immunofluorescence and/or automated quantitative analysis (e.g., Genoptix's AQUA);
• (b) ELISA approaches including, but not limited to, high-throughput ELISA, InCell ELISAs, or quantitative western analyses (e.g., Licor and related systems), and related ELISA methodologies, and flow cytometry-based analyses (e.g., Affymetrix's Luminex assay and related approaches);
• (c) PCR coupled with MS approaches including, but not limited to, MALDI-TOF MS (e.g., Sequenom's MassARRAY system and related approaches);
• (d) mass spectroscopy based methods including, but not limited to, NanoLC coupled with ESI-MS (e.g., Bruker Daltonics/Eksigent Technologies system and related approaches), LC-MS, LC-MS/MS, and other MS systems designed to generate accurate-mass, high-resolution data on heterogeneous samples;
• and (e) isoelectric focusing, agarose/polyacrylamide gel electrophoresis, Southern blotting, Western blotting, Northern blotting, enzyme/substrate activity assay, X-ray crystallography, and other related analytic methodologies. (a) fluorescence in situ hybridization (FISH), nucleic acid microarray analysis, immunohistochemistry (IHC), radioimmunoassay (RIA), quantitative immunofluorescence and/or automated quantitative analysis (e.g., Genoptix's AQUA);
• (b) ELISA approaches including, but not limited to, high-throughput ELISA, InCell ELISAs, or quantitative western analyses (e.g., Licor and related systems), and related ELISA methodologies, and flow cytometry-based analyses (e.g., Affymetrix's Luminex assay and related approaches);
• (c) PCR coupled with MS approaches including, but not limited to, MALDI-TOF MS (e.g., Sequenom's MassARRAY system and related approaches);
• (d) mass spectroscopy based methods including, but not limited to, NanoLC coupled with ESI-MS (e.g., Bruker Daltonics/Eksigent Technologies system and related approaches), LC-MS, LC-MS/MS, and other MS systems designed to generate accurate-mass, high-resolution data on heterogeneous samples;
• and (e) isoelectric focusing, agarose/polyacrylamide gel electrophoresis, Southern blotting, Western blotting, Northern blotting, enzyme/substrate activity assay, X-ray crystallography, and other related analytic methodologies.

A method to determine the dosage of the sulfur-containing, amino acid-specific small molecules of the present invention required to be administered to provide the maximal therapeutic benefit to a subject with one or more types of cellular metabolic anomalies or other undesirable physiological conditions that exhibit evidence of:

• (i) abnormal biochemical activity and/or (ii) abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif;
• wherein said method is comprised of quantitatively determining (i) the abnormal biochemical activity and/or (ii) the abnormal expression of any combination of said target molecules and then using the results obtained to select the amount of the sulfur-containing, amino acid-specific small molecules of the present invention to administer to provide a therapeutic benefit to said subject in need thereof;
• and
• wherein said method for quantitatively ascertaining the amount of the sulfur-containing, amino acid-specific small molecules of the present invention required to be administered to provide the maximal therapeutic benefit to a subject with one or more types of cellular metabolic anomalies or other undesirable physiological conditions that exhibit evidence of:
• (i) abnormal biochemical activity and/or (ii) abnormal expression of any combination of target molecules selected from the group consisting of:
• (a) fluorescence in situ hybridization (FISH), nucleic acid microarray analysis, immunohistochemistry (IHC), radioimmunoassay (RIA), quantitative immunofluorescence and/or automated quantitative analysis (e.g., Genoptix's AQUA);
• (b) ELISA approaches including, but not limited to, high-throughput ELISA, InCell ELISAs, or quantitative western analyses (e.g., Licor and related systems), and related ELISA methodologies, and flow cytometry-based analyses (e.g., Affymetrix's Luminex assay and related approaches);
• (c) PCR coupled with MS approaches including, but not limited to, MALDI-TOF MS (e.g., Sequenom's MassARRAY system and related approaches);
• (d) mass spectroscopy based methods including, but not limited to, NanoLC coupled with ESI-MS (e.g., Bruker Daltonics/Eksigent Technologies system and related approaches), LC-MS, LC-MS/MS, and other MS systems designed to generate accurate-mass, high-resolution data on heterogeneous samples;
• and (e) isoelectric focusing, agarose/polyacrylamide gel electrophoresis, Southern blotting, Western blotting, Northern blotting, enzyme/substrate activity assay, X-ray crystallography, and other related analytic methodologies. (a) fluorescence in situ hybridization (FISH), nucleic acid microarray analysis, immunohistochemistry (IHC), radioimmunoassay (RIA), quantitative immunofluorescence and/or automated quantitative analysis (e.g., Genoptix's AQUA);
• (b) ELISA approaches including, but not limited to, high-throughput ELISA, InCell ELISAs, or quantitative western analyses (e.g., Licor and related systems), and related ELISA methodologies, and flow cytometry-based analyses (e.g., Affymetrix's Luminex assay and related approaches);
• (c) PCR coupled with MS approaches including, but not limited to, MALDI-TOF MS (e.g., Sequenom's MassARRAY system and related approaches);
• (d) mass spectroscopy based methods including, but not limited to, NanoLC coupled with ESI-MS (e.g., Bruker Daltonics/Eksigent Technologies system and related approaches), LC-MS, LC-MS/MS, and other MS systems designed to generate accurate-mass, high-resolution data on heterogeneous samples;
• and (e) isoelectric focusing, agarose/polyacrylamide gel electrophoresis, Southern blotting, Western blotting, Northern blotting, enzyme/substrate activity assay, X-ray crystallography, and other related analytic methodologies.

A method for quantitatively ascertaining the amount of the sulfur-containing, amino acid-specific small molecules of the present invention required to be administered to provide the maximal therapeutic benefit to a subject with:

• (a) one or more types of cancer or (b) one or more types of non-cancerous, cellular metabolic anomalies or other undesirable physiological conditions that exhibit evidence of:
• (i) abnormal biochemical activity and/or (ii) abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif, in cells which have been isolated from said subject with:
• (a) one or more types of cancer or (b) one or more types of non-cancerous, cellular metabolic anomalies or other pathophysiological conditions that exhibit evidence of:
• (i) abnormal biochemical activity;
• and/or (ii) abnormal expression of any combination of said multiple target molecules;
• of any combination of said target molecules and then using the results obtained to select the amount of the sulfur-containing, amino acid-specific small molecules of the present invention to administer to provide a therapeutic benefit to said subject in need thereof;
• wherein said method for quantitatively ascertaining the amount of the sulfur-containing, amino acid-specific small molecules of the present invention required to be administered to provide the maximal therapeutic benefit to a subject with one or more types of cellular metabolic anomalies or other undesirable physiological conditions that exhibit evidence of:
• (i) abnormal biochemical activity and/or (ii) abnormal expression of any combination of target molecules selected from the group consisting of:
• and
• wherein said method for quantitatively ascertaining the amount of the sulfur-containing, amino acid-specific small molecules of the present invention required to be administered to provide the maximal therapeutic benefit to a subject with (a) one or more types of cancer or (b) one or more types of non-cancerous, cellular metabolic anomalies or other pathophysiological conditions that exhibit evidence of:
• (i) abnormal biochemical activity;
• and/or (ii) abnormal expression of any combination of said multiple target molecules and then using the results obtained to select the amount of the sulfur-containing, amino acid-specific small molecules of the present invention to administer to provide a therapeutic benefit to said subject in need thereof;
• and
• wherein said method for quantitatively ascertaining the amount of the sulfur-containing, amino acid-specific small molecules of the present invention required to be administered to provide the maximal therapeutic benefit to a subject with (a) one or more types of cancer or (b) one or more types of non-cancerous, cellular metabolic anomalies or other pathophysiological conditions that exhibit evidence of:
• (i) abnormal biochemical activity;
• and/or (ii) abnormal expression of any combination of said multiple target molecules to a subject with one or more types of cellular metabolic anomalies or other undesirable physiological conditions that exhibit evidence of:
• (i) abnormal biochemical activity and/or (ii) abnormal expression of any combination of target molecules selected from the group consisting of:
• (a) fluorescence in situ hybridization (FISH), nucleic acid microarray analysis, immunohistochemistry (IHC), radioimmunoassay (RIA), quantitative immunofluorescence and/or automated quantitative analysis (e.g., Genoptix's AQUA);
• (b) ELISA approaches including, but not limited to, high-throughput ELISA, InCell ELISAs, or quantitative western analyses (e.g., Licor and related systems), and related ELISA methodologies, and flow cytometry-based analyses (e.g., Affymetrix's Luminex assay and related approaches);
• (c) PCR coupled with MS approaches including, but not limited to, MALDI-TOF MS (e.g., Sequenom's MassARRAY system and related approaches);
• (d) mass spectroscopy based methods including, but not limited to, NanoLC coupled with ESI-MS (e.g., Bruker Daltonics/Eksigent Technologies system and related approaches), LC-MS, LC-MS/MS, and other MS systems designed to generate accurate-mass, high-resolution data on heterogeneous samples;
• and (e) isoelectric focusing, agarose/polyacrylamide gel electrophoresis, Southern blotting, Western blotting, Northern blotting, enzyme/substrate activity assay, X-ray crystallography, and other related analytic methodologies. (a) fluorescence in situ hybridization (FISH), nucleic acid microarray analysis, immunohistochemistry (IHC), radioimmunoassay (RIA), quantitative immunofluorescence and/or automated quantitative analysis (e.g., Genoptix's AQUA);
• (b) ELISA approaches including, but not limited to, high-throughput ELISA, InCell ELISAs, or quantitative western analyses (e.g., Licor and related systems), and related ELISA methodologies, and flow cytometry-based analyses (e.g., Affymetrix's Luminex assay and related approaches);
• (c) PCR coupled with MS approaches including, but not limited to, MALDI-TOF MS (e.g., Sequenom's MassARRAY system and related approaches);
• (d) mass spectroscopy based methods including, but not limited to, NanoLC coupled with ESI-MS (e.g., Bruker Daltonics/Eksigent Technologies system and related approaches), LC-MS, LC-MS/MS, and other MS systems designed to generate accurate-mass, high-resolution data on heterogeneous samples;
• and (e) isoelectric focusing, agarose/polyacrylamide gel electrophoresis, Southern blotting, Western blotting, Northern blotting, enzyme/substrate activity assay, X-ray crystallography, and other related analytic methodologies.

A method for use in:

• (a) the selection of subjects for treatment;
• (b) the determination of the most effective cancer treating agent(s) to be administered in combination with the administration of the sulfur-containing, amino acid-specific small molecules of the present invention;
• (c) the dosage of the cancer treating agent(s) to be administered;
• (d) the determination of the length and/or number of treatment cycles;
• (e) adjustment of the specific cancer treating agent(s) used and the dosage administered during treatment;
• and/or (f) ascertaining the potential treatment responsiveness of the specific cancer to the cancer treating agent(s) selected for administration to said subject having one or more types of cancer;
• wherein said method is comprised of quantitatively determining the expression levels and/or the biochemical activity of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif, and then using this expression level and/or biochemical activity data in determining:
• (i) the specific subjects to be treated;
• (ii) the cancer treating agent(s) to be administered in combination with the administration of the sulfur-containing, amino acid-specific small molecules of the present invention;
• (iii) the dosage of the cancer treating agent(s) to be administered;
• (iv) the length and/or number of cancer treating cycles to be administered;
• (v) the adjustment of the specific cancer treating agent(s) used and the dosages administered during the treatment regimen;
• and/or (vi) ascertaining the potential treatment responsiveness of the specific cancer to the cancer treating agents (s) selected to be administered to said subject having one or more types of cancer;
• and
• wherein the method for quantitatively determining the dosage of the most effective chemotherapeutic agent(s) and the sulfur-containing, amino acid-specific small molecules of the present invention required to be administered to provide the maximal therapeutic benefit to a subject with one or more types of cancer that exhibits evidence of abnormal biochemical activity and/or abnormal expression of any combination of said multiple target molecules is selected from the group consisting of:
• (a) fluorescence in situ hybridization (FISH), nucleic acid microarray analysis, immunohistochemistry (IHC), radioimmunoassay (RIA), quantitative immunofluorescence and/or automated quantitative analysis (e.g., Genoptix's AQUA);
• (b) ELISA approaches including, but not limited to, high-throughput ELISA, InCell ELISAs, or quantitative western analyses (e.g., Licor and related systems), and related ELISA methodologies, and flow cytometry-based analyses (e.g., Affymetrix's Luminex assay and related approaches);
• (c) PCR coupled with MS approaches including, but not limited to, MALDI-TOF MS (e.g., Sequenom's MassARRAY system and related approaches);
• (d) mass spectroscopy based methods including, but not limited to, NanoLC coupled with ESI-MS (e.g., Bruker Daltonics/Eksigent Technologies system and related approaches), LC-MS, LC-MS/MS, and other MS systems designed to generate accurate-mass, high-resolution data on heterogeneous samples;
• and (e) isoelectric focusing, agarose/polyacrylamide gel electrophoresis, Southern blotting, Western blotting, Northern blotting, enzyme/substrate activity assay, X-ray crystallography, and other related analytic methodologies.

A method for use in:

• (a) the selection of specific subjects for treatment;
• (b) the determination of the most effective medicinal agent(s) in combination with the administration of the sulfur-containing, amino acid-specific small molecules of the present invention;
• (c) the selection of the dosage of the medicinal agent(s) to be administered;
• (d) the determination of the length and/or number of treatment cycles to be administered;
• (e) adjustment of the specific medicinal agent(s) used and the dosages administered during treatment;
• and/or (f) ascertaining the potential treatment responsiveness of the specific disease to the medicinal agents(s) selected to be administered to a subject having one or more types of non-cancerous, cellular metabolic anomalies or other pathophysiological conditions;
• wherein said method is comprised of quantitatively determining the expression levels and/or biochemical activity of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif, and then using this expression level and/or biochemical activity data in determining:
• (i) the specific subjects to be treated;
• (ii) the medicinal agent(s) to be administered in combination with the administration of the sulfur-containing, amino acid-specific small molecules of the present invention;
• (iii) determining the dosage of the medicinal agent(s) to be administered;
• (iv) the length and/or number of treatment cycles to be administered;
• (v) the adjustment of the specific medicinal agent(s) administered and the dosages administered during treatment regimen;
• and/or (vi) ascertaining the potential treatment responsiveness of the specific disease to the medicinal agents (s) selected to be administered to said subject having one or more types of cellular metabolic anomalies or other pathophysiological conditions;
• and
• wherein the method for quantitatively determining the dosages of the most effective medicinal agent(s) and the sulfur-containing, amino acid-specific small molecules of the present invention required to be administered to provide the maximal therapeutic benefit to said subject with one or more types of non-cancerous, cellular metabolic anomalies or other undesirable physiological conditions that exhibit evidence of abnormal biochemical activity and/or abnormal expression of any combination of said multiple target molecules is selected from the group consisting of:
• (a) fluorescence in situ hybridization (FISH), nucleic acid microarray analysis, immunohistochemistry (IHC), radioimmunoassay (RIA), quantitative immunofluorescence and/or automated quantitative analysis (e.g., Genoptix's AQUA);
• (b) ELISA approaches including, but not limited to, high-throughput ELISA, InCell ELISAs, or quantitative western analyses (e.g., Licor and related systems), and related ELISA methodologies, and flow cytometry-based analyses (e.g., Affymetrix's Luminex assay and related approaches);
• (c) PCR coupled with MS approaches including, but not limited to, MALDI-TOF MS (e.g., Sequenom's MassARRAY system and related approaches);
• (d) mass spectroscopy based methods including, but not limited to, NanoLC coupled with ESI-MS (e.g., Bruker Daltonics/Eksigent Technologies system and related approaches), LC-MS, LC-MS/MS, and other MS systems designed to generate accurate-mass, high-resolution data on heterogeneous samples;
• and (e) isoelectric focusing, agarose/polyacrylamide gel electrophoresis, Southern blotting, Western blotting, Northern blotting, enzyme/substrate activity assay, X-ray crystallography, and other related analytic methodologies.

A contemporaneous, heterogeneously-oriented method for maximizing or extending the length of time before there is cancer progression in a subject who has one or more types of cancers that exhibit evidence of:

• (i) abnormal biochemical activity and/or (ii) abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif;
• wherein said method comprises the administration of the sulfur-containing, amino acid-specific small molecules of the present invention which function to delay the reoccurrence and/or progression of said cancer or cancers in the subject by modifying and/or modulating:
• (i) the abnormal biochemical activity and/or (ii) the abnormal expression of any combination of said target molecules.

A kit for use in the treatment of a subject having one or more cancers that are resistant to the cancer treating agent or agents being used to treat said subject with cancer, wherein said cancers are any cancer which exhibits evidence of:

• (i) abnormal biochemical activity and/or (ii) abnormal expression of one or more target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and/or other target protein (possessing a similar active site or structural motif)-mediated resistance to the chemotherapeutic agent or agents being used to treat said subject with cancer;
• wherein said kit comprises:
• (a) one or more cancer treating agents;
• (b) the sulfur-containing, amino acid-specific small molecules of the present invention;
• and (c) instructions for administering said cancer treating agents and the sulfur-containing, amino acid-specific small molecules of the present invention to a subject with one or more types of cancer which are resistant to the chemotherapeutic agent or agents being used to treat said subject with cancer.

A kit for use in the treatment of a subject having one or more cancers that are resistant to the cancer treating agent or agents being used to treat said subject with cancer, wherein said cancers are any cancer which exhibit evidence of:

• (i) abnormal expression of and/or (ii) abnormal biochemical activity in the target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and/or other target proteins possessing a similar active site or structural motif-mediated resistance to the cancer treating agent or agents being used to treat said subject with cancer;
• wherein said kit comprises:
• (a) one or more cancer treating agents;
• (b) the sulfur-containing, amino acid-specific small molecules of the present invention;
• and (c) instructions for administering said cancer treating agent(s) and the sulfur-containing, amino acid-specific small molecules of the present invention to a subject with one or more types of cancer which are resistant to the cancer treating agent or agents being used to treat said subject with cancer.

A cancer treating agent which modifies and/or modulates the expression levels and/or biochemical activity of one or more of the target molecules selected from the group consisting of:

• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif;
• wherein said cancer treating agent is the sulfur-containing, amino acid-specific small molecules of the present invention administered in an amount sufficient to provide a therapeutic benefit to a subject having one or more types of cancer which exhibit evidence of:
• (i) the abnormal expression level;
• and/or (ii) the abnormal biochemical activity of one or more of said target molecules;
• and wherein the abnormal expression level and/or the abnormal biochemical activity of said target molecules must be modified and/or modulated in order to treat said subject having one or more types of cancer.

A medicament which modifies and/or modulates the expression levels and/or biochemical activity of one or more of the target molecules selected from the group consisting of:

• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif;
• wherein said medicament is the sulfur-containing, amino acid-specific small molecules of the present invention administered in an amount sufficient to provide a therapeutic benefit to a subject having one or more types of cellular metabolic anomalies or other undesirable physiological conditions which exhibit evidence of:
• (i) the abnormal expression level;
• and/or (ii) the abnormal biochemical activity of one or more of said target molecules;
• and wherein the abnormal expression level and/or the abnormal biochemical activity of said target molecules must be modified and/or modulated in order to treat said subject having one or more cellular metabolic anomalies or other undesirable physiological conditions.

A method for the prophylactic use of the sulfur-containing, amino acid-specific small molecules of the present invention administered in an amount sufficient to provide a prophylactic benefit to a subject who has previously suffered from one or more types of cancers that exhibited evidence of:

• (i) abnormal biochemical activity and/or (ii) abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif;
• wherein the sulfur-containing, amino acid-specific small molecules of the present invention function to mitigate or prevent the reoccurrence of said cancer or cancers in said subject by modifying and/or modulating:
• (i) the abnormal biochemical activity and/or (ii) the abnormal expression of any combination of said target molecules.

A method for the prophylactic use of the sulfur-containing, amino acid-specific small molecules of the present invention administered in an amount sufficient to provide a prophylactic benefit to a subject who has previously suffered from one or more types of cellular metabolic anomalies or other undesirable physiological conditions that exhibited evidence of:

• (i) abnormal biochemical activity and/or (ii) abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif;
• wherein the sulfur-containing, amino acid-specific small molecules of the present invention function to mitigate or prevent the reoccurrence of said cellular metabolic anomalies or other undesirable physiological conditions in said subject by modifying and/or modulating:
• (i) the abnormal biochemical activity and/or (ii) the abnormal expression of any combination of said target molecules.

A method for the maintenance of a subject, who has one or more cancers, in a constant, steady physiological state such that said cancer(s) do not progress;

• wherein said method is comprised of the contemporaneous, heterogeneously-oriented metabolic modification and/or modulation of:
• (i) the expression level and/or (ii) the biochemical function of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif;
• and wherein the method is comprised of the administration of the sulfur-containing, amino acid-specific small molecules of the present invention in an amount sufficient to provide the maximal therapeutic benefit to a subject having one or more types of cancer which exhibit evidence of the expression level and/or biochemical function of one or more target molecules being abnormal;
• and wherein metabolic modification and/or modulation of the target molecule(s) exhibiting evidence of:
• (i) abnormal expression level and/or (ii) abnormal biochemical function is used to treat said subject in need thereof.

A method for the formation of adducts comprising the covalent-binding of one or more sulfur-containing, amino acid-specific small molecules of the present invention to one or more cysteine amino acid residues within a target molecule selected from the group consisting of:

• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif;
• wherein said adduct formation comprising the covalent-binding of one or more sulfur-containing, amino acid-specific small molecules of the present invention to one or more cysteine amino acid residues within said target molecule(s) has the ability to modify and/or modulate abnormal expression and/or biochemical activity of said target molecule(s) so as to provide a therapeutic benefit to a subject with one or more types of cellular metabolic anomalies or other undesirable physiological conditions that exhibit evidence of:
• (i) abnormal biochemical activity and/or (ii) abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), tubulin, and other target molecules possessing a similar active site or structural motif.

A method for quantitatively determining the level of DNA, mRNA, and/or protein of a target molecule selected from the group consisting of:

• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif, in cells which have been isolated from a patient who has been already been diagnosed or is suspected of having a non-cancerous cellular metabolic anomaly or other undesirable physiological condition;
• wherein the method used to quantitatively determine the levels of the DNA, mRNA, and/or protein of a target molecule(s) is selected from the group consisting of:
• (a) fluorescence in situ hybridization (FISH), nucleic acid microarray analysis, immunohistochemistry (IHC), radioimmunoassay (RIA), quantitative immunofluorescence and/or automated quantitative analysis (e.g., Genoptix's AQUA);
• (b) ELISA approaches including, but not limited to, high-throughput ELISA, InCell ELISAs, or quantitative western analyses (e.g., Licor and related systems), and related ELISA methodologies, and flow cytometry-based analyses (e.g., Affymetrix's Luminex assay and related approaches);
• (c) PCR coupled with MS approaches including, but not limited to, MALDI-TOF MS (e.g., Sequenom's MassARRAY system and related approaches);
• (d) mass spectroscopy based methods including, but not limited to, NanoLC coupled with ESI-MS (e.g., Bruker Daltonics/Eksigent Technologies system and related approaches), LC-MS, LC-MS/MS, and other MS systems designed to generate accurate-mass, high-resolution data on heterogeneous samples;
• and (e) isoelectric focusing, agarose/polyacrylamide gel electrophoresis, Southern blotting, Western blotting, Northern blotting, enzyme/substrate activity assay, X-ray crystallography, and other related analytic methodologies.

A method for quantitatively determining the level of DNA, mRNA, and/or protein of a target molecule selected from the group consisting of:

• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), ribonucleotide reductase, tubulin, farnesyltransferase, and other target molecules possessing a similar active site or structural motif, in cells which have been isolated from a patient who has already been diagnosed with cancer or is suspected of having cancer;
• wherein the method used to quantitatively determine the levels of the DNA, mRNA, and/or protein of a target molecule(s) is selected from the group consisting of:
• (a) fluorescence in situ hybridization (FISH), nucleic acid microarray analysis, immunohistochemistry (IHC), radioimmunoassay (RIA), quantitative immunofluorescence and/or automated quantitative analysis (e.g., Genoptix's AQUA);
• (b) ELISA approaches including, but not limited to, high-throughput ELISA, InCell ELISAs, or quantitative western analyses (e.g., Licor and related systems), and related ELISA methodologies, and flow cytometry-based analyses (e.g., Affymetrix's Luminex assay and related approaches);
• (c) PCR coupled with MS approaches including, but not limited to, MALDI-TOF MS (e.g., Sequenom's MassARRAY system and related approaches);
• (d) mass spectroscopy based methods including, but not limited to, NanoLC coupled with ESI-MS (e.g., Bruker Daltonics/Eksigent Technologies system and related approaches), LC-MS, LC-MS/MS, and other MS systems designed to generate accurate-mass, high-resolution data on heterogeneous samples;
• and (e) isoelectric focusing, agarose/polyacrylamide gel electrophoresis, Southern blotting, Western blotting, Northern blotting, enzyme/substrate activity assay, X-ray crystallography, and other related analytic methodologies.

A method for improving biological system stability by altering the level of non-clonal chromosomal aberrations (NCCAs) in a subject having one or more types of cellular metabolic anomalies or other pathophysiological conditions, including cancer;

• wherein the relative level of non-clonal chromosomal aberrations (NCCAs) is impacted by:
• (i) the abnormal biochemical activity and/or (ii) the abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), tubulin, ribonucleotide reductase (RNR), farnesyltransferase, and other target proteins possessing a similar active site or structural motif;
• and
• wherein said method is comprised of the administration of the sulfur-containing, amino acid-specific small molecules of the present invention in an amount sufficient to provide a therapeutic benefit by altering the relative level of non-clonal chromosomal aberrations (NCCAs) in the subject having one or more types of cellular metabolic anomalies or other pathophysiological conditions, including cancer.

A method for improving biological system stability in a subject with one or more types of cancer, where the system stability is altered by:

• (i) the abnormal biochemical activity and/or (ii) the abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), tubulin, ribonucleotide reductase (RNR), farnesyltransferase, and other target proteins possessing a similar active site or structural motif;
• and
• wherein said method is comprised of the administration of the sulfur-containing, amino acid-specific small molecules of the present invention in an amount sufficient to provide a therapeutic benefit by altering:
• (i) the abnormal biochemical activity and/or (ii) the abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), tubulin, ribonucleotide reductase (RNR), farnesyltransferase, and other target proteins possessing a similar active site or structural motif relative level of non-clonal chromosomal aberrations (NCCAs) in the subject having one or more types of cellular metabolic anomalies or other pathophysiological conditions, including cancer.

A method for the adjuvant treatment of a subject who has one or more types of cancer that involve:

• (i) the abnormal biochemical activity and/or (ii) the abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), tubulin, ribonucleotide reductase (RNR), farnesyltransferase, and other target proteins possessing a similar active site or structural motif;
• wherein said method is comprised of the administration of the sulfur-containing, amino acid-specific small molecules of the present invention in an amount sufficient to provide a therapeutic benefit to the subject suffering from one or more types of cancer that involve:
• (i) the abnormal biochemical activity and/or (ii) the abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), tubulin, ribonucleotide reductase (RNR), farnesyltransferase, and other target proteins possessing a similar active site or structural motif.

A method for the neo-adjuvant treatment of a subject who has one or more types of cancer that involve:

• (i) the abnormal biochemical activity and/or (ii) the abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), tubulin, ribonucleotide reductase (RNR), farnesyltransferase, and other target proteins possessing a similar active site or structural motif;
• wherein said method is comprised of the administration of the sulfur-containing, amino acid-specific small molecules of the present invention prior to the subsequent administration of the primary chemotherapeutic regimen in an amount sufficient to provide a therapeutic benefit to the subject suffering from one or more types of cancer that involve:
• (i) the abnormal biochemical activity and/or (ii) the abnormal expression of any combination of target molecules selected from the group consisting of:
• anaplastic lymphoma kinase (ALK), mesenchymal epithelial transition (MET) kinase, the receptor tyrosine kinase (ROS1), epidermal growth factor receptor (EGFR), peroxiredoxin (Prx), excision repair cross-complementing protein 1 (ERCC1), insulin growth factor 1 receptor (IGF1R), tubulin, ribonucleotide reductase (RNR), farnesyltransferase, and other target proteins possessing a similar active site or structural motif.